thanks for sharing the abstract with the rest of us. I found its subject very interesting. By coincidence, a dear friend of mine sent me the full article of the same study few days ago, and thus gave me a good reason to visit this thread again.
Well, basicly the abstract says it all. According to the researchers metabolic dysfunction in oligodendrocytes might be able to cause both axonal degeneration and focal inflammation. If that was the case, oligodendrocyte apoptosis and axonal degeneration would be the primary processes in MS, and inflammation would cause only "collateral damage".dignan wrote:I think this abstract sounds interesting, although it would be more interesting if we could read the whole article...
Anyway, here's a short quote from the article:
Recent findings have initiated a possible shift of paradigms, with inflammatory demyelination not only being caused by ‘primary’ immune defects, which is of obvious relevance to MS. Investigating the driving force behind inflammatory changes in the white matter, making use of novel mouse models with a primary defect in glial cell function and metabolism, will be a necessary next step. It is possible that an entire spectrum of inflammatory demyelinating diseases exist, in which multifocal white matter lesions (including classical MS lesions) reveal a final common pathway in brain pathology and the intrinsic susceptibility of oligodendrocytes to stimulate a local immune response. Alterations of lipid metabolism may play a key role.