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George Perry

Adjunct Clinical Assistant & Professor
Department of Obstetrics and Gynecology
Union Graduate College
Azerbaijan

Biography

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 bachelor 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 900 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 is recognized internationally for his work. He is a Foreign Correspondent Member of the Spanish Royal Academy of Sciences, the Academy of Science Lisbon, and a Foreign Member of the Mexican National Academy of Sciences. He is also a recent recipient of the National Plaque of Honor from the Republic of Panama Ministry of Science and Technology.  

Research Interest

Perrys research is primarily focused on the mechanism of formation and physiological consequences of the cytopathology of Alzheimer disease. He has played a key role in elucidating oxidative damage as the initial cytopathological abnormality in Alzheimer disease. He is currently working to determine the sequence of events leading to neuronal oxidative damage and the source of the increased oxygen radicals. His current studies focus on two issues: (i) the metabolic basis for the mitochondrial damage restricted to vulnerable neurons; and (ii) the consequences of RNA oxidation on protein synthesis rate and fidelity.

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