UCHL1 and Alzheimer disease: Despite its putative antioxidant role, UCH-L1 remains one of the main targets of oxidative damage; in 2004, Choi and colleagues showed that the massive oxidation of five methionine residues (Met-1, Met-6, Met-12, Met-124, and Met-179) as well as at a single cysteine site (Cys-220) eventually results in the irreversible alteration of UCH-L1 physiological activities, and these events have been described both in AD and PD post-mortem brains [21].