Back to Main

Faculty Detail    
Name MICHELLE GRAY
 
Campus Address CIRC 525B Zip 0021
Phone 205-996-4748
E-mail mccgray@uab.edu
Other websites https://www.uab.edu/medicine/neurology/faculty/gray
     


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Neurology   Neurology Chair Office Assistant Professor
Secondary  Neurobiology  Neurobiology Assistant Professor
Center  General Clinical Research Center  Comprehensive Neuroscience Center Assistant Professor
Center  Ctr for Glial Bio in Med  Ctr for Glial Bio in Med Assistant Professor
Center  Neurology   Ctr Neurodegeneration & Exp Ther (CNET) Assistant Professor

Biographical Sketch 
Graduate of Alabama State University, Montgomery, AL; 1997 B.S. in biology
Received Ph.D. from Ohio State University, Columbus, OH, in Molecular, Cellular, and Developmental Biology in 2003 Postdoctoral fellow in the Semel Institute of Neuroscience and Human Behavior at the University of California, Los Angeles.
Joined the UAB Center for Neurodegeneration and Experimental Therapeutics (CNET) in the Department of Neurology, September 2008 as an Instructor of Neurology and Dixon Scholar in Neuroscience and was promoted to Assistant Professor, June 2010.

Research/Clinical Interest
Title
Pathogenesis of Huntington's Disease
Description
My work is focused broadly on uncovering the mechanisms that contribute to Huntington’s Disease (HD) pathogenesis. Huntington’s Disease is an autosomal dominant neurodegenerative disorder characterized by motor, psychiatric and cognitive deficits. The disease is caused by a repeat expansion in the ubiquitously expressed huntingtin protein. Although the protein is widely expressed, only a subset of neurons is affected in disease. My current work is focused on understanding the overall contribution of glial cells (which constitute about 50% of cells in the brain) to HD pathology. This includes understanding the normal function of the huntingtin protein in glial cells and determining how the mutant protein in glial cells contributes to neuronal dysfunction in HD. We use conditional mouse genetic models to dissect cell type contribution to disease. We employ BAC transgenesis technology to generate animal models that are then characterized using molecular, cellular, biochemical and neuropathological techniques.

Keywords
Huntington's disease, neurodegeneration, neuroscience, astrocytes