In Alzheimer’s disease, accumulation of fibrillar peptide amyloid-β after phagocytosis releases cathepsin B that is sensed by NLRP3 (and at a lesser extent NLRP1) and induces activation of NLRP1 and 3 inflammasomes [219], which in turn have been found to worsen Alzheimer’s disease patient conditions [220–223]. The gene discussed is NLRP3; the disease is early-onset autosomal dominant Alzheimer disease.