Remyelination is a regenerative process in the central nervous system (CNS) that produces new myelin sheaths from adult stem cells. The decline in remyelination that occurs with advancing age poses a significant barrier to therapy in the CNS, particularly for long-term demyelinating diseases such as multiple sclerosis (MS). Here we show that remyelination of experimentally induced demyelination is enhanced in old mice exposed to a youthful systemic milieu through heterochronic parabiosis. Restored remyelination in old animals involves recruitment to the repairing lesions of blood-derived monocytes from the young parabiotic partner, and preventing this recruitment partially inhibits rejuvenation of remyelination. These data suggest that enhanced remyelinating activity requires both youthful monocytes and other factors, and that remyelination-enhancing therapies targeting endogenous cells can be effective throughout life.
Couldn't resist it.......The Franklinstein Mouse (with permission from House of Mouse)
We have commented on the important of age and remyelination before. It has been shown that in young mice that the default pathway following any insult that causes demyelination is repair and remyelination. However, it has been found that old mice do not repair that well.
As MSers accumulate more damage as the the disease progresses as you get older, then did this mean that the repair process fails because of age? Importantly is this is an irreversible process that time can not stop? The answer to this question is NO, you can still turn back the effects of age........We should have known this look at any aging star on the tele.
How did the do this?
Well they did this through parabiosis. Now we discussed the concept of parabiosis with you previously and in fact we talked about the ethics and the experimental design of the very same experiments as reported in this new article back in september, when you decided that the ends justify the means as far as your ethical use of animals go. So now you can see the actual results.
So in this paper they stiched the blood supply of two mice together to ask the question whether the failure of old mice to remyelinate is an intrinsic problem to old age or whether there is something in the the young mice that facilitated repair. In the previous studies we saw that there was a product in young blood that stimulated the growth of nerves. In this study the blood product that stimulated repair was the macrophages/monocytes (engulfing cells). The engulfing cells were the problem in old mice and if you could supply young monocytes then they can repair.
We know that these cells are vital in clearing up the debris after demyelination and without this repair does not occur. This means that if we find the trigger switches in monocytes then we have the potential to repair. So it is therefore interesting that we also reported some of work about a macrophage type cell in the brain that promotes repair. So more pieces of the jigsaw on how to crack this remyelination problem are appearing all the time and with increasing regulatity....so this is good news.