2007
DOI: 10.2217/14796708.2.6.689
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Growth factor regulation of remyelination: behind the growing interest in endogenous cell repair of the CNS

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, inhi… Show more

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Cited by 23 publications
(11 citation statements)
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References 61 publications
(83 reference statements)
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“…It may be that a residual pool of A2B5+ OPCs remains in the slice following complement mediated lysis and these cells subsequently proliferate and repopulate the entire lineage. Alternatively, a pre-OPC population (Armstrong, 2007; Baracskay et al, 2007; Nait-Oumesmar et al, 1999) could regenerate the entire lineage. Several sources of pre-OPCs have been described (Nait-Oumesmar et al, 1999; Wu et al, 2009).…”
Section: Discussionmentioning
confidence: 99%
“…It may be that a residual pool of A2B5+ OPCs remains in the slice following complement mediated lysis and these cells subsequently proliferate and repopulate the entire lineage. Alternatively, a pre-OPC population (Armstrong, 2007; Baracskay et al, 2007; Nait-Oumesmar et al, 1999) could regenerate the entire lineage. Several sources of pre-OPCs have been described (Nait-Oumesmar et al, 1999; Wu et al, 2009).…”
Section: Discussionmentioning
confidence: 99%
“…Failed differentiation of oligodendrocyte lineage cells (OLCs) may contribute to poor remyelination in chronic MS lesions and prolonged neurological deficits [9]. Multiple molecular signaling pathways inhibit differentiation of oligodendrocyte progenitor (OP) cells and limit remyelination in experimental models [1]. Modifying inhibitory signals in lesion areas could potentially enhance functional recovery in MS patients by improving the remyelination capacity of immature OLCs that persist in MS lesions [4, 9].…”
Section: Introductionmentioning
confidence: 99%
“…However, these mechanisms sometimes cannot fully compensate for the demyelination. This has been related to an age factor [38], but also to the possibility that intensity or chronicity of demyelination eventually outpaces the remyelinating capacity, as may be the case in multiple sclerosis [39].…”
Section: Discussionmentioning
confidence: 99%