Abstract
Remyelination can be very effective in human. However, this process ultimately fails in multiple sclerosis (MS). In this paper, we discuss the possibility of stimulating endogenous oligodendrocyte precursors to participate in remyelination in experimental models (rat and primate Callithrix jacchus) of MS through thyroid hormone (TH) administration. TH is in fact known to be a key signal in brain development, oligodendrocyte development and myelin protein gene expression regulation.
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