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Faculty Detail    
Name MICHELLE GRAY
  
Campus Address CIRC 425 Zip 0021
Phone  (205) 996-4748
E-mail  mccgray@uab.edu
Other websites http://labs.uab.edu/mccgray/
     


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Neurology Chair Office  Neurology Chair Office Associate Professor
Secondary  Neurobiology  Neurobiology Assistant Professor
Center  Comprehensive Neuroscience Center  Comprehensive Neuroscience Center Associate Professor
Center  Ctr for Exercise Medicine (Org Ret)  Ctr for Exercise Medicine (Org Ret) Associate Professor
Center  Ctr for Glial Bio in Med  Ctr for Glial Bio in Med Associate Professor
Center  Ctr Neurodegeneration & Exp Ther (CNET)  Ctr Neurodegeneration & Exp Ther (CNET) Associate Professor
Center  Evelyn F. McKnight Brain Institute  Evelyn F. McKnight Brain Institute Associate Professor

Graduate Biomedical Sciences Affiliations
Biochemistry and Structural Biology 
Cell, Molecular, & Developmental Biology 
Genetics, Genomics and Bioinformatics 
Neuroscience 
Pathobiology and Molecular Medicine 

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