Title of article
Is oxidative damage the fundamental pathogenic mechanism of Alzheimer’s and other neurodegenerative diseases?
Author/Authors
George Perry، نويسنده , , Akihiko Nunomura، نويسنده , , Keisuke Hirai، نويسنده , , Xiongwei Zhu، نويسنده , , Mar Prez، نويسنده , , Jess Avila، نويسنده , , Rudolph J. Castellani، نويسنده , , Craig S. Atwood، نويسنده , , Gjumrakch Aliev، نويسنده , , Lawrence M. Sayre، نويسنده , , Atsushi Takeda، نويسنده , , Mark A. Smith، نويسنده ,
Issue Information
روزنامه با شماره پیاپی سال 2002
Pages
5
From page
1475
To page
1479
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.
Keywords
Amyloid-? , Alzheimer’s Disease , antioxidants , Homeostasis , Neurofibrillary tangles , oxidative stress , Redox balance , Senile plaque , ? , free radicals
Journal title
Free Radical Biology and Medicine
Serial Year
2002
Journal title
Free Radical Biology and Medicine
Record number
519328
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