BACE1 and Alzheimer disease: Zhang et al. (2014) used APP23/PS45 double transgenic AD model mice, overexpressing UCH-L1 by intracerebral injection of UCH-L1 expressing recombinant adeno-associated virus, and the results showed that UCH-L1 overexpression could regulate the degradation of BACE1, which in turn reduced the production of APP CTF and the level of Aβ, inhibited the formation of neuritic plaques, and ameliorated the memory deficits in the AD transgenic model mice to slow down the progression of AD.