Member SpotlightsOxidative Stress and its Role in the Pathogenesis of Alzheimer disease Dr. George Perry A Science Advisory Board Member Since 1997  Dr. Perry is a Dean and a Professor in the College of Sciences at the University of Texas at San Antonio. Educational Background: Dr. Perry received a B.A. in Zoology from the University of California, Santa Barbara. He subsequently studied at The Scripps Institution of Oceanography – UCSD/Stanford University and was awarded his Ph.D in Marine Biology. Honors and Awards: NIH Research Career Development Award, 1987-1993 Fellow, American Association for the Advancement of Science, 1998 Faculty of 1000 Biology, Member, Neurobiology of Disease and Regeneration Section, 2004 Doctorado Honoris Causa (Hon. D.), Universidad Arturo Prat, Iquique, Chile, 2007 Highly Cited – Institute for Scientific Information, 2008 Iberoamerican Molecular Biology Organization, 2008 Denham Harman Award, American Aging Association, 2008 Foreign member, Royal Society of Spain, 2010 Distinguished Professional Mentor Award, Society for the Advancement of Chicanos and Native Americans in Science (SACNAS), 2010 Alzheimer Award, Journal of Alzheimer’s Disease, 2010 Professional Memberships: -Editor-In-Chief, Journal of Alzheimer Disease -Past President, American Association of Neuropathology What is the primary focus of your current research?: Our research is on the pathogenesis of Alzheimer disease (AD) with focus on the role of oxidative stress, signal transduction and cell cycle abnormalities. My current position is Dean of the College of Sciences, University of Texas at San Antonio. In this role my major activity is leading the development of a research-intensive university while building on strength as an Hispanic service institution. Presently, in my research we are focusing on the physiology/biochemistry that underlies these diseases and would be most open to therapeutic intervention. We have often contrasted this view to one that attempts to find a single-cause effect for the diseases. While genetic or protein alterations have provided some insight, they have not provided a route to therapeutics. As a group, chronic degenerative diseases have defied treatment for reasons we think underlie the nature of the homeostatic changes that form them. In this light, efforts to simply remove or “treat” single changes of the disease are unlikely to be efficacious. What motivated you to pursue this research?: Since my graduate student days I have been interested in the role of oxidative stress in pathology and physiology. In my early work I examined the role of oxidative stress in fertilization, while I now study the end of life. Several features attracted me to this area. First, there was incredible opportunity; when I began, most work was on the negative aspects of oxidative stress and damage. I thought it was analogous to where calcium studies had been 70 years ago. Second, the ambiguity of oxidative stress and response and role of antioxidants appealed to my own concept of scientific truth. Third, the founders of the oxidative stress field were unusually open to scientific innovation. I have not been disappointed. Looking back, is your current career path what you expected it would be?: The administrative part is a surprise even to me, but the science is exactly as I expected and planned. In my formative days I was highly introverted, probably the result of growing up on an isolated farm. As I learned, success in science is highly social and it was my wife’s coaxing and my own work to resolve academic inequalities that brought me to leadership positions. Even more surprising is my leadership in minority education, which developed as I came to realize that Azorean-Americans share lower educational attainment with other Hispanics. These issues, and the opportunity to work in a dynamic university, brought me to UTSA. In science I wanted to work in an area where my persistence and ability to connect relationships could make novel contributions. I have found that in my research in oxidative stress. Doing so was not without detours--I think the most important was that I unsuccessfully tried to adapt the explicit approach of others to science to my own work instead of adapting my own strengths to the task at hand through empirical observation. By this means I learned through the example of others and my own strength. I wish I could have known this would be my path at an earlier point in my career. Do you have timeline predictions, such as: What type of breakthrough may occur in the future and when? When will new technology be available that will increase the speed & productivity of your research?: The major limitation is new insights. Technically new developments in mass spectrometry and other approaches that allow unbiased analysis of insoluble aggregates will advance the field. I think that increased insights will continue for degenerative conditions but major advances will require paradigm shifts. The rapid progress of biology through linear/reductionist approaches based on the central dogma of biology have also impeded our understanding of the most important diseases afflicting modern society where people are changing lifestyle and longevity faster than genes can be selected to support them. What are your other hobbies, interests, activities?: My outside interests are focused on family and resolving educational inequity and self-realization. Genealogy has been an important tool for linking my Portuguese heritage and science. Any other comments you may have about the future and progress of neurodegenerative diseases?: There will be improved therapeutics in the next several years but it is likely their impact will be small until we understand their primary driver—ageing. Understanding age-related neurodegenerative diseases will lead to opening the complexity of biological homeostasis adaptation to a post-genetic world. For more information about Dr. Perry's research, please refer to one of the following links or publications; -http://bio.utsa.edu/faculty/perry.html -http://en.wikipedia.org/wiki/George_Perry_%28neuroscientist%29 -http://www.researcherid.com/rid/A-8611-2009 Publications: Lee H-g, Zhu X, Casadesus G, Pallàs M, Camins A, O’Neill MJ, Nakanishi S, Perry G, Smith MA. The effect of mGluR2 activation on signal transduction pathways and neuronal cell survival. Brain Res 1249:244-250, 2009. Gelfand SL, Vento M, Sastre J, Lust WD, Smith MA, Perry G, Walsh M, Martin R. A new model of oxidative stress in rat pups. Neonatology 94:293-299, 2008. Dwyer BE, Zacharski LR, Balestra DJ, Lerner AJ, Perry G, Zhu X, Smith MA. Getting the iron out: Phlebotomy for Alzheimer’s disease? Med Hypoth 72:504-509, 2009. Dwyer BE, Stone ML, Gorman N, Sinclair PR, Perry G, Smith MA, Zhu X. Heme-a, the heme prosthetic group of cytochrome c oxidase, is increased in Alzheimer’s disease Neurosci Lett 461:302-305, 2009. Wang X, Su B, Lee H-g, Li X, Perry G, Smith MA, Zhu X. Impaired balance of mitochondrial fission and fusion in Alzheimer’s disease. J Neurosci 29:9090-9103, 2009 Garrett M, Raina AK, Rottkamp CA, Cash AD, Sayre LM, Perry G, Smith MA. Acetylation: a novel posttranslational modification in Alzheimer disease (accepted pending revision). Bonda DJ, Evans TA, Santocanale C, Llosá JC, Viña J, Bajic VP, Castellani RJ, Siedlak SL, Perry G, Smith MA, Lee H-g. Evidence for the progression through S-phase in the ectopic cell cycle re-entry of neurons in Alzheimer disease. Aging 1:382-388, 2009. Cash AD, Harris PLR, Siedlak SL, Smith MA, Perry G. Defining the mechanism for nitrotyrosine formation in Alzheimer disease (in preparation). Lee H-g, Casadesus G, Nunomura A, Zhu X, Castellani RJ, Richardson SL, Perry G, Felsher DW, Petersen RB, Smith MA. The neuronal expression of MYC causes a neurodegenerative phenotype in a novel transgenic mouse. Amer J Pathol 174:891-897, 2009. Chan HW, Liu T, Verdile G, Bishop GM, Haasl RJ, Smith MA, Perry G, Martins RN, Atwood CS. Copper induces apoptosis of neuroblastoma cells via post-translational regulation of the expression of Bcl-2-family proteins and the txJ mouse is a better model of hepatic than brain Cu toxicity.Int J Clin Exp Med 1:76-88, 2008. Siedlak SL, Casadesus G, Webber KM, Pappolla MA, Atwood CS, Smith, MA, Perry G. Chronic antioxidant therapy reduces oxidative stress in a mouse model of Alzheimer’s disease Free Rad Res 43:156-164, 2009. ### << Previous Next >> [ View All Member Spotlights ] |
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