The prevalence of Alzheimer's disease (AD) has been increasing worldwide due to the aging population, placing a substantial burden on both society and families. To date, the underlying pathogenesis of AD has not been comprehensively elucidated, and advancements in drug development for this disease have been relatively slow. Astrocytes are crucial for maintaining the homeostasis of the brain microenvironment. Astrocyte dysfunction has been closely linked to AD onset and progression. The Rac1 protein, which belongs to the Rho GTPase family, exhibits hyperactivation in the astrocytes of AD model mice. Nevertheless, the exact role of Rac1 in the pathogenesis of AD remains ambiguous. The TLR4/Rac1/NLRP3 signaling pathway is involved in diverse cellular activities and inflammatory responses and plays a significant role in the AD neuroinflammatory process. This review explores the mechanism of action of Rac1 in astrocytes in the context of AD and how the TLR4/Rac1/NLRP3 pathway influences the pathological process, offering novel theoretical foundations and potential therapeutic targets for preventing and treating this disease.