Philip Haydon, Ph.D., the Annetta and Gustav Grisard Professor of Neuroscience and chair of the Department of Neuroscience, is one of the world’s foremost experts in neuron-glia interactions. Work in the Haydon Lab integrates a variety of technical approaches to illuminate roles played by glia in molecular genetics, electrophysiology, imaging, and behavioral studies. In the 1990s, Haydon and colleagues were the first to discover that astrocytes, a subtype of glial cell, exhibit the regulated release of chemical transmitters that were previously thought to be released only from neurons. Haydon is the founder of Glia-Cure, a start-up biotech company using new discoveries about glial cells to develop new drug therapies for Alzheimer’s and other diseases.
Giuseppina Tesco, M.D., Ph.D., and colleagues are studying one of the central mechanisms governing Alzheimer’s disease, namely the regulation and accumulation of beta-amyloid plaques in the brains of people with Alzheimer’s. These plaques are thought to be the cause of memory loss, cognitive impairment, confusion, and personality changes. Tesco’s research focuses on the beta-site APP-cleaving enzyme, BACE1, also known as betasecretase, and its regulatory role in the production of beta-amyloid. BACE1 is a primary target for Alzheimer’s treatment. Tesco’s group has shown that BACE1 is increased in the brain of people with Alzheimer’s disease and after stroke and head trauma, which are known risk factors for the development of Alzheimer’s. One of the most exciting results of Tesco’s recent work is the discovery of a novel mechanism of BACE1 regulation mediated by the molecule GGA3, which may pinpoint new targets for drug therapy.
Leon Reijmers, Ph.D., and colleagues are working to understand the molecular basis of memories, or how networks of neurons encode and retrieve memories. Current projects in the Reijmers Lab include identifying proteins that are synthesized by neurons during memory encoding, mapping connections among memory-encoding neurons, and studying the process of memory encoding in a mouse model of Alzheimer’s disease.