NLRP3 and Alzheimer disease: The inflammasome also drives AD pathologies by recognizing and translating Aβ into inflammation; phagocytosis of Aβ by microglia stimulates lysosomal breakdown and consequent release of cathepsin B, an endogenous trigger of NLRP3 inflammasome activation that promotes neurotoxic IL-1β and caspase-1 release (Halle et al., 2008), which is essential for the downstream neuroinflammatory events observed in the AD brain.