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Promoting myelin repair and return of function in multiple sclerosis
Author(s) -
Zhang Jingya,
Kramer Elisabeth G.,
Asp Linnea,
Dutta Dipankar J.,
Navrazhina Kristina,
Pham Trinh,
Mariani John N.,
Argaw Azeb Tadesse,
Melendez-Vasquez Carmen V.,
John Gareth R.
Publication year - 2011
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2011.08.017
Subject(s) - multiple sclerosis , myelin , medicine , neuroscience , neuropathology , oligodendrocyte , myelin oligodendrocyte glycoprotein , exacerbation , axon , pathology , immunology , experimental autoimmune encephalomyelitis , disease , central nervous system , biology
Multiple sclerosis (MS) is an inflammatory demyelinating disease of the CNS. Conduction block in demyelinated axons underlies early neurological symptoms, but axonal transection and neuronal loss are believed to be responsible for more permanent chronic deficits. Several therapies are approved for treatment of relapsing‐remitting MS, all of which are immunoregulatory and clinically proven to reduce the rate of lesion formation and exacerbation. However, existing approaches are only partially effective in preventing the onset of disability in MS patients, and novel treatments to protect myelin‐producing oligodendrocytes and enhance myelin repair may improve long‐term outcomes. Studies in vivo in genetically modified mice have assisted in the characterization of mechanisms underlying the generation of neuropathology in MS patients, and have identified potential avenues for oligodendrocyte protection and myelin repair. However, no treatments are yet approved that target these areas directly, and in addition, the relationship between demyelination and axonal transection in the lesions of the disease remains unclear. Here, we review translational research targeting oligodendrocyte protection and myelin repair in models of autoimmune demyelination, and their potential relevance as therapies in MS.