Samuel K. Jensen

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Multiple sclerosis is an inflammatory demyelinating disease of the central nervous system characterized by plaque formation containing lost oligodendrocytes, myelin, axons, and neurons. Remyelination is an endogenous repair mechanism whereby new myelin is produced subsequent to proliferation, recruitment, and differentiation of oligodendrocyte precursor(More)
Remyelination is the generation of new myelin sheaths after injury facilitated by processes of differentiating oligodendrocyte precursor cells (OPCs). Although this repair phenomenon occurs in lesions of multiple sclerosis patients, many lesions fail to completely remyelinate. A number of factors have been identified that contribute to remyelination(More)
Despite an appreciation of the importance of myelination and the consequences of pathological demyelination, the fundamental mechanisms regulating myelination are only now being resolved. Neuronal activity has long been considered a plausible regulatory signal for myelination. However, controversy surrounding its dispensability in certain contexts and the(More)
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