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Brain Sci. 2013, 3(3), 1282-1324; doi:10.3390/brainsci3031282

Myelin Recovery in Multiple Sclerosis: The Challenge of Remyelination

Department of Neurology, Institute of Molecular Medicine and Genetics, Georgia Regents University, 1120 15th Street, Augusta, GA 30912-2620, USA
Department of Neurosciences, Medical University of South Carolina, 171 Ashley Avenue, Charleston, SC 29425-6160, USA
Laboratory of Signaling Proteins, Polish Academy of Sciences, Ludwik Hirszfeld Institute of Immunology & Experimental Therapy, Rudolfa Weigla 12, Wrocław 53-114, Poland
Department of Microbiology, National University of Ireland Galway, University Road, Galway, Ireland
Author to whom correspondence should be addressed.
Received: 8 July 2013 / Revised: 12 August 2013 / Accepted: 12 August 2013 / Published: 28 August 2013
(This article belongs to the Special Issue Myelin Repair)
View Full-Text   |   Download PDF [1599 KB, uploaded 28 August 2013]   |  


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. View Full-Text
Keywords: calpain; central nervous system; demyelination; fingolimod; glycolipids; lipids; multiple sclerosis; myelin; myelination; NKT cells; oligodendrocytes; remyelination; T cells calpain; central nervous system; demyelination; fingolimod; glycolipids; lipids; multiple sclerosis; myelin; myelination; NKT cells; oligodendrocytes; remyelination; T cells

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This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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Podbielska, M.; Banik, N.L.; Kurowska, E.; Hogan, E.L. Myelin Recovery in Multiple Sclerosis: The Challenge of Remyelination. Brain Sci. 2013, 3, 1282-1324.

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