Int. J. Mol. Sci. 2013, 14(1), 1031-1049; doi:10.3390/ijms14011031
Review

Signalling Pathways that Inhibit the Capacity of Precursor Cells for Myelin Repair

Centre for Neuroscience Research, Department of Anatomy and Neuroscience, University of Melbourne, Melbourne Brain Centre, Kenneth Myer Building, 30 Royal Parade, Parkville, Vic 3010, Australia
* Author to whom correspondence should be addressed.
Received: 27 November 2012; in revised form: 21 December 2012 / Accepted: 31 December 2012 / Published: 7 January 2013
(This article belongs to the Special Issue Recent Advances in the Research of Multiple Sclerosis)
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Abstract: In demyelinating disorders such as Multiple Sclerosis (MS), targets of injury are myelin and oligodendrocytes, leading to severe neurological dysfunction. Regenerative therapies aimed at promoting oligodendrocyte maturation and remyelination are promising strategies for treatment in demyelinating disorders. Endogenous precursor cells or exogenous transplanted cells are potential sources for remyelinating oligodendrocytes in the central nervous system (CNS). Several signalling pathways have been implicated in regulating the capacity of these cell populations for myelin repair. Here, we review neural precursor cells and oligodendrocyte progenitor cells as potential sources for remyelinating oligodendrocytes and evidence for the functional role of key signalling pathways in inhibiting regeneration from these precursor cell populations.
Keywords: oligodendrocyte progenitor cell (OPC); neural precursor cell (NPC); bone morphogenic protein (BMP); central nervous system (CNS)

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MDPI and ACS Style

Sabo, J.K.; Cate, H.S. Signalling Pathways that Inhibit the Capacity of Precursor Cells for Myelin Repair. Int. J. Mol. Sci. 2013, 14, 1031-1049.

AMA Style

Sabo JK, Cate HS. Signalling Pathways that Inhibit the Capacity of Precursor Cells for Myelin Repair. International Journal of Molecular Sciences. 2013; 14(1):1031-1049.

Chicago/Turabian Style

Sabo, Jennifer K.; Cate, Holly S. 2013. "Signalling Pathways that Inhibit the Capacity of Precursor Cells for Myelin Repair." Int. J. Mol. Sci. 14, no. 1: 1031-1049.

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