UCHL1 and Alzheimer disease: Additional evidence pointing to a potential role of ubiquitin dyshomeostasis in triggering an AD-like “dying-back”-type neurodegenerative phenotype comes from UCHL-1 (PGP9.5), a neuron-specific ubiquitin C-terminal hydrolase involved in disease pathogenesis (Pasinetti, 2001; Choi et al., 2004; Gong et al., 2006) which is enriched at nerve terminals (Liu et al., 2002) where it controls their physiopathological structural reshaping via ubiquitin recycling (Cartier et al., 2009).