NLRP3, an intracellular sensor that can detect a wide range of microbial substrates, has been shown to elevate the levels of pro-inflammatory cytokines IL-1β and IL-18 by activating caspase-1.[79] In AD models, administration of the NLRP3 inhibitor Mcc950 attenuated Tau-induced IL-1β responses and reduced neuroinflammation as well as amyloid deposition associated with AD pathology.[36] GABAAP is also thought to affect the NLRP3 inflammasome-dependent inflammatory response by mediating mitochondrial mass in macrophages.[80]. Here, IL18 is linked to Alzheimer disease.