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タイトル: | A mouse model of 22q11.2 deletions: Molecular and behavioral signatures of Parkinson's disease and schizophrenia |
著者: | Sumitomo, Akiko Horike, Kouta Hirai, Kazuko Butcher, Nancy Boot, Erik Sakurai, Takeshi Nucifora, Frederick C. Bassett, Anne S. Sawa, Akira Tomoda, Toshifumi |
著者名の別形: | 住友, 明子 堀家, 康太 櫻井, 武 澤, 明 友田, 利文 |
発行日: | 1-Aug-2018 |
出版者: | American Association for the Advancement of Science (AAAS) |
誌名: | Science Advances |
巻: | 4 |
号: | 8 |
論文番号: | eaar6637 |
抄録: | Individuals with chromosome 22q11.2 deletions are at increased risk of developing psychiatric conditions, most notably, schizophrenia (SZ). Recently, clinical studies have also implicated these recurrent 22q11.2 deletions with the risk of early-onset Parkinson’s disease (PD). Thus far, the multiple mouse models generated for 22q11.2 deletions have been studied primarily in the context of congenital cardiac, neurodevelopmental, and psychotic disorders. One of these is the Df1/+ model, in which SZ-associated and developmental abnormalities have been reported. We present the first evidence that the mouse model for the 22q11.2 deletion exhibits motor coordination deficits and molecular signatures (that is, elevated α-synuclein expression) relevant to PD. Reducing the α-synuclein gene dosage in Df1/+ mice ameliorated the motor deficits. Thus, this model of the 22q11.2 deletion shows signatures of both SZ and PD at the molecular and behavioral levels. In addition, both SZ-associated and PD-relevant deficits in the model were ameliorated by treatment with a rapamycin analog, CCI-779. We now posit the utility of 22q11.2 deletion mouse models in investigating the mechanisms of SZ- and PD-associated manifestations that could shed light on possible common pathways of these neuropsychiatric disorders. |
記述: | 神経細胞のオートファジー機能の低下と精神疾患との関連を実証 --精神疾患の新たな治療戦略の開発に期待--. 京都大学プレスリリース. 2018-09-03. |
著作権等: | © 2018 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution NonCommercial License 4.0 (CC BY-NC). This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial license, which permits use, distribution, and reproduction in any medium, so long as the resultant use is not for commercial advantage and provided the original work is properly cited. |
URI: | http://hdl.handle.net/2433/234197 |
DOI(出版社版): | 10.1126/sciadv.aar6637 |
PubMed ID: | 30116778 |
関連リンク: | https://www.kyoto-u.ac.jp/ja/research-news/2018-09-03 |
出現コレクション: | 学術雑誌掲載論文等 |
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