While Alzheimer's Disease (AD) is characterized by plaques and tangles composed mostly of β-amyloid, recent clinical trials focused on amyloid therapies have been disappointing and the ability to improve or prevent the decline in memory of most, if not all, currently developed AD therapies are questionable. We have developed a drug that will work to improve memory functions through a mechanism not previously explored in the AD field. However, the receptor system that the drug binds to has been extensively documented to regulate cognition. Transgenic mouse models I created have confirmed that function. The biggest hurdle in this area of research is that this receptor system also regulates blood pressure and most drugs that activate this receptor also cause an increase in blood pressure. The drug we designed has circumvented the blood pressure issues by only being active in the brain and by not increasing the signals that regulate blood pressure in the blood vessels throughout the body. We are currently testing this drug in a mouse model of AD and want to expand this effort by making further compounds to optimize its effects, to confirm that this drug reaches its intended target in the brain, and to determine its stability in an animal.