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Home: Community: Researcher Profiles
Researcher Profile

RESEARCHER INFORMATION
First Name:George
Last Name:Perry
Title:Dean
Advanced Degrees:Ph.D.
Affiliation:University of Texas at San Antonio
Department:College of Sciences
Street Address 1:One UTSA Circle
City:San Antonio
State/Province:TX
Zip/Postal Code:78249
Country/Territory:U.S.A.
Phone:210-458-4450
Fax:210-458-4445
Email Address: 
Disclosure:
(view policy) 
Member reports the following financial or other potential conflicts of interest: [Last Modified: 30 July 2008]

I am a consultant for and have stock options in Voyager Pharmaceutical Corporation and Panacea Pharmaceutical Company.
View all comments by George Perry
Clinical Interests:
Alzheimer Disease, Neurodevelopmental Disorders (Down syndrome, etc.), Tauopathies, Aging Process, Prion Diseases, Neuromuscular Disorders (ALS, etc.), Parkinson Disease
Research Focus:
A-beta PP/A-beta, Animal Models, Apoptosis/Cell cycle, Oxidative Stress, Tau/Cytoskeleton, Microscopy, Molecular and Cell biology, Neuropathology, Protein structure/chemistry
Work Sector(s):
University
Web Sites:
Personal: http://bio.utsa.edu/faculty/perry.html
Professional: http://www.utsa.edu/
Researcher Bio
Education:
University of California, Santa Barbara, B.A., 1974, Zoology
University of California, San Diego, Ph.D., 1979, Marine Biology
Baylor College of Medicine, Houston, Texas, Fellow, 1982, Cell Biology

Professional Positions:
1982-1989 Assistant Professor of Pathology, Case Western Reserve University, Cleveland, Ohio
1989-1994 Associate Professor of Pathology and Neuroscience, Case Western Reserve University, Cleveland, Ohio
1994-present Professor and Pathology and Neuroscience, Case Western Reserve University, Cleveland, Ohio
2001-2005 Interim-Chair, Department of Pathology, Case Western Reserve University, Cleveland, Ohio
2006-present Dean, College of Sciences, The University of Texas at San Antonio, San Antonio, Texas

Other Experience and Professional Memberships:
Neurological Sciences I, ad hoc Member 1988-89, Member 1989-93, Chair 1991-93
Neurological Sciences III, Member, 1995
Associate Editor, American Journal of Pathology 1994-2000
Editor-in-Chief, Journal of Alzheimer's Disease, 1998-

Honors and Awards:
NIH Research Career Development Award, 1987-1993
Fellow, American Association for the Advancement of Science, 1998
Zenith Fellows Award, Alzheimer's Association, 2007
Top Papers
Smith MA, Harris PLR, Sayre LM, Perry G. Iron accumulation in Alzheimer disease is a source of redox-generated free radicals. Proc Natl Acad Sci USA 94:9866-9868, 1997.

Nunomura A, Perry G, Pappolla MA, Wade R, Hirai K, Chiba S, Smith MA. RNA oxidation is a prominent feature of vulnerable neurons in Alzheimer's disease. J Neurosci 19:1959-1964, 1999.

Nunomura A, Perry G, Hirai K, Chiba S, Smith MA. Neuronal oxidative stress precedes amyloid-ß deposition in Down's syndrome. J Neuropathol Exp Neurol 59:1011-1017, 2000.

Rottkamp CA, Raina AK, Zhu X, Gaier E, Bush AI, Atwood CS, Chevion M, Perry G, Smith MA. Redox-active iron mediates amyloid-ß toxicity. Free Radic Biol Med 30:447-450, 2001.

Nunomura A, Perry G, Aliev G, Hirai K, Takeda A, Balraj EK, Jones PK, Wataya T, Shimohama S, Chiba S, Atwood CS, Petersen RB, Smith MA. Oxidative damage is an early event in Alzheimer disease. J Neuropathol Exp Neurol 60:759-767, 2001.

Hirai K, Aliev G, Nunomura A, Russell RL, Atwood CS, Johnson AB, Kress Y, Vinters HV, Tabaton M, Cash A, Siedlak SL, Jones PK, Petersen RB, Perry G, Smith MA. Mitochondrial DNA turnover is decreased in oxidatively stressed pyramidal neurons of the Alzheimer's disease brain. J Neurosci 21:3017-3023, 2001.

Cash AD, Aliev G, Siedlak SL, Nunomura A, Fujioka H, Zhu X, Raina AK, Vinters HV, Tabaton M, Johnson AB, Paula-Barbosa M, Avíla J, Jones PK, Castellani RJ, Smith MA, Perry G. Microtubule reduction in Alzheimer’s disease and aging is independent of τ filament formation. Am J Pathol 162:1623-1627, 2003.

Nunomura A, Chiba S, Lippa CF, Cras P, Kalaria RN, Takeda A, Honda K, Smith MA, Perry G. Neuronal RNA oxidation is a prominent feature of familial Alzheimer’s disease. Neurobiol Dis 17:108-113, 2004.

Liu Q, Smith MA, Avila J, De Bernardis J, Kansal M, Takeda A, Zhu X, Nunomura A, Honda, K, Moreira PI, Oliveira CR, Santos MS, Shimohama S, Aliev G, de la Torre J, Ghanbari HA, Siedlak SL, Harris PLR, Sayre LM, Perry G. Alzheimer-specific epitopes of tau represent lipid peroxidation induced conformations. Free Radic Biol Med 38:746-754, 2005.

Honda K, Smith MA, Zhu X, Baus D, Merrick WC, Tartakoff AM, Hattier T, Harris PL, Siedlak SL, Fujioka H, Liu Q, Moreira P, Miller F, Nunomura A, Shimohama S, Perry G. Ribosomal RNA in Alzheimer disease is oxidized by bound redox-active iron. J Biol Chem 280:20978-20986, 2005.
What is the greatest void to date in our knowledge of Alzheimer's Disease?
Etiology and pathogenesis
If resources were not limited, what research projects would you pursue?
Mechanisms regulating oxidative damage
What is your leading hypothesis?
Brain hypometabolism
What piece of missing evidence would help prove it?
A model showing a clear cause-effect relationship
What is your fallback position?
Oxidative stress

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