In this study, we tested the hypothesis that there is a compromising interaction between neuroinflammation—noted as excessive levels of IL-1α and β in AD—and the early advent of autophagic failure—noted as the abundance of undigested ubiquitinated intraneuronal aggregates (P-tau) and extracellular aggregates (Aβ) in AD. The gene discussed is MAPT; the disease is Alzheimer disease.