Here we show that in the context of elevated IL-1β: (i) the steady-state levels of parkin and P-parkin are increased; (ii) PINK1 and P-Ub levels are decreased; (iii) NEDD8 is translocated from nucleus-to-cytoplasm in AD and in IL-1β treated neurons; (iv) parkin is activated by binding of NEDD8 at the same location as P-Ub, allowing for exposure of and phosphorylation of parkin Ser65; (v) PINK1 levels are reduced, and (vi) P-parkin levels are elevated via IL-1β-induced levels and activation of GSK3β. This evidence concerns the gene NEDD8 and Alzheimer disease.