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Involvement of oxidative stress in Alzheimer disease
https://asahikawa-med.repo.nii.ac.jp/records/1611
https://asahikawa-med.repo.nii.ac.jp/records/1611b82ece0a-ad70-4261-b132-41e1eb639907
| 名前 / ファイル | ライセンス | アクション |
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2141.pdf (1.2 MB)
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| Item type | 学術雑誌論文 / Journal Article_02(1) | |||||||||||||||||||
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| 公開日 | 2009-05-15 | |||||||||||||||||||
| タイトル | ||||||||||||||||||||
| タイトル | Involvement of oxidative stress in Alzheimer disease | |||||||||||||||||||
| 言語 | en | |||||||||||||||||||
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| 言語 | eng | |||||||||||||||||||
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| 資源タイプ | journal article | |||||||||||||||||||
| 著者 |
布村, 明彦
× 布村, 明彦
× Castellani, RJ
× Zhu, X
× Moreira, PI
× Perry, G
× Smith, MA
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| 著者 ローマ字 | ||||||||||||||||||||
| Nunomura, Akihiko | ||||||||||||||||||||
| 著者 ローマ字 | ||||||||||||||||||||
| en | ||||||||||||||||||||
| 書誌情報 |
Journal of Neuropathology and Experimental Neurology 巻 65, 号 7, p. 631-641, 発行日 2006-07-01 |
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| 収録物識別子タイプ | ISSN | |||||||||||||||||||
| 収録物識別子 | 0022-3069 | |||||||||||||||||||
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| 関連タイプ | isVersionOf | |||||||||||||||||||
| 識別子タイプ | DOI | |||||||||||||||||||
| 関連識別子 | 10.1097/01.jnen.0000228136.58062.bf | |||||||||||||||||||
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| 内容記述タイプ | Other | |||||||||||||||||||
| 内容記述 | http://www.ncbi.nlm.nih.gov/pubmed/16825950 | http://www.ncbi.nlm.nih.gov/pubmed/16825950 | |||||||||||||||||||
| 抄録 | ||||||||||||||||||||
| 内容記述タイプ | Abstract | |||||||||||||||||||
| 内容記述 | 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. | |||||||||||||||||||
| 言語 | en | |||||||||||||||||||
| 注記 | ||||||||||||||||||||
| 内容記述タイプ | Other | |||||||||||||||||||
| 注記 | his is a non-final version of an article published in final form in Nunomura, Akihiko ; Castellani, Rudy J. ; Zhu, Xiongwei ; Moreira, Paula I. ; Perry, George ; Smith, Mark A., Involvement of oxidative stress in Alzheimer disease, NJournal of Neuropathology and Experimental Neurology 65(7), JUL 2006, pp. 631-641 \nauthor |
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| 言語 | en | |||||||||||||||||||
| 資源タイプ | ||||||||||||||||||||
| 内容記述タイプ | Other | |||||||||||||||||||
| 資源タイプ | text | |||||||||||||||||||
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| 出版タイプ | AM | |||||||||||||||||||
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| 内容記述タイプ | Other | |||||||||||||||||||
| 内容記述 | application/pdf | |||||||||||||||||||
| ID(XooNIps) | ||||||||||||||||||||
| 16825950 | ||||||||||||||||||||
| 閲覧数(XooNIps) | ||||||||||||||||||||
| ダウンロード数(XooNIps) | ||||||||||||||||||||
| 1764 | ||||||||||||||||||||
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Cite as
布村, 明彦, Castellani, RJ, Zhu, X, Moreira, PI, Perry, G, Smith, MA, n.d., Involvement of oxidative stress in Alzheimer disease: 631–641 p.
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