This Is MS Multiple Sclerosis Community: Knowledge & Support

I like that they were able to remyelinate even after chronic demyelination in this study -- lucky mice.



Endogenous Cell Repair of Chronic Demyelination.

J Neuropathol Exp Neurol. 2006 Mar;65(3):245-256.
Armstrong RC, Le TQ, Flint NC, Vana AC, Zhou YX.
From the Department of Anatomy, Physiology, and Genetics (RCA, TQL, NCF, Y-XZ) and the Program in Neuroscience (RCA, NCF, ACV), Uniformed Services University of the Health Sciences, Bethesda, Maryland.

In multiple sclerosis lesions, remyelination typically fails with repeated or chronic demyelinating episodes and results in neurologic disability. Acute demyelination models in rodents typically exhibit robust spontaneous remyelination that prevents appropriate evaluation of strategies for improving conditions of insufficient remyelination.

In the current study, we used a mouse model of chronic demyelination induced by continuous ingestion of 0.2% cuprizone for 12 weeks. This chronic process depleted the oligodendrocyte progenitor population and impaired oligodendrocyte regeneration. Remyelination remained limited after removal of cuprizone from the diet.

Fibroblast growth factor 2 (FGF2) expression was persistently increased in the corpus callosum of chronically demyelinated mice as compared with nonlesioned mice. We used FGF2 mice to determine whether removal of endogenous FGF2 promoted remyelination of chronically demyelinated areas.

Wild-type and FGF2 mice exhibited similar demyelination during chronic cuprizone treatment. Importantly, in contrast to wild-type mice, the FGF2 mice spontaneously remyelinated completely during the recovery period after chronic demyelination. Increased remyelination in FGF2 mice correlated with enhanced oligodendroglial regeneration. FGF2 genotype did not alter the density of oligodendrocyte progenitor cells or proliferating cells after chronic demyelination.

These findings indicate that attenuating FGF2 created a sufficiently permissive lesion environment for endogenous cells to effectively remyelinate viable axons even after chronic demyelination.

<shortened url>

although i love these studies, i find it frustrating when i cant find anything on the net that i can do to increase my FGF2

...and that might be a good thing. The FGF2 mice are most likely genetic knockouts where the function of the gene has been turned off. I found the article confusing as well. However, the key statement was "attenuating FGF2" in the abstract.

NHE