In AD, microglia are drawn to neuritic plaques to consume aggregated Aβ, triggering NLRP3 inflammasome activation, resulting in the release of proinflammatory cytokines (IL-1β and IL-18) and potentially neurotoxic factors, which can worsen the effects of Aβ and exacerbate AD pathology. This evidence concerns the gene IL1B and Alzheimer disease.