| Item type |
学術雑誌論文 / Journal Article_02(1) |
| 公開日 |
2009-05-15 |
| タイトル |
|
|
タイトル |
Neuronal death and survival under oxidative stress in Alzheimer and Parkinson diseases |
|
言語 |
en |
| 言語 |
|
|
言語 |
eng |
| 資源タイプ |
|
|
資源タイプ |
journal article |
| 著者 |
布村, 明彦
Moreira, PI
Lee, HG
Zhu, X
Castellani, RJ
Smith, MA
Perry, G
|
| 著者 ローマ字 |
|
|
|
Nunomura, Akihiko |
| 著者 ローマ字 |
|
|
|
en |
| 書誌情報 |
CNS & Neurological Disorders Drug Targets
巻 6,
号 6,
p. 411-423,
発行日 2007-12-01
|
| ISSN |
|
|
収録物識別子タイプ |
ISSN |
|
収録物識別子 |
1871-5273 |
| DOI |
|
|
関連タイプ |
isVersionOf |
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|
識別子タイプ |
DOI |
|
|
関連識別子 |
10.2174/187152707783399201 |
| リンクURL |
|
|
内容記述タイプ |
Other |
|
内容記述 |
http://www.bentham.org/cdtcnsnd/ | http://www.bentham.org/cdtcnsnd/ |
| 抄録 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
Neuronal death is a common feature in neurodegenerative diseases including Alzheimer disease (AD) and Parkinson disease (PD). This occurs over years, not the minutes of classically defined apoptosis, and neurons show both responses of apoptosis and regeneration, evidenced by accumulated oxidative insult and attempts at cell cycle re-entry. There is recent evidence suggesting that several known gene mutations in causing familial AD (amyloid beta protein precursor, presenilin-1, or presenilin-2 gene) and familial PD (Parkin, PINK-1, or DJ-1 gene) are associated with increased oxidative stress. Also, several known genetic (e.g. Apolipoprotein Eepsilon4 variant) and environmental (e.g. metals or pesticides exposure) risk factors of sporadic AD and/or PD are associated with increased oxidative stress. In concord, patients at the preclinical stages of AD and PD as well as cellular and animal models of the diseases provide consistent evidence that oxidative insult is a significant early event in the pathological cascade of AD and PD. In contrast to the general aspects of the pathological hallmarks, aggregation of the disease-specific proteins such as amyloid-beta, tau, and alpha-synuclein may act as a compensatory (survival) response against the oxidative insult via the mechanism that the disease-specific structures sequester redox-active metals. Expanding knowledge of the molecular mechanisms of organism longevity indicates that pro-longevity gene products such as forkhead transcription factors and sirtuins are involved in the insulin-like signaling pathway and oxidative stress resistance against aging. An enhancement of the pro-longevity signaling (e.g. caloric restriction) may be a promising approach as anti-oxidative strategy against age-associated neurodegenerative diseases. |
|
言語 |
en |
| 注記 |
|
|
内容記述タイプ |
Other |
|
注記 |
author |
|
言語 |
en |
| 資源タイプ |
|
|
内容記述タイプ |
Other |
|
資源タイプ |
text |
| 著者版フラグ |
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|
出版タイプ |
AM |
| フォーマット |
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内容記述タイプ |
Other |
|
内容記述 |
application/pdf |
| ID(XooNIps) |
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|
|
18220780 |
| 閲覧数(XooNIps) |
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| ダウンロード数(XooNIps) |
|
|
|
3461 |
2148.pdf (1.3 MB)
