This Is MS Multiple Sclerosis Community: Knowledge & Support

MS is caused by a defect in the body's immune system, which turns in on itself, and attacks the fatty myelin sheath.

Thanks Ian, although I think it's just you and I in this echoey old warehouse of a website. Seems most everyone else is convinced that MS/CCSVI, if they do indeed ever prove to be related, is of a vascular cause.

On a sidenote, regarding your immune system directed treatment, any further progression these last few years? How are the beaches of spain?

The beirut study you guys seem to love showed that CCSVI and MS are related. Please stop spreading misinformation.

Is it (CCSVI) the ONLY likely cause(?) of "MS" ... probably not ... but it's linked and you can't argue it - so please stop trying to do so.

Thanks Ian, although I think it's just you and I in this echoey old warehouse of a website. Seems most everyone else is convinced that MS/CCSVI, if they do indeed ever prove to be related, is of a vascular cause.

Keep bashing CCSVI ... it's rather amusing. You're silly.

Funny, because aside from your 4 skeptic friends, that's all the rest of us see in your posts.

blah, blah, blah

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.

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.

If you disagree with someone, please succintly state why and let it go at that. Point, counterpoint, counter-counter point, etc. is not useful-- the reality is that after the first disagreement, you will rarely convince another of something they feel strongly about unless you have shocking new information to share. The drawn-out debates also turn people off from reading the messages in the first place. If you really have to get something off your chest, please send that person a Private Message-- there is no need to have a long argument in public.