| Item type |
学術雑誌論文 / Journal Article(1) |
| 公開日 |
2010-08-18 |
| タイトル |
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|
タイトル |
＜Symposium IV＞Oligomeric Aβ is the sole culprit molecule to cause Alzheimer's disease? |
| 言語 |
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言語 |
eng |
| キーワード |
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主題Scheme |
Other |
|
主題 |
Alzheimer’s disease |
| キーワード |
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主題Scheme |
Other |
|
主題 |
amyloid genetics |
| キーワード |
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主題Scheme |
Other |
|
主題 |
oligomeric Aβ |
| 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 |
|
資源タイプ |
journal article |
| 著者 |
Mori, Hiroshi
Tomiyama, Takami
Ishibashi, Kennichi
Ohnishi, Kiyouhisa
Teraoka, Rie
Fukushima, Akiko
Takuma, Hiroshi
Shimada, Hiroyuki
Ataka, Suzuka
Umeda, Tomohiro
Kitajima, Erika
Fujita, Yuki
Yamashita, Yuki
Yamamoto, Keiichi
Miki, Takami
Matsuyama, Shogo
Iso, Hiroyuki
Nagata, Tetsu
Nishizaki, Tomoyuki
Wada, Yasuhiro
Yoshioka, Eito
Watanabe, Yasuyoshi
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| 著者所属 |
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|
値 |
Department of Neuroscience and Neurology,Osaka City University Medical School |
| 著者所属 |
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値 |
Department of Neuroscience and Neurology,Osaka City University Medical School |
| 著者所属 |
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値 |
Department of Neuroscience and Neurology,Osaka City University Medical School |
| 著者所属 |
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値 |
Department of Neuroscience and Neurology,Osaka City University Medical School |
| 著者所属 |
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値 |
Department of Neuroscience and Neurology,Osaka City University Medical School |
| 著者所属 |
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値 |
Department of Neuroscience and Neurology,Osaka City University Medical School |
| 著者所属 |
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値 |
Department of Neuroscience and Neurology,Osaka City University Medical School |
| 著者所属 |
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値 |
Department of Neuroscience and Neurology,Osaka City University Medical School |
| 著者所属 |
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値 |
Department of Neuroscience and Neurology,Osaka City University Medical School |
| 著者所属 |
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|
値 |
Department of Neuroscience and Neurology,Osaka City University Medical School |
| 著者所属 |
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|
値 |
Department of Neuroscience and Neurology,Osaka City University Medical School |
| 著者所属 |
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|
値 |
Department of Neuroscience and Neurology,Osaka City University Medical School |
| 著者所属 |
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|
値 |
Department of Neuroscience and Neurology,Osaka City University Medical School |
| 著者所属 |
|
|
値 |
Department of Neuroscience and Neurology,Osaka City University Medical School |
| 著者所属 |
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値 |
Department of Neuroscience and Neurology,Osaka City University Medical School |
| 著者所属 |
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値 |
Department of Pharmaceutical Sciences, Himeji Dokkyo University |
| 著者所属 |
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値 |
Department of Behavior Science, Hyogo University of Health Sciences |
| 著者所属 |
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値 |
Department of Physiology, Hyogo College of Medicine |
| 著者所属 |
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値 |
Department of Physiology, Hyogo College of Medicine |
| 著者所属 |
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値 |
Department of Physiology, Osaka City University Medical School |
| 著者所属 |
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値 |
Department of Physiology, Osaka City University Medical School |
| 著者所属 |
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値 |
Department of Physiology, Osaka City University Medical School |
| 抄録 |
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内容記述タイプ |
Abstract |
|
内容記述 |
Alzheimer's disease (AD) is the major and common disease usually for aged people to show progressive neurodegenerative disorder with the dementia. Amyloid-beta （also β-protein and referred here to as Aβ） is a wellestablished seminal peptide in AD that is produced from the amyloid precursor protein （APP） by consecutive digestions with β-secretase of BACE and gamma-secretase of the presenilin complex. Abnormal cerebral accumulation of Aβ such as insoluble fi brils in senile plaques and cerebral amyloid angiopathy （CAA） are observed as a neuropathological hallmark of AD. In contrast to such insoluble fi brillary Aβ, a soluble oligomeric complex is discussed as ADDLs, Aβ oligomer, low-n oligomer Aβ, Aβ*56 or so. Despite their diff erent names, it is proposed as the current hypothesis that oligomeric Aβ is the direct molecule to cause synaptic toxicity and cognitive dysfunction in the early stages of AD. We identifi ed a novel APP mutation （E693delta; referred to as the Osaka mutation） in a pedigree with probable AD resulting in a variant Aβ lacking glutamate at position 22. Based on theoretical prediction and in vitro studies on synthetic mutant Aβ peptides, the mutated Aβ peptide showed a unique aggregation property of enhanced oligomerization but no fi brillization. This was further confi rmed by PiB-PET analysis on the proband patient. Collectively together, we conclude that the Osaka mutation is the fi rst human evidence for the hypothesis that oligomeric Aβ is involved in AD. |
| 引用 |
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内容記述タイプ |
Other |
|
内容記述 |
弘前医学. 61(Suppl.), 2010, p.S105-S110 |
| 書誌情報 |
弘前医学
巻 61,
号 Supplement,
p. S105-S110,
発行日 2010-07-08
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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 |
0439-1721 |
| 書誌レコードID |
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収録物識別子タイプ |
NCID |
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収録物識別子 |
AN00211444 |
| 著者版フラグ |
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出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| 日本十進分類法 |
|
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主題Scheme |
NDC |
|
主題 |
490 |
| NIIサブジェクト |
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|
主題Scheme |
Other |
|
主題 |
医学 |
| 出版者 |
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|
出版者 |
弘前大学大学院医学研究科・弘前医学会 |
| 資源タイプ |
|
|
値 |
Article |
HirosakiMedJ_61_S105.pdf (199.7 kB)
