The mechanism for the accumulation of Ub proteins involved in AD has been ascribed in part to the reaction of PGJ2 and Δ12-PGJ2 with a thiol on ubiquitin C-terminal hydrolase L1 (Uch-L1) [65], a major neurological protein that functions to remove ubiquitin from misfolded proteins that need to be directed to the proteasome pathway [73]. This evidence concerns the gene UCHL1 and Alzheimer disease.