Open AccessFailed remyelination of the nonhuman primate optic nerve leads to axon degeneration, retinal damages, and visual dysfunction
Author(s) -
Nadège Sarrazin,
Estelle Chavret-Reculon,
Corinne Bachelin,
Mehdi Felfli,
Rafik Arab,
Sophie Gilardeau,
Elena Brazhnikova,
Élisabeth Dubus,
Lydia Yaha-Cherif,
Jean Lorenceau,
Serge Picaud,
Serge G. Rosolen,
Pierre Moissonnier,
Pierre Pouget,
Anne Baron-Van Evercooren
Publication year - 2022
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.2115973119
Subject(s) - remyelination , neuroscience , multiple sclerosis , axonal degeneration , primate , optic nerve , axon , myelin , degeneration (medical) , retinal degeneration , white matter , medicine , biology , retina , central nervous system , pathology , magnetic resonance imaging , immunology , radiology
Significance Promotion of remyelination has become a new therapeutic avenue to prevent neuronal degeneration and promote recovery in white matter diseases, such as multiple sclerosis (MS). 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.