Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (575 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
An autoimmune disorder mainly affecting young adults and characterized by destruction of myelin in the central nervous system. Pathologic findings include multiple sharply demarcated areas of demyelination throughout the white matter of the central nervous system. Clinical manifestations include visual loss, extra-ocular movement disorders, paresthesias, loss of sensation, weakness, dysarthria, spasticity, ataxia, and bladder dysfunction. The usual pattern is one of recurrent attacks followed by partial recovery (see multiple sclerosis, relapsing-remitting), but acute fulminating and chronic progressive forms (see multiple sclerosis, chronic progressive) also occur. (Adams et al., Principles of Neurology, 6th ed, p903)
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Sclerosis, Multiple; MS (Multiple Sclerosis); Sclerosis, Disseminated; Disseminated Sclerosis; Multiple Sclerosis, Acute Fulminating.
Where it fits in the MeSH classification
- Broader topics
- Demyelinating Autoimmune Diseases, CNS
- Narrower topics
- Multiple Sclerosis, Chronic Progressive; Multiple Sclerosis, Relapsing-Remitting
- See also
- Myelitis, Transverse
Related concepts
- Multiple Sclerosis
- Relapsing-Remitting
- Chronic Progressive
Research landscape
PubMed indexes 79,296 records tagged with the MeSH heading “Multiple Sclerosis” (counts retrieved 2026-10-29). 20,414 of them (25.7%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 25,081 records.
Reviews account for 14,148 records (17.8%) and meta-analyses for 1,159. Randomized controlled trials number 2,749 (3.5%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 18,850 |
| 2000-2009 | 14,951 |
| 2010-2019 | 25,081 |
| 2020 onward | 20,414 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 14,148 | 17.8% |
| Meta-analyses | 1,159 | 1.5% |
| Randomized controlled trials | 2,749 | 3.5% |
Method: PubMed query "Multiple Sclerosis"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in neuroscience
Neuroscience draws on tools with different strengths: cellular and animal work can manipulate circuits directly, while human imaging and electrophysiology observe the living brain at lower resolution. Small imaging studies are prone to false positives, and findings in animals do not always carry over to people. Clinical neurology and psychiatry rely on trials and cohort studies whose outcomes are often symptom scales. Check the species, the sample size, how the outcome was measured and whether results were replicated.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| The exercise hormone irisin has neuroprotective effects in a mouse model of multiple sclerosis | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42168599 · DOI · PMC13218937 |
| Interaction between smoking and HLA-A*02:01 in multiple sclerosis progression | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42397838 · DOI · PMC13385633 |
| Targeting progressive multiple sclerosis: Toward mechanism-informed precision medicine | 2026 | Review article Design not recorded in structured metadata | 1 | cc by PMID 42482223 · DOI · PMC13429007 |
The exercise hormone irisin has neuroprotective effects in a mouse model of multiple sclerosis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Aerobic exercise is a disease-modifying intervention in multiple sclerosis (MS) that ameliorates several progressive neurological symptoms in people with MS.
- Closing excerpt
- Taken together, these findings suggest that irisin induction in response to exercise confers direct neuroprotective effects in an inflammation-driven neurodegenerative condition, making it an attractive therapeutic candidate for MS.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (150 words)
Aerobic exercise is a disease-modifying intervention in multiple sclerosis (MS) that ameliorates several progressive neurological symptoms in people with MS. Here we show that the exercise hormone irisin mediates neuroprotective effects of exercise in the experimental autoimmune encephalomyelitis (EAE) mouse model of MS. We demonstrate that voluntary free-wheel running exercise protects against inflammation-induced neurodegeneration in EAE, but these neuroprotective effects are abrogated in mice lacking Fndc5/irisin. Peripheral delivery of irisin increases irisin plasma levels and reduces both clinical symptoms and neuronal loss in EAE. Although peripheral irisin does not alter peripheral and central immune responses in EAE, it induces a direct neuroprotective gene programme in spinal cord neurons and preserves synapses and mitochondrial activity, probably through direct binding to motor neurons. Taken together, these findings suggest that irisin induction in response to exercise confers direct neuroprotective effects in an inflammation-driven neurodegenerative condition, making it an attractive therapeutic candidate for MS.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42168599 · DOI · PMC13218937
Interaction between smoking and HLA-A*02:01 in multiple sclerosis progression [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundGene-environment interactions between smoking and HLA genotypes have been reported in multiple sclerosis (MS) susceptibility, although their relevance beyond disease onset remains unclear.
- Closing excerpt
- ConclusionThese findings suggest that the impact of smoking on MS progression varies according to immunogenetic background.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (202 words)
BackgroundGene-environment interactions between smoking and HLA genotypes have been reported in multiple sclerosis (MS) susceptibility, although their relevance beyond disease onset remains unclear.ObjectivesTo examine whether the effect of smoking on disability progression differs according to HLA-A*02:01 and HLA-DRB1*15:01 status.MethodsPatients from two population-based case-control cohorts were classified by smoking status at diagnosis and by HLA-A*02:01 and HLA-DRB1*15:01 status and were followed for up to 15 years through the Swedish MS registry (n = 6807). Cox regression models were used to estimate hazard ratios (HRs) with 95% confidence intervals (CIs) for 24-week confirmed disability worsening (CDW) and time to Expanded Disability Status Scale (EDSS) 3, 4, and 6. Interaction was assessed on the additive scale.ResultsCompared with HLA-A*02:01-positive non-smokers, smoking at diagnosis was associated with a higher risk of disability progression primarily among individuals who lacked HLA-A*02:01, with consistently elevated risks of CDW (HR = 1.15, 95% CI = 1.06-1.26), EDSS 3 (HR = 1.26, 95% CI = 1.08-1.47), and EDSS 4 (HR = 1.50, 95% CI = 1.25-1.79). No clear effect of smoking was observed among HLA-A*02:01 carriers, and no evidence of interaction was detected between smoking and HLA-DRB1*15:01.ConclusionThese findings suggest that the impact of smoking on MS progression varies according to immunogenetic background.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42397838 · DOI · PMC13385633
Targeting progressive multiple sclerosis: Toward mechanism-informed precision medicine [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Multiple sclerosis has undergone a therapeutic revolution over the past three decades.
- Closing excerpt
- Future management will require mechanism-informed treatment algorithms that align therapeutic choice with dominant disease drivers while incorporating comorbidity management, de-escalation strategies and potential EBV-targeted preventive approaches to optimize outcomes across the entire disease course.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (223 words)
Multiple sclerosis has undergone a therapeutic revolution over the past three decades. Randomized clinical trials and real-world data demonstrate that modern disease-modifying therapies substantially reduce relapse rates and acute inflammatory activity detected by magnetic resonance imaging (MRI). However, disability accumulation increasingly occurs independent of relapse activity, highlighting progression biology as the principal unmet need. Converging epidemiological and molecular evidence supports a pivotal role for Epstein-Barr virus (EBV) infection in disease initiation, whereas later stages appear dominated by brain-intrinsic mechanisms, including compartmentalized inflammation, microglial activation, failure of remyelination and accelerated biological ageing. Population-based cohorts demonstrate that early high-efficacy therapy improves long-term outcomes, yet the risk of progression rises markedly after midlife despite effective relapse suppression. Emerging biomarkers, such as serum neurofilament light chain, glial fibrillary acidic protein, paramagnetic rim lesions and advanced quantitative MRI metrics, now enable more granular monitoring of progressive pathology. Integration of imaging, fluid biomarkers, genetics and machine learning offers opportunities for individualized benefit-risk stratification. Brain-penetrant Bruton's tyrosine kinase inhibitors, CD40 ligand-targeting biologics, refined B-cell-depleting strategies and emerging chimeric antigen receptor T-cell therapies represent promising approaches to target different aspects of compartmentalized inflammation and smoldering disease biology. Future management will require mechanism-informed treatment algorithms that align therapeutic choice with dominant disease drivers while incorporating comorbidity management, de-escalation strategies and potential EBV-targeted preventive approaches to optimize outcomes across the entire disease course.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42482223 · DOI · PMC13429007
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Disease-associated oligodendrocyte responses across neurodegenerative diseases [4]
- Research article Clinical Features of Late-Onset Multiple Sclerosis: a Systematic Review and Meta-analysis [5]
- Research article Cerebrospinal fluid kappa free light chains for the diagnosis of multiple sclerosis: A systematic review and meta-analysis [6]
- Research article The impact of aerobic and resistance training intensity on markers of neuroplasticity in health and disease [7]
- Research article Effect of home-based virtual reality training and telerehabilitation on balance in individuals with Parkinson disease, multiple sclerosis, and stroke: a systematic review and meta-analysis [8]
- Research article Is Aerobic or Resistance Training the Most Effective Exercise Modality for Improving Lower Extremity Physical Function and Perceived Fatigue in People With Multiple Sclerosis? A Systematic Review and Meta-analysis [9]
References
- Rosenkranz SC, da Rocha JF, Moreira L, Schlachter P, Bier J, Healy K, et al.. The exercise hormone irisin has neuroprotective effects in a mouse model of multiple sclerosis. . 2026. PMID 42168599 · DOI · PMC13218937
- Hedström AK, Stridh P, Hillert J, Olsson T, Alfredsson L. Interaction between smoking and HLA-A*02:01 in multiple sclerosis progression. . 2026. PMID 42397838 · DOI · PMC13385633
- Piehl F, Castelo-Branco G, Jagodic M, Olsson T. Targeting progressive multiple sclerosis: Toward mechanism-informed precision medicine. . 2026. PMID 42482223 · DOI · PMC13429007
- Pandey S, Shen K, Lee SH, Shen YA, Wang Y, Otero-García M, et al.. Disease-associated oligodendrocyte responses across neurodegenerative diseases. Cell Rep. 2022. PMID 36001972 · DOI
- Naseri A, Nasiri E, Sahraian MA, Daneshvar S, Talebi M. Clinical Features of Late-Onset Multiple Sclerosis: a Systematic Review and Meta-analysis. Mult Scler Relat Disord. 2021. PMID 33571792 · DOI
- Hegen H, Walde J, Berek K, Arrambide G, Gnanapavan S, Kaplan B, et al.. Cerebrospinal fluid kappa free light chains for the diagnosis of multiple sclerosis: A systematic review and meta-analysis. Mult Scler. 2023. PMID 36453167 · DOI · PMC9925892
- Hortobágyi T, Vetrovsky T, Balbim GM, Sorte Silva NCB, Manca A, Deriu F, et al.. The impact of aerobic and resistance training intensity on markers of neuroplasticity in health and disease. Ageing Res Rev. 2022. PMID 35853549 · DOI
- Truijen S, Abdullahi A, Bijsterbosch D, van Zoest E, Conijn M, Wang Y, et al.. Effect of home-based virtual reality training and telerehabilitation on balance in individuals with Parkinson disease, multiple sclerosis, and stroke: a systematic review and meta-analysis. Neurol Sci. 2022. PMID 35175439 · DOI · PMC9023738
- Taul-Madsen L, Connolly L, Dennett R, Freeman J, Dalgas U, Hvid LG. Is Aerobic or Resistance Training the Most Effective Exercise Modality for Improving Lower Extremity Physical Function and Perceived Fatigue in People With Multiple Sclerosis? A Systematic Review and Meta-analysis. Arch Phys Med Rehabil. 2021. PMID 33901439 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.