Investigator: Christopher Reid, Bryant University

Scientific Theme: Neuroscience

Abstract: The Lyme disease epidemic in the U.S. is far worse than doctors and public health professionals have predicted. Last year the Centers for Disease Control and Prevention (CDC) reported over 30,000 cases of Lyme disease in the United States. It is estimated that unreported cases of Lyme disease brings the total in excess of 300,000 annually. This large number is due to the belief that Lyme disease is significantly underreported due to the broad physiological manifestations of the disease causing difficulty in diagnosis. While our knowledge and understanding of Borellia burgdorferi (Bb) physiology and pathogenesis is contstantly improving, exactly how Bb interacts with the CNS to cause disease is still a black box in our understanding of Lyme disease. In order for Bb to cause neuropathologies, it must interact with nerve cells. Gangliosides, a subfamily of glycosphingolipids, are particularly concentrated in the membranes of nervous tissue. These glycolipids serve as a distinguishing surface marker for cell recognition and cell-to-cell communication. We plan to use a bioinformatic approach to identify potential ganglioside binding proteins in Bb by probing the 17 available Bb genomes with a non-homologous database of known ganglioside binding proteins. We will use a feature-incorporated alignment method (FIA) to identify putative carbohydrate binding modules and ligand binding residues in the putative Bb ganglioside binding proteins. Once putative ganglioside binding proteins are identified, they will be cloned and biochemically characterized.

Human Health Relevance: This research program will provide valuable information regarding the pathogenesis of neuroborreliosis by identifying the mechanism by which Bb recognizes and binds to neural tissue. This research could lead to potential therapeutic intervention for neuroborreliosis.