Studies in AD brains have shown that Uch-L1 deficits are linked to the accumulation of Aβ in the ascending gracile tract as demonstrated by a mouse model of gracile axonal dystrophy (GAD; Osaka et al., 2003), and there is an association between Uch-L1 gene S18Y polymorphisms and sporadic AD (Xue and Jia, 2006; Zetterberg et al., 2010). Here, UCHL1 is linked to Alzheimer disease.