NLRP3 and Alzheimer disease: In sporadic AD human brains, extracellular lipopolysaccharide (LPS) and aggregated Aβ1-42 co-localize (Zhan et al., 2016) and activate microglia by interacting with toll-like receptor (TLR) 4, which primes nucleotide-binding domain, leucine-rich–containing family, and pyrin domain–containing-3 (NLRP3), and stimulate nuclear factor-kappa B (NF-κB), thereby promoting neuroinflammation.