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Bruce Lyeth, Ph.D.

Bruce Lyeth

Clinical/Research Interests

Dr. Lyeth's research interests focus on the pathophysiology of traumatic brain injury, excitotoxic cascades affecting signal transduction and behavior, and the development of therapeutic interventions for brain injury. Dr. Lyeth's laboratory uses a variety of pharmacological, behavioral and neuroanatomical methods to investigate the neural mechanisms involved in traumatic brain injury pathology. The ultimate goal of this research program is to develop novel clinical therapeutic strategies targeted at reducing the debilitating consequences of traumatic brain injury in patients. Pre-clinical testing of novel therapeutic strategies and compounds are routinely performed in this laboratory. Previous efforts have led to ongoing clinical trials evaluating hypothermia and glutamate receptor antagonists as therapeutic interventions for traumatic brain injury patients. Dr. Lyeth is investigating the role of early astrocyte damage following TBI and the consequences on neuronal cell death, the involvement of the neuropeptide NAAG in brain injury , and the role of HDAC inhibitors in modulating excitotoxicity.

Title:

 Professor IR

Specialty:

 Neurological Surgery

Education:

 Virginia Commonwealth University
Richmond, Virginia
Ph.D. 1986

Education:

 Christopher Newport College
Newport News, Virginia
B.A. 1974

Fellowships:

 Medical College of Virginia
Richmond, Virginia
1986-1987
Traumatic Brain Injury

Professional Memberships:

 Editorial Board, Journal of Neurotrauma
Member, Executive Council National Neurotrauma Society
UCLA Brain Injury Research Center Advisory Board

Select Recent Publications:

Zhang B, West EJ, Van KC, Gurkoff GG, Zhou, J, Zhang X-M, Kozikowski AP, Lyeth BG.. HDAC inhibitor increases histone H3 acetylation and reduces microglia inflammatory response following traumatic brain injury in rats. Brain Research, 1226: 181-191, 2008.

Cox CD, West EJ, Liu MC, Wang KK, Hayes RL, Lyeth BG. Dicyclomine, an M1 muscarinic antagonist, reduces biomarker levels, but not neuronal degeneration, in fluid percussion brain injury. J Neurotrauma, 25(11): 1355-65, 2008.

Zhao X, Gorin FA, Berman RF, Lyeth BG. Differential hippocampal protection when blocking intracellular sodium and calcium entry during traumatic brain injury in rats. J Neurotrauma, 25(10): 1195-205, 2008.

Di Giorgio AM, Hou Y, Zhao X, Zhang B, Lyeth BG, Russell MJ. Dimethyl sulfoxide provides neuroprotection in a traumatic brain injury model. Restor Neurol Neurosci, 26(6): 501-7, 2008.

Folkerts MM, Parks EA, Dedman J, Kaetzel M, Lyeth BG, Berman RF. Phosphorylation of calcium calmodulin-dependent protein kinase II following lateral-fluid percussion brain injury in rats. J Neurotrauma, 24(4):638-650, 2007.

Floyd CL, Lyeth BG. Astroglia: Important Mediators of Traumatic Brain Injury. In: Neurotrauma: New Insights into Pathology and Treatment. Progress in Brain Research., 161, eds Weber JT, Mass AIR, Elsevier, Amsterdam, 2007.

Zhong C, Zhao X, Van KC, Bzdega T, Smyth A, Zhou J, Kozikowski AP, Jiang J, O'Connor WT, Berman RF, Neale JH, Lyeth BG. NAAG peptidase inhibitor increases dialysate NAAG and reduces glutamate, aspartate and GABA levels in the dorsal hippocampus following fluid-percussion injury in the rat. J Neurochemistry, 97:1015-1025, 2006.

Zhong C, Zhao X, Sarva J, Kozikowski A, Neale JH, Lyeth BG. NAAG peptidase inhibitor reduces acute neuronal degeneration and astrocyte damage following lateral-fluid percussion TBI in rats. J Neurotrauma, 22(2):266-276, 2005.

Van Putten HP, Bouwhuis MG, Muizelaar JP, Lyeth BG, Berman RJ. Diffusion-weighed imaging of edema following traumatic brain injury in rats: Effects of secondary edema. J Neurotrauma, 22(8):857-872, 2005.

Floyd CL, Gorin FA, Lyeth BG. Mechanical strain injury to cultured astrocytes increases intracellular sodium and reverses Na+/Ca++ exchange. GLIA, 51(1):35-46, 2005.