Alzheimer’s disease is thought to be caused by an excess of the peptide amyloid beta. This peptide greatly impacts synapses, leading to their inability to function normally. This is achieved, at least in part, by driving the loss of an important synaptic protein, PSD-95. This project seeks to leverage recent findings from our laboratory indicating that synapses can be protected from amyloid beta by increasing the amount of PSD-95 at synapses. The most exciting finding is that this can be achieved pharmacologically, using drugs that are being developed for human use. These studies should provide important preclinical data, paving the way for human trials with these drugs.