| Project/Area Number |
24591615
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Embryonic/Neonatal medicine
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| Research Institution | Keio University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
Inoe Ken 国立精神・神経医療研究センター, 神経研究所疾病研究第二部, 室長 (30392418)
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| Research Collaborator |
Kubo Ken-ichiro 慶應義塾大学, 医学部, 講師 (20348791)
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| Project Period (FY) |
2012-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 超早産児 / 後遺症 / 認知機能障害 / 脳虚血 / モデルマウス / 神経細胞 / 虚血性脳障害 / 微細組織構築 / 行動解析 / 神経幹細胞 / 発達障害 / 治療法開発 / マウスモデル |
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| Outline of Final Research Achievements |
Many extremely preterm infants (EPIs) subsequently develop cognitive impairment of unknown etiology. We observed fewer neural progenitors and larger numbers of ectopic neurons in the white matter (WM) of human EPI brains and hypothesized that EPIs develop cognitive dysfunction because of altered neuronal generation and migration. To test our hypothesis we produced ischemic brain damage in mouse embryos by occluding maternal uterine arteries. The mice showed decreased proliferation of neuronal progenitors, delayed neuronal migration, and altered neocortical structures. Similar to human EPIs the surviving mice exhibited abnormal cognitive function. These findings supported our hypothesis that altered neuronal generation and migration underlies the serious risk of subsequent cognitive impairment of EPIs.
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