Item type |
学術雑誌論文 / Journal Article(1) |
公開日 |
2017-10-03 |
タイトル |
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タイトル |
Endogenous secretory receptor for advanced glycation end-products inhibits amyloid-β 1-42 uptake into mouse brain |
言語 |
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言語 |
eng |
資源タイプ |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
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資源タイプ |
journal article |
ID登録 |
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ID登録 |
10.24517/00013703 |
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ID登録タイプ |
JaLC |
著者 |
Sugihara, Takahiro
Munesue, Seiichi
Yamamoto, Yasuhiko
Sakurai, Shigeru
Akhter, Nasima
Kitamura, Yoji
Shiba, Kazuhiro
Watanabe, Takuo
Yonekura, Hideto
Hayashi, Yasuhiko
Hamada, Jun-ichiro
Yamamoto, Hiroshi
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著者別表示 |
杉原, 崇大
棟居, 聖一
山本, 靖彦
櫻井, 繁
北村, 暘二
柴, 和弘
渡邊, 拓夫
米倉, 秀人
林, 靖彦
濱田, 潤一郎
山本, 博
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書誌情報 |
Journal of Alzheimer's Disease
巻 28,
号 3,
p. 709-720,
発行日 2012-01-01
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ISSN |
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収録物識別子タイプ |
ISSN |
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収録物識別子 |
1387-2877 |
NCID |
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収録物識別子タイプ |
NCID |
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収録物識別子 |
AA11545428 |
DOI |
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関連タイプ |
isVersionOf |
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識別子タイプ |
DOI |
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関連識別子 |
10.3233/JAD-2011-110776 |
出版者 |
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出版者 |
IOS Press |
抄録 |
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内容記述タイプ |
Abstract |
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内容記述 |
The cell-surface receptor for advanced glycation end-products (RAGE) has been implicated in the development of diabetic vascular complications and Alzheimer's disease. RAGE has been considered to be involved in amyloid-β 1-42 (Aβ 1-42) uptake into brain. In the present study, we demonstrate that endogenous secretory RAGE (esRAGE), a decoy form of RAGE generated by alternative RNA processing, is able to inhibit Aβ 1-42 influx into mouse brain. Surface plasmon resonance and competitive binding assays revealed that human Aβ 1-42 interacted with human esRAGE within the immunoglobulin V type region. We next examined the uptake and distribution of 125I-labeled human Aβ 1-42 in various organs and body fluids of newly created mice overexpressing human esRAGE as well as RAGE-null and wild-type (WT) mice. The transition of the 125I-labeled Aβ 1-42 from circulation to brain parenchyma peaked at 30 min after the injection into WT mice, but this was significantly blunted in esRAGE-overexpressing and RAGE-null mice. Significant reduction in 125I-labeled Aβ 1-42-derived photo-stimulated luminescence were marked in ventricles, cerebral cortex, hippocampus, especially CA1 and CA3 regions, putamen, and thalamus. The results thus suggest the potential of esRAGE in protection against the development of Alzheimer's disease. © 2012 - IOS Press and the authors. All rights reserved. |
内容記述 |
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内容記述タイプ |
Other |
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内容記述 |
Thesis of Sugihara Takahiro / 学位論文 医学甲第2227 杉原 崇大 |
著者版フラグ |
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出版タイプ |
AM |
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出版タイプResource |
http://purl.org/coar/version/c_ab4af688f83e57aa |