IL1B and Alzheimer disease: Further, based on our findings that, (i) not only does parkin and NEDD8 interact in AD brain, but, (ii) our finding of IL-1β-induction of NEDD8 translocation from nucleus to cytoplasm, and, (iii) of NEDD8 interaction with and activation of parkin, it is logical to conclude that the AD-associated excess levels of IL-1β play a role in the neuropathologically defined AD-associated parkin pathology.