Our demonstration of IL-1β downregulation of the levels of PINK1 that may appear simultaneous with upregulation of both the levels and activity of GSK3β and a resultant increase in the levels of P-Parkin is consistent with the idea that the increase in IL-1β in AD may lead to known deleterious effects of GSK3β activation through the IL-1β-mediated decrease in PINK1 but that these may be counterbalanced by NEDD8-dependent activation of parkin via GSK3β activation. Here, IL1B is linked to Alzheimer disease.