Abstract

Ras-related C3 botulinum toxin substrate (Rac1) is a small GTPase that monitors external signals and activates downstream cascades by transmitting information from membrane-bound receptors to exert its physiological and pathological effects. It is essential for regulating actin cytoskeleton polymerization, organization, function, and dynamics. Rac1 is a widely studied molecule, and its role in various brain disorders and diseases has been studied in rodent and vitro models. This review discusses the involvement of Rac1 in the pathophysiology of neurological diseases, its molecular pathway in different neurological diseases, and its beneficial and detrimental pathophysiological role in different cell-type and neurological disease phases.

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