Supporting evidence for this hypothesis includes: (i) elevated LPS levels detected in the blood and brains of AD patients; (ii) AD risk factors associated with increased LPS levels or heightened responses; (iii) LPS-induced upregulation, aggregation, inflammation, and neurotoxicity of Aβ; (iv) LPS-driven tau phosphorylation, aggregation, and propagation; (v) LPS-mediated microglial priming, activation, and neurotoxicity; and (vi) LPS-induced synaptic and neuronal loss and memory impairment in AD mouse models, as well as cognitive deficits observed in humans. This evidence concerns the gene MAPT and Alzheimer disease.