Upon activation by microbial components, aggregated Aβ, or oxidative stress—all of which are hallmarks of AD pathogenesis—the NLRP3 inflammasome triggers the cleavage of pro-caspase-1 into its active form, thereby promoting maturation and secretion of pro-inflammatory cytokines like IL-1β, a central driver of neuroinflammation in AD [51,52]. Here, IL1B is linked to Alzheimer disease.