George Perry (born April 12, 1953 in Lompoc, California) is a neuroscientist and 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 Alzheimer's disease research particularly for his work on oxidative stress.
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Perry received his bachelor's of arts degree in Zoology from University of California, Santa Barbara. After graduation, he headed to Scripps Institution of Oceanography and also studied at Hopkins Marine Station of Stanford University and the Marine Biological Laboratory of Woods Hole and obtained his PhD 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, Joseph Bryan and Anthony R. Means at Baylor College of Medicine where he laid the foundation for his observations of cytoskeletal abnormalities.
In 1995, Perry joined the faculty of Case Western Reserve University, where he currently holds an adjunct appointment. He is currently dean of the College of Sciences and professor of biology at the University of Texas at San Antonio. He is distinguished as one of the top Alzheimer’s disease researchers[1][2] with over 900 publications, one of the top 100 most-cited scientists[3] in Neuroscience & Behavior and one of the top 25 scientists in free radical research.[4] Perry has been cited over 29,000 times (H=88) and is recognized as an ISI highly cited researcher.[5][6] Perry is editor for numerous journals and is editor-in-chief for the Journal of Alzheimer's Disease. He is fellow of the American Association for the Advancement of Sciences and past-president of the American Association of Neuropathologists.
Perry's 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.