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George Perry

Researcher at University of Texas at San Antonio

Publications -  956
Citations -  84451

George Perry is an academic researcher from University of Texas at San Antonio. The author has contributed to research in topics: Alzheimer's disease & Oxidative stress. The author has an hindex of 139, co-authored 923 publications receiving 77721 citations. Previous affiliations of George Perry include University of South Alabama & Michigan State University.

Papers
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Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes

Daniel J. Klionsky, +235 more
- 16 Feb 2008 - 
TL;DR: A set of guidelines for the selection and interpretation of the methods that can be used by investigators who are attempting to examine macroautophagy and related processes, as well as by reviewers who need to provide realistic and reasonable critiques of papers that investigate these processes are presented.
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Oxidative damage is the earliest event in Alzheimer disease.

TL;DR: The observations indicate that increased oxidative damage is an early event in AD that decreases with disease progression and lesion formation and suggest that AD is associated with compensatory changes that reduce damage from reactive oxygen.
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Mitochondrial abnormalities in Alzheimer's disease.

TL;DR: Morphometric analysis showed that mitochondria are significantly reduced in Alzheimer's disease, and the relationship shown here between the site and extent of mitochondrial abnormalities and oxidative damage suggests an intimate and early association between these features in dementia.
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Iron accumulation in Alzheimer disease is a source of redox-generated free radicals.

TL;DR: It is found, using a modified histochemical technique that relies on the formation of mixed valence iron complexes, that redox-active iron is associated with the senile plaques and neurofibrillary tangles-the pathological hallmark lesions of Alzheimer disease.