Establishment and analysis of a new mouse model of ischemic brain injuries in extremely preterm infants
| 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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Report
(5 results)
Research Products
(16 results)
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[Journal Article] Epidemiological, clinical, and genetic landscapes of hypomyelinating leukodystrophies.2014
Author(s)
Numata Y, Gotoh L, Iwaki A, Kurosawa K, Takanashi J, Deguchi K, Yamamoto T, Osaka H, Inoue K.
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Journal Title
J Neurol.
Volume: 261(4)
Issue: 4
Pages: 752-758
DOI
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Peer Reviewed
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[Presentation] Abnormal brain cytoarchitecture as one of the micro-endophenotypes of neuropsychiatric disorders (精神疾患のマイクロエンドフェノタイプとしての微細な脳組織構築の異常)2014
Author(s)
Ken-ichiro Kubo, Kazuhiro Ishii, Toshihiro Endo, Seico Benner, Taku Nagai, Wei Shan, Kimiko Deguchi, Ken Inoue, Kiyofumi Yamada, Chiharu Tohyama, Masaki Kakeyama, and Kazunori Nakajima
Organizer
第36回日本生物学的精神医学会・第57回日本神経化学会大会
Place of Presentation
奈良県文化会館・奈良県新公会堂、奈良（奈良県）
Year and Date
2014-09-29 – 2014-10-01
Related Report
Invited
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[Presentation] Preclinical studies for the treatment of Pelizaeus-Merzbacher disease with clinically applicable compounds, curumin and chloroquine.2013
Author(s)
Inoue K, Morimura T, Numata Y, Yu L-H, Gotoh L, Yamamoto R, Inoue N, Antalfy B, Deguchi K, Osaka H, Goto Y
Organizer
23nd Meeting of the European Neurological Society (ENS)
Place of Presentation
Convention Centre Gran Via, Barcelona, Spain
Related Report
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[Presentation] Treating Pelizaeus-Merzbacher disease with clinically applicable compounds, curumin and chloroquine: preclinical studies.2012
Author(s)
Ken Inoue, Toshifumi Morimura, Yurika Numata, Li-Hua Yu, Leo Gotoh, Ryoko Yamamoto, Naoko Inoue, Barbara Antalfy, Kimiko Deguchi, Hitoshi Osaka , Yu-ichi Goto
Organizer
62nd Annual meeting of the American Society of Human Genetics
Place of Presentation
San Francisco, USA
Related Report
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