Age is one of the many factors that influence remyelination following CNS demyelination, although it is not clear whether it is the extent or rate of remyelination that is affected. To resolve this issue these investigators compared remyelination in young and old adult rats following toxin-induced demyelination.
An old paper that may be of interest to anybody concerned about the ageing debate.
Shields et al. Remyelination occurs as extensively but more slowly in old rats compared to young rats following gliotoxin-induced CNS demyelination. Glia. 1999 Oct;28(1):77-83.
Remyelination of areas of demyelination reached completion by 4 weeks in young adult rats (2 months) but was not complete until 9 weeks in old adult rats (9-12 months).
They have also shown that remyelination in another model of demyelination in the spinal cord white matter of old adult rats (18 months) can be extensive, with longer survival times (8 weeks) than have previously been examined.
They concluded that it is the rate rather than the extent of remyelination that changes in the ageing CNS.
These results have had a major influence on our understanding of the mechanisms of remyelination.
“This may be why investigators set upper age limits when testing treatment strategies in MS’ers. The younger the population the better they are likely to do.”
“This is something we see clinically as well. In MS’ers with highly active MS the earlier you treat the MS the more likely you are to see improvements in functioning. This observation was also noted in the rituximab primary progressive study; it was the PPMS’ers less than 50 years of age that derived the benefit of the treatment, not the group that were older than 50 years of age.”
Previous post of interest:
14 May 2011
The latter study is based on the observations from a subgroup analysis of the Rituximab PPMS trial that showed younger patients (<51 years) and those with active MRI scans (Gd-enhancing lesions) responded to treatment;