How to Use the Cuprizone Model to Study De- and Remyelination

Abstract

Multiple sclerosis (MS) is an autoimmune and inflammatory disorder affecting the central nervous system whose cause is still largely unknown. Oligodendrocyte degeneration results in demyelination of axons, which can eventually be repaired by a mechanism called remyelination. Prevention of demyelination and the pharmacological support of remyelination are two promising strategies to ameliorate disease progression in MS patients. The cuprizone model is commonly employed to investigate oligodendrocyte degeneration mechanisms or to explore remyelination pathways. During the last decades, several different protocols have been applied, and all have their pros and cons. This article intends to offer guidance for conducting pre-clinical trials using the cuprizone model in mice, focusing on discovering new treatment approaches to prevent oligodendrocyte degeneration or enhance remyelination.

CNS Resident Innate Immune Cells: Guardians of CNS Homeostasis

“…The inducible models comprise the experimental autoimmune encephalomyelitis (EAE) [22] and the cuprizone-induced model for demyelination [23]. MS is an exclusively human disease that does not occur spontaneously in non-human organisms [24].…”