Evidence map›Paper›PMID 24961530›Full record

ArticleBrain sciences2013

Myelin recovery in multiple sclerosis: the challenge of remyelination.

Maria Podbielska, Naren L Banik, Ewa Kurowska, Edward L Hogan

Open access · goldAbstract read
In one paragraph

Article in Brain sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 135 citations in OpenAlex.

  1. Pooled it
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  15. Article
  16. Cladribine tablets in the new multiple sclerosis era.Therapeutic advances in neurological disorders · 2025
    Review
  17. Review
  18. Article
  19. Article
  20. Article

5 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 3 countries.

Maria PodbielskaDepartment of Neurology, Institute of Molecular Medicine and Genetics, Georgia Regents University, 1120 15th Street, Augusta, GA 30912-2620, USA. kurowska@iitd.pan.wroc.pl.
Naren L BanikDepartment of Neurosciences, Medical University of South Carolina, 171 Ashley Avenue, Charleston, SC 29425-6160, USA. baniknl@musc.edu.
Ewa KurowskaLaboratory of Signaling Proteins, Polish Academy of Sciences, Ludwik Hirszfeld Institute of Immunology & Experimental Therapy, Rudolfa Weigla 12, Wrocław 53-114, Poland. kurowska@iitd.pan.wroc.pl.
Edward L HoganDepartment of Neurology, Institute of Molecular Medicine and Genetics, Georgia Regents University, 1120 15th Street, Augusta, GA 30912-2620, USA. hoganel@musc.edu.
Ludwik Hirszfeld Institute of Immunology and Experimental Therapy · PLMedical University of South Carolina · USOllscoil na Gaillimhe – University of Galway · IE

Funding

CALPAIN ACTIVATION OF T CELLS IN DEMYELINATING DISEASER01NS041088 · NINDS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BANIK, NAREN L · 2001 to 2009
$2.9M
Attenuation of Axonal Damage and Neuronal Death in EAER01NS056176 · NINDS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BANIK, NAREN L · 2006 to 2010
$1.6M
Inflammation and Degeneration of Optic Nerve in EAER01NS065456 · NINDS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BANIK, NAREN L · 2009 to 2013
$1.6M
CALPAIN IN THE PATHOPHYSIOLOGY OF DEMYELINATING DISEASER01NS038146 · NINDS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BANIK, NAREN L · 1999 to 2003
$918k
NINDS NIH HHS R01 NS038146NINDS NIH HHS R01 NS041088NINDS NIH HHS R01 NS056176NINDS NIH HHS R01 NS065456
6 · The paper itself

Abstract

Multiple sclerosis (MS) is the most common demyelinating and an autoimmune disease of the central nervous system characterized by immune-mediated myelin and axonal damage, and chronic axonal loss attributable to the absence of myelin sheaths. T cell subsets (Th1, Th2, Th17, CD8+, NKT, CD4+CD25+ T regulatory cells) and B cells are involved in this disorder, thus new MS therapies seek damage prevention by resetting multiple components of the immune system. The currently approved therapies are immunoregulatory and reduce the number and rate of lesion formation but are only partially effective. This review summarizes current understanding of the processes at issue: myelination, demyelination and remyelination-with emphasis upon myelin composition/ architecture and oligodendrocyte maturation and differentiation. The translational options target oligodendrocyte protection and myelin repair in animal models and assess their relevance in human. Remyelination may be enhanced by signals that promote myelin formation and repair. The crucial question of why remyelination fails is approached is several ways by examining the role in remyelination of available MS medications and avenues being actively pursued to promote remyelination including: (i) cytokine-based immune-intervention (targeting calpain inhibition), (ii) antigen-based immunomodulation (targeting glycolipid-reactive iNKT cells and sphingoid mediated inflammation) and (iii) recombinant monoclonal antibodies-induced remyelination.

Identifiers

PMID24961530
PMCPMC4061877
OpenAlexW2171125850

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.