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Non-steroidal anti-inflammatory drugs have anti-amyloidogenic effects for Alzheimer's β-amyloid fibrils in vitro
http://hdl.handle.net/2297/7405
http://hdl.handle.net/2297/7405f096ceef-ba8d-4019-b2c7-9bba2be62cb6
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
HO-PR-YAMADA-M-1088.pdf (1.6 MB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2017-10-05 | |||||
| タイトル | ||||||
| タイトル | Non-steroidal anti-inflammatory drugs have anti-amyloidogenic effects for Alzheimer's β-amyloid fibrils in vitro | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
| 資源タイプ | journal article | |||||
| 著者 |
Hirohata, Mie
× Hirohata, Mie× Ono, Kenjiro× Naiki, Hironobu× Yamada, Masahito |
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| 提供者所属 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | 金沢大学医学部附属病院放射線部 | |||||
| 書誌情報 |
Neuropharmacology 巻 49, 号 7, p. 1088-1099, 発行日 2005-12-01 |
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| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 0028-3908 | |||||
| NCID | ||||||
| 収録物識別子タイプ | NCID | |||||
| 収録物識別子 | AA00754812 | |||||
| DOI | ||||||
| 関連タイプ | isVersionOf | |||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | 10.1016/j.neuropharm.2005.07.004 | |||||
| 出版者 | ||||||
| 出版者 | Elsevier | |||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | The pathogenesis of Alzheimer's disease (AD) is characterized by cerebral deposits of amyloid β-peptides (Aβ) and neurofibrillary tangles which are surrounded by inflammatory cells. Long-term use of non-steroidal anti-inflammatory drugs (NSAIDs) reduces the risk of developing AD and delays the onset of the disease. In the present study, we used fluorescence spectroscopy with thioflavin T and electron microscopy to examine the effects of NSAIDs such as ibuprofen, aspirin, meclofenamic acid sodium salt, diclofenac sodium salt, ketoprofen, flurbiprofen, naproxen, sulindac sulfide and indomethacin on the formation, extension, and destabilization of β-amyloid fibrils (fAβ) at pH 7.5 at 37°C in vitro. All examined NSAIDs dose-dependently inhibited formation of fAβ from fresh Aβ(1-40) and Aβ(1-42), as well as their extension. Moreover, these NSAIDs dose-dependently destabilized preformed fAβs. The overall activity of the molecules examined was in the following order: ibuprofen ≈ sulindac sulfide ≥ meclofenamic acid sodium salt > aspirin ≈ ketoprofen ≥ flurbiprofen ≈ diclofenac sodium salt > naproxen ≈ indomethacin. Although the mechanisms by which these NSAIDs inhibit fAβ formation from Aβ, and destabilize preformed fAβ in vitro are still unclear, NSAIDs may be promising for the prevention and treatment of AD. © 2005 Elsevier Ltd. All rights reserved. | |||||
| 著者版フラグ | ||||||
| 出版タイプ | AM | |||||
| 出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
