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Brent T. Harris MD, PhD

Contact Information:
Phone: (603) 650-7171
Fax: (603) 650-4845
Email: not given

Website: http://www.dartmouth.edu/~btharris/

Dartmouth Medical School page

Institution Affiliations:
Assistant Professor of Pathology
Department of: PATHOLOGY
Section: Pathology
Specialty: Anatomic Pathology/Neuropathology
Joined Staff: 2002

Cancer Center Membership:
Neuro-Oncology Group
Pediatric Oncology Group

Clinical Interests:
Brain Tumors
Neurodegeneration
ALS
Regeneration
Board Certified:
Anatomic Pathology and Neuropathology, 2003
Degree(s): MD, PhD
Georgetown University School of Medicine, Washington, DC 1995

Internship(s):

Residency:
Stanford University, Stanford, CA, (Pathology, Anatomic) , Chief Resident 1997-1998 1997-99

Fellowship(s):
Stanford University Medical Center, Stanford, CA, (Neuropathology) 1997-99

Biography:
Dr. Harris is a neuropathologist and neuroscientist interested in glial-neuronal interactions, pediatric head trauma, neuronal cell survival, CNS/PNS tumors, and neurodegenerative diseases. He is one of the co-founders of the ALS Center at DHMC and is actively involved in educating undergraduate, graduate, and medical students at Dartmouth College and Dartmouth Medical School.

Research Interests:
Our ability to move our arms and legs depends on the integrity of our spinal motor neurons, which relay electrical signals from our brain to our muscles. When these motor neurons die, as can occur in injury or in a variety of degenerative diseases that affect infants and children (spinal muscular atrophies) or adults (ALS) irreversible paralysis or even death may ensue. Cortical upper motor neurons extend their axons great distances down to the spinal cord. For unknown reasons in ALS, this select group of neurons in the cerebrum atrophy and die similar to the lower motor neurons in the spinal cord. A number of transgenic animal models for ALS exist based on the superoxide dismutase (SOD1) gene mutations found in a portion of familial ALS patients. These animals display similar clinical symptoms and histopathology to that found in human motor neuron disease. Thus, it is now possible and crucial to understand the signaling mechanisms that normally promote upper and lower motor neuron survival and how these processes go awry in motor neuron diseases.

Selected Publications:
Stommel, EW, Cohen, JA, Fadul, CE, Cogbill, CH, Graber, DJ, Kingman, L, Mackenzie, T, Harris,BT. Efficacy of Thalidomide for the Treatment of Amyotrophic Lateral Sclerosis: A Phase II Open Label Clinical Trial. Amyotrophic Lateral Sclerosis Jan 28:1-12, 2009.
Hitoshi, Y., Harris, B.T., Lui, H., Popko, B., Israel, M.A. Spinal glioma: platelet–derived growth factor mediated oncogenesis in the spinal cord. Cancer Research,68(20):8507-15, 2008.
Stommel, E.W. Langford, G., van Hoff, R., Bercury, K., Harris, B.T. Mitochondrial localization in motor neurons in response to tumor necrosis factor alpha: implication for amyotrophic lateral sclerosis. Neuroscience,146(3):1013-9, 2007.
  

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