UCHL1 and Alzheimer disease: This premise is supported by studies showing that overexpressing Uch-L1 or pharmacologically enhancing Uch-L1 activity, improves long term potentiation (LTP) and cognition in AD transgenic mouse models (Gong et al., 2006), whereas knocking out Uch-L1 or pharmacologically inhibiting Uch-L1 causes a decline in cognition (Kurihara et al., 2001; Gong et al., 2006; Chen et al., 2010; Figure 2).