Perry joined the UTSA faculty in 2006 from Case Western Reserve University where he was Professor of Pathology and Neurosciences and Chair of the Department of Pathology. 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 has been cited over 50,000 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 Alzheimer′s Disease. He is a fellow of the American Association for the Advancement of Sciences, the Microscopy Society of America, 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 Lisbon Academy of Sciences. Perry joined the UTSA faculty in 2006 from Case Western Reserve University where he was Professor of Pathology and Neurosciences and Chair of the Department of Pathology. 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 has been cited over 50,000 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 Alzheimer′s Disease. He is a fellow of the American Association for the Advancement of Sciences, the Microscopy Society of America, 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 Lisbon Academy of Sciences.

Our studies are focused on the mechanism of formation and physiological consequences of the cytopathology of Alzheimer disease. We have shown that oxidative damage is the initial cytopathology in Alzheimer disease. We are working to determine the sequence of events leading to neuronal oxidative damage and the source of the increased oxygen radicals. Our current studies focus on (i) the mechanism for RNA-based redox metal binding; (ii) the consequences of RNA oxidation on protein synthesis rate and fidelity; (iii) the role of redox active metals in mediating prooxidant and antioxidant properties; (iv) the signal transduction pathways altered in Alzheimer disease that allow neurons to evade apoptosis; and (v) mechanism of phosphorylation control of oxidative damage to neurofilament proteins.