Relevantly, changes in UCHL-1 -the most abundant, neuron-specific ubiquitin C-terminal hydrolase which regulates the structure and function(s) of synaptic terminals by controlling the local ubiquitin dynamics (Cartier et al., 2009)- are known to be involved in the pathogenesis of AD (Pasinetti, 2001; Choi et al., 2004; Gong et al., 2006). This evidence concerns the gene UCHL1 and Alzheimer disease.