Wednesday, June 4, 2003
Boston Cure Project for Multiple Sclerosis
There are many hypotheses to explain why lesions fail to remyelinate fully in MS. The depletion hypothesis states that repeated episodes of demyelination and remyelination in an area eventually uses up that area's supply of oligodendrocyte progenitor cells (OPCs). A new study argues against that hypothesis using a technique that induces targeted demyelinating lesions in the brain of an animal.
In these experiments, researchers injected a gliotoxin, ethidium bromide, into a specific area of the brain of rats. Up to three injections were made in the same area with a period of several weeks in between injections to allow for complete remyelination. Examination of the brain tissue showed that concentrations of OPCs were similar to that in normal white matter, even after repeated episodes of demyelination. In addition, repeated episodes of demyelination did not appear to impair remyelination.
While this study does not explain what actually causes failure of remyelination
in MS, it does demonstrate that repeated demyelination does not automatically
cause a progressive depletion of OPCs (at least not in rats and not after
three targeted lesions -- perhaps a higher number of episodes would have
produced a different outcome). Rather, these findings tend to support the
hypothesis that failure to remyelinate is due to the presence of inhibitory
factors in an MS lesion, and/or the absence of critical pro-remyelinating
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