A major consequence of AD neuroinflammation is that Aβ-induced microglial NLRP3 inflammasome activation results in the extracellular release of ASC specks, which may act as binding cores for Aβ, promoting the formation and propagation of Aβ oligomers and aggregates and providing evidence in favour of the theory that AD pathology worsens through inflammasome activation [156,157]. Here, NLRP3 is linked to Alzheimer disease.