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Significance Myelin sheaths insulate the neuronal axons and speed the transmission of electrical impulses. The demyelination process occurs in many human diseases, including multiple sclerosis (MS). Using multiple mouse models of MS, we demonstrate in this study the role of MLKL, a protein known to function in a form of regulated necrosis (necroptosis), in facilitating demyelination in a necroptosis-independent manner in the central nervous system. An RIP1 kinase inhibitor was shown to block the progression of MS in an immune-induced demyelination model, and it does so at the stage after antibody generation but before breakdown of the blood–brain barrier, at a likely step of monocyte elevation. These findings provide insights into the demyelination process and potential new therapeutic agents for MS.

RIP1 kinase inhibitor halts the progression of an immune-induced demyelination disease at the stage of monocyte elevation