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Review
. 2011 Oct;8(4):650-8.
doi: 10.1007/s13311-011-0065-x.

Myelin Regeneration in Multiple Sclerosis: Targeting Endogenous Stem Cells

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Free PMC article
Review

Myelin Regeneration in Multiple Sclerosis: Targeting Endogenous Stem Cells

Jeffrey K Huang et al. Neurotherapeutics. .
Free PMC article

Abstract

Regeneration of myelin sheaths (remyelination) after central nervous system demyelination is important to restore saltatory conduction and to prevent axonal loss. In multiple sclerosis, the insufficiency of remyelination leads to the irreversible degeneration of axons and correlated clinical decline. Therefore, a regenerative strategy to encourage remyelination may protect axons and improve symptoms in multiple sclerosis. We highlight recent studies on factors that influence endogenous remyelination and potential promising pharmacological targets that may be considered for enhancing central nervous system remyelination.

Figures

Fig. 1
Fig. 1
Pharmacological targets of central nervous system (CNS) remyelination. The diagram illustrates the recruitment of an oligodendrocyte precursor cell (OPC) to an area of demyelination, and its differentiation into a remyelinating oligodendrocyte. Chronically demyelinated axons that do not acquire remyelinated sheaths are liable to undergo degeneration. Conversely, stimulation of remyelination preserves the integrity of axons. Several molecular pathways known to regulate oligodendrocyte differentiation are possible pharmaceutical targets of CNS remyelination. Semaphorin 3A and 3F are involved in OPC recruitment into the lesion. Lingo-1, Wnt/β-catenin, Semaphorin 3A, and canonical Notch signalling pathways negatively regulate CNS remyelination by preventing OPC differentiation, whereas retinoid X receptor (RXR)-γ and the noncanonical Notch signalling pathways enhance CNS remyelination by stimulating OPC differentiation

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