Interestingly, the activation of the cerebral, endogenous NLRP3 inflammasome was restricted to the microglia surrounding the plaques, and the microglial-specific disruption of the NLRP3 inflammasome skewed the microglial phenotypes toward M2, which could potentially reduce Aβ load and protect against cognitive decline [35], suggesting that microglia-specific activation of the NLRP3 inflammasome is important for AD pathogenesis. Here, NLRP3 is linked to Alzheimer disease.