There are more than 70,000 Oklahomans who suffer from Alzheimer's disease (AD) and it is estimated that 96,000 patients will be diagnosed with AD by 2025 in Oklahoma. Cognitive decline in Alzheimer's disease is thought to be the result of disturbed neuronal communication due to synaptic dysfunction. Aggregated amyloid beta protein accumulates in AD, a process dependent on synaptic activity. In this series of studies we investigate how synaptobrevin1, an essential synaptic protein, regulates amyloid secretion. Maintaining physiological synaptic function while reducing amyloid secretion may provide a breakthrough to design effective therapies that halt progression of dementia in Alzheimer's disease.