With Alzheimer’s disease being one of the most debilitating, prevalent, deadly, and costly disease in the United States, research into treatments has increased drastically in the recent years. In Alzheimer’s disease, a misfolded protein, called amyloid-beta, aggregates to form plaques. These plaques interrupt neuronal transmission at the synapse, degrade neurons and glia, and produce swelling—all of which contribute to decreased neurological function and Alzheimer’s disease. There is currently no cure. Treatments are available to alleviate symptoms. One successful strategy includes reducing the swelling caused by amyloid-beta plaques. The Adenosine A2A Receptor, a transmembrane G-Protein coupled receptor that activates adenylyl cyclase to produce the secondary messenger cAMP, is a target of interest in treating symptoms of Alzheimer’s disease. The receptor’s normal function is to regulate inflammation caused by the inflammatory response. It has been shown that inhibiting the receptor decreases long-term swelling and inflammation caused by amyloid-beta plaques. In this study, we endeavored to discover a novel antagonist of the adenosine A2A receptor. Using HEK-293 cells expressing this receptor, we measured cAMP concentration inside of the cells to quantify the effects of previously untested benzothiazoles, on receptor activity relative to known antagonists.

Previously untested benzothiazoles as a blockade of the adenosine A2a receptor, as a possible treatment for Alzheimer's disease

251st National Meeting (2016)

The official archive and repository for all ACS Meetings & Expositions abstracts and select posters or presentations.