Growth factor regulation of remyelination: behind the growing interest in endogenous cell repair of the CNS. (November 2007)

• Record Type: Journal Article
• Authors: Armstrong, Regina C
• Is Part Of: Future neurology. Volume 2:Number 6(2007)
• Page Start: 689
• Page End: 697
• Publication Date: 2007-11
• Subjects: cuprizone -- demyelinating disease -- FGF -- multiple sclerosis -- myelin -- oligodendrocyte -- PDGF -- progenitors -- remyelination; Neurology -- Research -- Periodicals; 611.8005
• DOI: 10.2217/14796708.2.6.689
• Languages: English
• ISSNs: 1479-6708

Abstract

Remyelination facilitates recovery of saltatory conduction along demyelinated axons and may help prevent axon damage in patients with demyelinating diseases, such as multiple sclerosis. The extent of remyelination in multiple sclerosis lesions varies dramatically, indicating a capacity for repair that is not fulfilled in lesions with poor remyelination. In experimental models of demyelinating disease, remyelination is limited by chronic disease that depletes the oligodendrocyte progenitor (OP) population, inhibits OP differentiation into remyelinating oligodendrocytes and/or perturbs cell survival in the lesion environment. Manipulating the activity of growth factor signaling pathways significantly improves the ability of endogenous OP cells to accomplish extensive remyelination. Specifically, growth factors have been identified that can regulate OP proliferation, differentiation and survival in demyelinated lesions. Therefore, growth factors may be key signals for strategies to improve conditions with poor remyelination.