Studies have shown that NLRP3 promotes the release of pro-inflammatory cytokines such as IL-1β and IL-18 in the brain by inducing the activation of caspase-1, which further promotes the aggregation of intrinsic immune cells and initiates the downstream inflammatory cascade response, and ultimately accelerates the pathological progression of AD, which is a major mechanism of neuroinflammatory response [36–40]. This evidence concerns the gene IL18 and Alzheimer disease.