Cece wrote: The link was to an article about remyelination. Whether or not MS has a vascular cause (and I know you know which side of that I land on), remyelination is huge and beneficial to those of us with demyelination.
Although I don't want to minimize the situation a helluva recent advance was going from thinking that re-myelinsation is something that doesn't happen to realizing that it does happen, although admittedly inadequately.
Still, it's a huge advancement to go from "not possible" to only having to "speed up the process".
Regulation of Oligodendrocyte Differentiation and Myelination
* Ben Emery
Science 5 November 2010: 779-782. wrote:A major future challenge will be translating our knowledge of oligodendrocyte development and myelination into therapeutic approaches aimed at promoting remyelination in human diseases such as the leukodystrophies and MS. In early MS, remyelination can occur relatively robustly, but becomes less efficient with disease progression. Given that mature oligodendrocytes are relatively inefficient in initiating new myelin segments (13, 52), it seems likely that strategies promoting remyelination in such diseases will need to be targeted toward promoting the division, recruitment, and differentiation of OPCs and their subsequent myelination. It is not clear whether all mechanisms that regulate developmental myelination will have identical roles in remyelination; for example, unlike in development, Notch signaling does not appear to be a ratelimiting step in experimentally induced remyelination (53). Encouragingly, however, many of the mechanisms thus far identified as controlling developmental myelination do have conserved roles in remyelination. For instance, modulation of Lingo-1, known to regulate developmental myelination (5), also modulates remyelination in animal models of demyelination (54). Similarly, SVZ-derived OPCs receive synaptic input in the whitematter in a mouse model of remyelination, indicating that, like developmental myelination, remyelination may be in part mediated by neuronal activity (26). We are still a long way from fully applying our understanding of mechanisms of myelin in a therapeutic context; however, the discoveries described here will provide an important basis for such work.