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doi:10.1016/S0891-5849(02)01113-9 
Copyright © 2002 Elsevier Science Inc. All rights reserved.
Serial review: oxidatively modified proteins in aging and disease
Is oxidative damage the fundamental pathogenic mechanism of Alzheimer’s and other neurodegenerative diseases?*1
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George Perry*, Akihiko Nunomura*, †, Keisuke Hirai*, ‡, Xiongwei Zhu*, Mar Prez§, Jess Avila§, Rudolph J. Castellani*, Craig S. Atwood*, Gjumrakch Aliev¶, Lawrence M. Sayre
, Atsushi Takeda*, # and Mark A. Smith
, 
, *
* Institute of Pathology, Case Western Reserve University, Cleveland, OH, USA
† Department of Psychiatry and Neurology, Asahikawa Medical College, Asahikawa, Japan
‡ Pharmaceutical Research Laboratories I, Takeda Chemical Industries Ltd., Osaka, Japan
§ Centro de Biologia Molecular, Universidad Autonoma de Madrid, Madrid, Spain
¶ Department of Anatomy, Case Western Reserve University, Cleveland, OH, USA
Department of Chemistry, Case Western Reserve University, Cleveland, OH, USA
# Tohoku University School of Medicine, Department of Neurology, Sendai, Japan
Received 12 February 2002;
Abstract
In less than a decade, beginning with the demonstration by Floyd, Stadtman, Markesbery et al. [1] of increased reactive carbonyls in the brains of patients with Alzheimer’s disease (AD), oxidative damage has been established as a feature of the disease. Here, we review the types of oxidative damage seen in AD, sites involved, possible origin, relationship to lesions, and compensatory changes, and we also consider other neurodegenerative diseases where oxidative stress has been implicated. Although much data remain to be collected, the broad spectrum of changes found in AD are only seen, albeit to a lesser extent, in normal aging with other neurodegenerative diseases showing distinct spectrums of change.
Author Keywords: Alzheimer’s disease; Amyloid-β; Antioxidants; Homeostasis; Neurofibrillary tangles; Oxidative stress; Redox balance; Senile plaque; τ; Free radicals
Article Outline
*1 Guest Editor: Earl Stadtman
