NLRP3 and Parkinson disease: It is noteworthy that the characteristic pathological product of PD—fibrillated α-synuclein aggregates—can also act as an endogenous danger signal to activate the NLRP3 inflammasome: studies have confirmed that microglia phagocytose α-synuclein fibrils derived from Lewy bodies, releasing cathepsin B through lysosomal membrane rupture, accompanied by a large generation of ROS, which synergistically activates the NLRP3-caspase-1 axis, driving the maturation and release of IL-1β (Yu et al., 2024; Li G. et al., 2024; Li M. M. et al., 2024; Codolo et al., 2013; Martinon et al., 2002).