Mark S. Kindy, Ph.D.

Director, Neuroscience Institute; Associate Director of the Center on Aging;
Director of the Stroke Program; Associate Director of the South Carolina Spinal Cord Injury Center.

Medical University of South Carolina, Charleston, SC.

Phone: (843) 792-0808
Fax: (843) 792-4423
Email: kindyms@musc.edu

Education:

B.S. in Zoology University of Massachusetts, Amherst, MA
Ph.D. in Biochemistry, Boston University School of Medicine, Boston, MA
Post-Doctorate in Molecular Biology and Virology, Salk Institute, San Diego, CA

Research Interests:

The molecular basis of disease. Identification of novel targets for drug therapy. Specifically, understanding the amyloid formation in Alzheimer's disease, identifying signal transduction pathways in stroke and spinal cord injury. The primary goal of the laboratory is to determine the underlying mechanisms of these diseases and identify targets and compounds for treatment.

Selected Recent Publications:

Yan, S.D., Zhu, H., Zhu, A., Golabek, A., Wolozin, B., Roher, A., Yu, J., Chaney, M., Soto, C., Schmidt, A.M., Stern, D., Kindy, M.S. RAGE and amyloid fibrils: receptor-dependent signaling by b-sheet fibrils mediates cellular stress in amyloidosis. Nature Medicine, 2000, 6:643-651.

Keller, J.N., Huang, F.F., Zhu, H., Yu, J., Ho, Y.-S., Kindy, M.S. Oxidative stress-associated impairment of proteosome activity during ischemia-reperfusion injury. J. Cereb. Blood Flow Metab. 2000, 20:1467-73.

Dubal, D.B., Zhu, H., Yu, J., Rau, S.W., Shughrue, P.J., Merchenthaler, I., Kindy, M.S., Wise, P.M. Estrogen Receptor -a, not -b, is Critical in Estradiol-Mediated Neuroprotection against Stroke Injury. PNAS, 2001, 98:1952-1957.

Zhu, H., Yu, J. and Kindy, M.S. Inhibition of Amyloidosis Using Low-Molecular-Weight Heparins. Molec. Med. 2001, 7:517-522.

Guo, J-T., Yu, J., Zhu, H., Grass, D., de Beer, F.C., Kindy, M.S. Inflammation dependent cerebral deposition of serum amyloid A protein in a mouse model of amyloidosis J. Neurosci, 2002, 22:5900-5909.

Kindy M et al. RAGE mediates amyloid-b peptide transport across the blood-brain barrier, suppression of cerebral blood flow and development of cerebral amyloidosis. Nature Medicine, 2002, in press.