George Perry (Born 12 April, 1953 in Lompoc, California, USA) is a neuroscientist ... at many universities and holds multiple degrees including a Bachelor of Arts ...
Meet Our Editorial Board Member
Current Aging Science, 2016, Vol. 9, No. 3
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Meet Our Editorial Board Member Dr. George Perry The University of Texas at San Antonio San Antonio, Texas, USA George Perry (Born 12 April, 1953 in Lompoc, California, USA) is a neuroscientist recognized in the field of Alzheimer’s disease research particularly for his work in oxidative stress. Dr. Perry has studied at many universities and holds multiple degrees including a Bachelor of Arts degree in Zoology from the University of California Santa Barbra and PhD in Marine Biology from the Scripps Institute of Oceanography. Dr. Perry is distinguished as one of the top Alzheimer’s disease researchers with over 1000 publications, more than 62,000 citations (H=125), one of the top 100 most-cited scientists in Neuroscience & Behavior and one of the top 25 scientists in free radical research. Dr. Perry is a Semmes Foundation Distinguished University chair in Neurobiology and is an active participant in many other scientific associations. In addition, Perry is an Editor of numerous scientific journals including Journal of Alzheimer’s Diseasewhich he founded in 1998. Today, Perry continues his research while working as Dean of the College of Sciences at The University of Texas at San Antonio. His major interest is unlocking the biological basis for the pathogenesis of neurodegenerative diseases. Instead of viewing these hallmarks of disease as ‘causative’, his studies have suggested they are protective responses responsible for the chronic slow progression of these age-related diseases. Study of these protective responses may reveal therapeutic targets to benefit patients. SELECTED PUBLICATIONS: [1] [2]
Blair JA, Siedlak SL, Wolfram JA, et al. Accumulation of intraneuronal amyloid- is common in normal brain. Curr Alzheimer Res 2014; 11: 317-24. Bowen RL, Perry G, Xiong C, Smith MA, Atwood CS. A clinical study of Lupron depot in the treatment of women with Alzheimer’s disease: Preservation of cognitive function in patients taking an acetylcholinesterase inhibitor and treated with high dose Lupron over 48 weeks. J Alzheimers Dis 2015; 44: 549-60.
[3]
Calderón-Garcidueñas L, Franco-Lira M, Perry G, et al. Mexico city normal weight children exposed to high concentrations of ambient PM2.5 show high blood leptin and endothelin-1, vitamin D deficiency, and food reward hormone dysregulation versus low pollution controls. Relevance for obesity and Alzheimer disease. Environmental Res 2015; 140: 579-92.
[4]
Fawver JN, Ghiwot Y, Koola C, et al. Islet amyloid polypeptide (IAPP): A second amyloid in Alzheimer’s disease. Curr Alzheimer Res 2014; 11: 92840.
[5]
Gerenu G, Liu K, Chojnacki JE, et al. Curcumin/melatonin hybrid, 5-(4-hydroxy-phenyl)-3-oxo-pentanoic acid [2-(5-methoxy-1H-indol-3-yl)-ethyl]amide, ameliorates AD-like pathology in the APP/PS1 mouse model. ACS Chem Neurosci 2015; 8: 1393-9.
[6]
Mondragón-Rodríguez S, Perry G, Luna-Muñoz J, Acevedo-Aquino MC, Williams S. Phosphorylation of tau protein at sites Ser396-404 is one of the earliest events in Alzheimer’s disease and Down syndrome. Neuropathol Appl Neurobiol 2014; 40: 121-35.
[7]
Rodriguez AR, Plascencia-Villa G, Witt CM, et al. Chlamydia pneumoniae promotes dysfunction of pancreatic beta cells. Cell Immunol 2015; 295: 83-91.
[8]
Sharoar MG, Shi Q, Ge Y, et al. Dysfunctional tubular endoplasmic reticulum constitutes a pathological feature of Alzheimer’s disease. Mol Psychiatry. doi: 10.1038/mp.2015.181.
[9]
Xia J, Rocke DM, Perry G, Ray M. Differential network analyses of Alzheimer’s disease identify early events in Alzheimer’s disease pathology. Int J Alzheimer’s Dis 2014; 2014: 721453.
[10]
Fan Zhang, Bo Su, Perry G, Zhu, et al. Posttranslational modifications of -tubulin in Alzheimer disease. Transl Neurodegen 2015; 4: 1-9.
