Journal Article

Semaphorin 3A and 3F: key players in myelin repair in multiple sclerosis?

Anna Williams, Gabrièle Piaton, Marie-Stéphane Aigrot, Aisha Belhadi, Marie Théaudin, Franziska Petermann, Jean-Léon Thomas, Bernard Zalc and Catherine Lubetzki

in Brain

Published on behalf of The Guarantors of Brain

Volume 130, issue 10, pages 2554-2565
Published in print October 2007 | ISSN: 0006-8950
Published online September 2007 | e-ISSN: 1460-2156 | DOI: http://dx.doi.org/10.1093/brain/awm202
Semaphorin 3A and 3F: key players in myelin repair in multiple sclerosis?

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The presence of demyelinated plaques in the central nervous system is the hallmark of multiple sclerosis (MS). Some plaques remyelinate but others do not, leaving permanent damage. The reasons for this failure of repair are many, but one possible reason is the lack of migration of oligodendrocyte precursor cells to the lesion. The guidance molecules Semaphorin 3A and 3F, already known to direct oligodendroglial migration in development, may also be active in controlling oligodendrocyte precursor cell migration in MS, and hence may determine the ability of plaques to remyelinate. Here, in MS tissue and an experimental model of demyelination, we demonstrate a local source of these molecules around active demyelinating lesions, but not chronic plaques. We also provide evidence for their up-regulation at a distance from the lesion, in the neuronal cell bodies corresponding to the demyelinated axons. We propose that both of these mechanisms influence remyelination.

Keywords: multiple sclerosis; demyelination; remyelination; myelin; semaphorin

Journal Article.  6261 words.  Illustrated.

Subjects: Neurology ; Neuroscience

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