Erik Roberson, M.D., Ph.D.
Associate Professor of Neurology
Virginia B. Spencer Scholar in Neuroscience
Associate Director, CNET - Center for Neurodegeneration and Experimental Therapeutics
Professional Background: A.B., Princeton University, 1990; M.D., Ph.D. (Neuroscience), Baylor College of Medicine, 1999
Office: SHEL 1106, 1825 University Blvd, Birmingham AL 35294-2182
Originally from Iowa, Dr. Roberson received his A.B. with highest honors from Princeton University in 1990. He earned an M.D. and Ph.D in neuroscience at Baylor College of Medicine in Houston before moving to the University of California San Francisco for neurology residency. He served as Chief Resident in Neurology at UCSF, then completed a clinical fellowship in behavioral neurology with Dr. Bruce Miller while resuming basic research in the laboratory of Dr. Lennart Mucke at the Gladstone Institute of Neurological Disease. He was appointed as Assistant Professor of Neurology at UCSF in 2005. In 2008, he moved to UAB where he is now Associate Professor of Neurology and Neurobiology and the Virginia B. Spencer Scholar in Neuroscience.
Specialty / Interests
Dr. Roberson is a physician-scientist interested in neurodegenerative diseases, particularly Alzheimer Disease (AD) and Frontotemporal Dementia (FTD). He sees patients with AD, FTD, and related disorders at The Kirklin Clinic, and directs a basic science laboratory devoted to understanding the neurobiology of AD and FTD and to helping develop better treatments for these conditions. His lab uses modern neuroscience approaches to study animal and cellular models of these conditions and unravel their underlying cellular and molecular mechanisms. Dr. Roberson has shown that reducing expression of the microtubule-associated protein tau makes the brain resistant to Alzheimer-related impairments, and the lab is using a variety of behavioral, electrophysiological, and biochemical techniques to better understand this protective effect. The lab is also testing new animal models of frontotemporal dementia to understand how mutations in tau and progranulin cause the social and behavioral dysfunction seen in this condition.