While the underlying cause of Alzheimer’s disease is unknown, evidence from human genetics and transgenic mouse studies implicate amyloid beta. This protein greatly impacts synapses—gaps between two neurons that serve as the sites of transmission of electrical or chemical information—leading to their inability to function normally. The Malinow laboratory seeks to leverage recent findings indicating that synapses can be protected from amyloid beta by increasing the amount of an important synaptic protein, PSD-95. This increase in PSD-95 at synapses can be achieved pharmacologically using drugs that are being developed for human use. These studies provide important pre-clinical data.