Abstract
The current issue of Brain contains four papers that illuminate different aspects of inflammatory demyelinating disease, especially multiple sclerosis (Black et al., 2006; Coman et al., 2006; Howell et al., 2006; Patrikios et al., 2006). One paper focuses on axonal protection, while the others describe aspects of spontaneous remyelination in the disease. Promoting remyelination is a major therapeutic goal in multiple sclerosis, but some observations from the current papers raise the possibility that remyelination may transiently render axons vulnerable to degeneration before long-term protection is achieved, as discussed below.

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