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Citation
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HERO ID
6816503
Reference Type
Journal Article
Subtype
Review
Title
Involvement of oxidative stress in Alzheimer disease
Author(s)
Nunomura, A; Castellani, RJ; Zhu, X; Moreira, PI; Perry, G; Smith, MA
Year
2006
Is Peer Reviewed?
Yes
Journal
Journal of Neuropathology and Experimental Neurology
ISSN:
0022-3069
EISSN:
1554-6578
Volume
65
Issue
7
Page Numbers
631-641
Language
English
PMID
16825950
DOI
10.1097/01.jnen.0000228136.58062.bf
Web of Science Id
WOS:000241692200001
Abstract
Genetic and lifestyle-related risk factors for Alzheimer disease (AD) are associated with an increase in oxidative stress, suggesting that oxidative stress is involved at an early stage of the pathologic cascade. Moreover, oxidative stress is mechanistically and chronologically associated with other key features of AD, namely, metabolic, mitochondrial, metal, and cell-cycle abnormalities. Contrary to the commonly held notion that pathologic hallmarks of AD signify etiology, several lines of evidence now indicate that aggregation of amyloid-beta and tau is a compensatory response to underlying oxidative stress. Therefore, removal of proteinaceous accumulations may treat the epiphenomenon rather than the disease and may actually enhance oxidative damage. Although some antioxidants have been shown to reduce the incidence of AD, the magnitude of the effect may be modified by individual factors such as genetic predisposition (e.g. apolipoprotein E genotype) and habitual behaviors. Because caloric restriction, exercise, and intellectual activity have been experimentally shown to promote neuronal survival through enhancement of endogenous antioxidant defenses, a combination of dietary regimen of low total calorie and rich antioxidant nutrients and maintaining physical and intellectual activities may ultimately prove to be one of the most efficacious strategies for AD prevention.
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