Ubiquitin hydrolase Uch-L1 rescues [beta]-amyloid-induced decreases in synaptic function and contextual memory

The effects of ubiquitin C-terminal hydrolase L1 (Uch-L1) inhibition on LTP and memory was investigated to determine the increasing Uch activity by the application of a fusion protein containing Uch-L1 rescues synaptic dysfunction in hippocampal slices treated with oligomeric A[beta]. The data results suggest that Uch-L1 could be an attractive target for the development of new therapeutic approaches to Alzheimer's disease (AD), either alone or in combination with therapies that alter A[beta] levels.