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To date most of these strategies have been developed in short-lived rodent models of demyelination, which spontaneously repair. Well-defined nonhuman primate models closer to man would allow us to efficiently advance therapeutic approaches. Here we present a nonhuman primate model of optic nerve demyelination that recapitulates several features of MS lesions. The model leads to failed remyelination, associated with progressive axonal degeneration and visual dysfunction, thus providing the missing link to translate emerging preclinical therapies to the clinic for myelin disorders such as MS.<\/jats:p>","DOI":"10.1073\/pnas.2115973119","type":"journal-article","created":{"date-parts":[[2022,3,2]],"date-time":"2022-03-02T14:42:57Z","timestamp":1646232177000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":16,"title":["Failed remyelination of the nonhuman primate optic nerve leads to axon degeneration, retinal damages, and visual dysfunction"],"prefix":"10.1073","volume":"119","author":[{"given":"Nad\u00e8ge","family":"Sarrazin","sequence":"first","affiliation":[{"name":"Institut du Cerveau, Sorbonne Universit\u00e9, INSERM, CNRS, F-75013 Paris, 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