David J. McAdoo, Ph.D.

Professor

Affiliations: Department of Human Biological Chemistry & Genetics; Marine Biomedical Institute

Phone: (409) 772-2939
Fax: (409) 762-3222
Email: djmcadoo@utmb.edu

Education

• B.A. 1963 Lafayette College
• Ph.D. 1971 Cornell University

research interests

The McAdoo group focuses on secondary damage by release of harmful substances following spinal cord injury. The goal of this work is to provide a foundation for improving ways to reduce the permanent impairments that follow spinal cord injury. Emphasis has been on the release and actions of the neurotransmitter and excitotoxin glutamic acid. Present efforts also include addressing the role of leukemia inhibitory factor in the outcome of spinal cord injury, proteomic (changes of large numbers of proteins and the consequences of those changes) of spinal cord injury, altered gene expression following spinal cord injury, and magnetic resonance imaging studies of the role of cholesterol trafficking in the outcome of spinal cord injury.

Selected Publications

De Castro, Jr., R.C., Burns, C., McAdoo, D.J. and Romanic, A.M. Metalloproteinase increases in the injured rat spinal cord. NeuroReport 11: 3551-3554, 2000.

McAdoo, D.J., Xu, G.-Y., Robak, G., Hughes, M.G. and Price, E.M. Evidence that reversed glutamate uptake contributes significantly to glutamate release following experimental injury to the rat spinal cord. Brain Res. 865: 283-285, 2000.

McAdoo, D.J., Robak, G., Xu, G.-Y., and Hughes, M.G. Adenosine release upon spinal cord injury. Brain Res. 854: 152-157, 2000.

McAdoo, D.J., Xu, G.Y., Robak, G. and Hughes, M.G. Changes in amino acid concentrations over time and space around an impact injury and their diffusion through the rat spinal cord. Exp. Neurol. 149: 538-544, 1999.

Liu, D., Xu, G.-Y., Pan, E. and McAdoo, D.J. Neurotoxicity of glutamate at the concentration released upon spinal cord injury. Neuroscience 93: 1383-1389, 1999.

Nesic, O., Xu, G.-Y., McAdoo, D.J., High, K., Hulsebosch, C. and Perez-Polo, R. Il-1 receptor antagonist prevents apoptosis of spinal cord cells after injury by decreasing caspase-3 activity. J. Neurotrauma, in press.