Incomplete remyelination via therapeutically enhanced oligodendrogenesis is sufficient to recover visual cortical function.

ABSTRACT: Myelin loss induces neural dysfunction and contributes to the pathophysiology of neurodegenerative diseases, injury conditions, and aging. Because remyelination is often incomplete, better understanding endogenous remyelination and developing remyelination therapies that restore neural function are clinical imperatives. Here, we use in vivo two-photon microscopy and electrophysiology to study the dynamics of endogenous and therapeutic-induced cortical remyelination and functional recovery after cuprizone-mediated demyelination in mice. We focus on the visual pathway, which is uniquely positioned to provide insights into structure-function relationships during de/remyelination. We show endogenous remyelination is driven by recent oligodendrocyte loss and is highly efficacious following mild

SUBMITTER: Della-Flora Nunes G 

PROVIDER: S-EPMC11739692 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature