Moreover, studies conducted on brain tissue samples from AD patients that had died because of intercurrent systemic infections and APP/PS1 AD-model mice revealed that any added proinflammatory insults intensified NLRP3 inflammasome’s assembly/activation and IL-1β, IL-6, and various chemokines release from microglia, astrocytes, and neurons while increasing the brain’s Aβs and p-Taues load. This evidence concerns the gene NLRP3 and Alzheimer disease.