Using PLA, we found that in all age-matched controls, the number of parkin-NEDD8 colocalized dots was less in comparison with their Alzheimer counterparts (Fig. 2d, f, p = 0.05, Wilcoxon rank sum test), suggesting that in response to the neuronal stress of AD, NEDD8 translocation occurs alongside elevated parkin and parkin-NEDD8 interaction, perhaps at the behest of elevated IL-1β. This evidence concerns the gene IL1B and Alzheimer disease.