The critical effects of UCH-L1 on PKA-CREB cascade was further investigated in a transgenic mouse model of AD: in this case, restoring UCH-L1 homeostatic functionality counteracts the Aβ-induced inhibition of long-term potentiation (LTP), rescuing basal neurotransmission and synaptic plasticity and boosting associative memory in APP/PS1 mice. This evidence concerns the gene UCHL1 and Alzheimer disease.