Additionally, the formation of the complement membrane attack complex (MAC) triggers increased cytosolic Ca2+ concentration, resulting in mitochondrial dysfunction and NLRP3 activation that causes caspase 1 activation and IL-1β secretion in vitro (203), which may further promote a pathogenic cycle of the TLR4-complement-NLRP3 inflammasome interactions in AD. This evidence concerns the gene NLRP3 and Alzheimer disease.