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
Link To Document :
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