Our findings show that (i) parkin is present in P-tau aggregates in neurons lying adjacent to activated IL-1α-laden glia in Alzheimer brain but not in control (AMC) brain; and (ii) the synthesis of IL-1α, IL-1β, and parkin is elevated months prior to the appearance of Aβ plaques in an animal model of AD but not in syngeneic littermates. Here, IL1B is linked to Alzheimer disease.