Our functional data show that Chlamydia pneumoniae infection is sufficient to induce NLRP3 activation, IL1β maturation, neurotoxicity, and Aβ42 accumulation in human neurons and to exacerbate neuroinflammation, Aβ plaque burden, and visuocognitive impairment in AD+ mice. This evidence concerns the gene NLRP3 and Alzheimer disease.