Department of Obstetrics and Gynecology
Union Graduate College
George Perry is dean of the College of Sciences and professor of biology at The University of Texas at San Antonio. Perry is recognized in the field of Alzheimers disease research particularly for his work on oxidative stress. Perry received his bachelors of arts degree in zoology with high honors from University of California, Santa Barbara. After graduation, he headed to Scripps Institution of Oceanography and obtained his Ph.D. in marine biology under David Epel in 1979. He then received a postdoctoral fellowship in the Department of Cell Biology in the laboratories of Drs. Bill Brinkley and Joseph Bryan at Baylor College of Medicine where he laid the foundation for his observations of abnormalities in cell structures. In 1982, Perry joined the faculty of Case Western Reserve University, where he currently holds an adjunct appointment. He is distinguished as one of the top Alzheimer’s disease researchers with over 800 publications, one of the top 100 most-cited scientists in neuroscience and behavior and one of the top 25 scientists in free radical research. Perry has been cited over 23,000 times and is recognized as an ISI highly cited researcher. Perry is editor for numerous journals and is editor-in-chief for the Journal of Alzheimers Disease. He is a fellow of the American Association for the Advancement of Sciences and past-president of the American Association of Neuropathologists, as well as a member of the Dana Alliance for Brain Initiatives. Perry is recognized internationally for his work. He is a Foreign Correspondent Member of the Spanish Royal Academy of Sciences and a Foreign Member of the Mexican National Academy of Sciences, and recent recipient of the National Plaque of Honor from the Republic of Panama Ministry of Science and Technology.
Perry′s research is primarily focused on how Alzheimer disease develops and the physiological consequences of the disease at a cellular level. He is currently working to determine the sequence of events leading to damage caused by and the source of increased oxygen radicals.