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U.S.A."],"published-print":{"date-parts":[[2017,11,7]]},"abstract":"<jats:title>Significance<\/jats:title>\n                  <jats:p>The hallmark of remyelination in the CNS has been proposed to be the presence of thin myelin sheaths. This has been demonstrated in multiple experimental models and in multiple sclerosis. It is the only surrogate marker of remyelination, and therefore a crucial fingerprint of myelin repair. However, this has been challenged recently in separate studies, in which, by implication, the degree or presence of remyelinated axons has been underestimated. In this article, we provide evidence from two different models that thin myelin sheaths and short internodes persist almost indefinitely. Future attempts to promote myelin repair in models of multiple sclerosis will be crucially dependent on a definitive marker of repair. 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