Faculty Detail   
Patsy W. and Charles A. Collat Professor of Neuroscience
Director, Alzheimer's Disease Center
Director, Center for Neurodegeneration and Experimental Therapeutics
Associate Director, Evelyn F. McKnight Brain Institute
Campus Address SHEL 1110 Zip 2182
E-mail  eroberson@uabmc.edu
Other websites Roberson Lab Website
CNET Website
Alzheimer's Disease Center website

Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Neurology Chair Office  Neurology Chair Office Professor
Secondary  Neurobiology  Neurobiology Professor
Center  Alzheimer's Disease Center  Alzheimer's Disease Center Professor
Center  Comprehensive Neuroscience Center  Comprehensive Neuroscience Center Professor
Center  Ctr for Clinical & Translational Sci  Ctr for Clinical & Translational Sci Professor
Center  Ctr for Glial Bio in Med  Ctr for Glial Bio in Med Professor
Center  Ctr Neurodegeneration & Exp Ther (CNET)  Ctr Neurodegeneration & Exp Ther (CNET) Professor
Center  Evelyn F. McKnight Brain Institute  Evelyn F. McKnight Brain Institute Professor
Center  Integrative Center for Aging Research  Integrative Center for Aging Research Professor
Center  Multiple Sclerosis Center  Multiple Sclerosis Center Professor

Graduate Biomedical Sciences Affiliations
Cell, Molecular, & Developmental Biology 
Cellular and Molecular Biology Program 
Medical Scientist Training Program 
Pathobiology and Molecular Medicine 

Biographical Sketch 
Dr. Roberson is a neurologist and neuroscientist whose research is focused on age-related cognitive impairment. He received his A.B. with highest honors from Princeton University, then earned his M.D. and Ph.D 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, where he also served as Chief Resident in Neurology. After residency, he completed a clinical fellowship in behavioral neurology at UCSF and resumed basic research at the Gladstone Institute of Neurological Disease. He joined the neurology faculty at UCSF in 2005 and moved to UAB in 2008.

The Roberson lab studies the neurobiology of Alzheimer’s disease and frontotemporal dementia (FTD), using mouse models to understand the cellular and molecular mechanisms of these disorders and identify new therapeutic strategies, with a particular focus on tau and progranulin. His lab is part of the UAB Center for Neurodegeneration and Experimental Therapeutics (CNET), which Dr. Roberson leads along with Dr. Andrew West.

Dr. Roberson is also active in clinical research and patient care, directing the UAB Alzheimer’s Disease Center, leading clinical trials, caring for patients with memory disorders and dementia at the Kirklin Clinic, and co-directing the Evelyn F. McKnight Brain Institute for research on cognitive aging.

Society Memberships
Organization Name Position Held Org Link
American Academy of Neurology    http://www.aan.com 
American Neurological Association    http://myana.org 
International Society to Advance Alzheimer Research and Treatment    http://www.alz.org/professionals_and_researchers_istaart.asp 
Molecular and Cellular Cognition Society    http://www.molcellcog.org/ 
Society for Neuroscience    http://www.sfn.org 

Research/Clinical Interest
Neurobiology of Alzheimer's Disease and Frontotemporal Dementia
The Roberson lab studies the neurobiology of two common neurodegenerative disorders, Alzheimer Disease and Frontotemporal Dementia, with a focus on understanding the underlying cellular and molecular mechanisms that will lead to better treatments. We apply modern neuroscience approaches to study animal and cellular models of these conditions. We have shown that reducing expression of the microtubule-associated protein tau makes the brain resistant to Alzheimer-related impairments, and are using a variety of behavioral, electrophysiological, and biochemical approaches to better understand this protective effect. We are also studying animal models of frontotemporal dementia to understand how mutations in tau and progranulin cause the social and behavioral dysfunction seen in this condition.

Neurodegeneration, Alzheimer's disease, frontotemporal dementia, tau, progranulin, excitability, signaling, plasticity, behavior