Erik Roberson, MD, PhD, is an associate professor of neurology and neurobiology and co-director of the Center for Neurodegeneration and Experimental Therapeutics at the University of Alabama at Birmingham (UAB). He received his bachelor’s degree with highest honors from Princeton University and then earned his MD and PhD in neuroscience at Baylor College of Medicine, where he studied molecular mechanisms of learning and memory. He completed a residency in neurology at the University of California, San Francisco (UCSF), where he also served as chief resident in neurology. After residency, he completed a clinical fellowship in behavioral neurology with Bruce Miller, MD, at UCSF and resumed basic research in the laboratory of Dr. Lennart Mucke, MD, at the Gladstone Institute of Neurological Disease, UCSF, initiating his current studies of neurodegenerative disease using mouse models. He joined the neurology faculty at UCSF in 2005, then moved to UAB in 2008. The Roberson lab studies the neurobiology of AD and frontotemporal dementia (FTD), with a focus on understanding the cellular and molecular mechanisms of these disorders and identifying new therapeutic strategies. The role of tau in neuronal dysfunction in AD and FTD is a major area of interest, and the lab also studies how progranulin deficiency causes FTD. In addition to directing his laboratory, Dr. Roberson co-director of the Center for Neurodegeneration and Experimental Therapeutics, which is dedicated to developing new therapies for age-related cognitive disorders and neurodegenerative disease. Dr. Roberson also cares for patients with memory disorders and dementia at the Kirklin Clinic and directs clinical trials related to tauopathies.
"As a physician-scientist, I am committed to translating basic science discoveries about AD as far as possible toward therapies. This work started about 10 years ago when we found that reducing tau in mouse models was protective. We reasoned that reducing tau in people would be difficult, so instead we have looked for a way to reduce the aberrant form of tau which, of course, remains somewhat of a mystery. Over the years, we have accumulated evidence that tau’s interaction with Fyn is important, so we started this drug discovery/development project to pursue a new therapeutic approach involving this pathway."