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Fasudil-Triggered Phagocytosis of Myelin Debris Promoted Meylin Regeneration via the Activation of TREM2/DAP12 Signaling Pathway in Cuprizone-Induced Mice
The inflammation and demyelination of the central nervous system (CNS) are mainly involved in multiple sclerosis (MS), in which the disorder of myelin regeneration leads to continual neurologic impairment. Fasudil, one of the ROCK inhibitors, has been shown protective functions in some models of demyelinating diseases. In this study, Fasudil treatment ameliorated the behavioral performance and myelin loss in CPZ-fed mice. Here, we demonstrated a new role of Fasudil, which triggered microglia todoi:10.21203/rs.3.rs-531893/v1 fatcat:hqnpr3zk2namdeqib3k2vql3me