Deposition of amyloid-β in Alzheimer's disease (AD) activates microglia, which drive cerebral neuroinflammation. This paper showed increased expression of caspase 1 (a component of the NLRP3 (NOD-, LRR- and pyrin domain-containing 3) inflammasome) in brain samples from patients with AD. Mice that lacked Nlrp3 or Casp1 and had mutations associated with familial AD were protected from loss of spatial memory and had enhanced amyloid-β clearance. In another mouse model of AD, Nlrp3 deficiency resulted in decreased deposition of amyloid-β, suggesting that targeting the NLRP3 inflammasome could be beneficial in AD.