As described in a previous study (Dempsey et al., 2017), Aβ accumulates in the AD brain to form characteristic plaques and then activates the NLRP3 inflammasome, triggering the pyroptosis via the NLRP3/caspase-1/GSDMD signaling pathway, and finally leading to levels of inflammatory factors IL-1β and IL-18 becoming elevated. This evidence concerns the gene CASP1 and Alzheimer disease.