In a transgenic mouse model of AD, NLRP3 or caspase-1 knockdown prevented spatial-memory impairments and decreased brain concentrations of caspase-1 and IL-1β, while increasing microglial phagocytosis able to remove Aβ, suggesting a role of NLRP3 inflammasome in the pathogenesis of AD. The gene discussed is CASP1; the disease is Alzheimer disease.