Alzheimer's Research Laboratory

Education: Ph.D., University of California, San Diego

Research Interests:
Several lines of evidence point to an underlying vascular component in the pathology of Alzheimer's disease (AD).Vascular diseases (hypertension, atherosclerosis, stroke) often precede or accompany the onset of AD. Endothelium dysfunction is an early event in these vascular diseases. An impaired endothelium response is also found in normal aging and Alzheimer's disease is an age dependent disease. We have shown that vascular dysfunction induced by the Alzheimer's peptide, b-amyloid (Ab), involves endothelial damage by superoxide radicals. Our current research is to investigate the mechanism of Ab induced dysfunction and the role of aging, stroke, and endogenous antioxidants (estrogen) in the Ab related vascular component of AD pathology.

FIGURE: Cannulated posterior cerebral rat artery used for in vitro experiments to test the effects of the Alzheimer's peptide, b-amyloid on vascular function.

Recent publications:

Price JM, Sutton ET, Hellermann A, Thomas T. b-amyloid induces cerebrovascular endothelial dysfunction in rat brain. Neurological Research 19: 534-538, 1997. PubMed File

Chi, X, Sutton, ET, Thomas, T. Price JM The protective effect of K+ channel openers on b-amyloid induced cerebrovascular endothelial dysfunction. Neurological Research 21(4): 345-351, 1999. PubMed File

Email: jprice@hsc.usf.edu
Phone: (813) 974-1559
Fax: (813) 974-3079
Mail Box: MDC Box 08