| Project/Area Number |
26870683
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neurochemistry/Neuropharmacology
Experimental pathology
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| Research Institution | Chiba University (2016)
The University of Tokyo (2014-2015) |
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Principal Investigator |
OUCHI YASUO 千葉大学, 大学院医学研究院, 特任助教 (70553858)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 幹細胞学 / 認知機能形成 / 成体神経新生 / 神経幹細胞 / 神経新生 / 認知機能 / 統合失調症 / 成体神経化細胞 / 成体神経幹細胞 |
|---|
| Outline of Final Research Achievements |
Recently, the role of adult hippocampal neurogenesis in cognitive function has attracted a lot of attention. In this study, to elucidate the molecular mechanism of the maintenance of adult neural stem cells and its role in cognitive function and development of schizophrenia, we focused on epigenetic regulation and analyzed the genome-wide DNA methylation profile of Dgcr8(+/-) mouse model of 22q11.2 deletion-associated schizophrenia. From this result, consistent with downregulation of IGF2 gene expression, we found that the DNA methylation status of the regulatory region of IGF2 gene, which is an important autocrine growth factor for hippocampal neural stem cells is altered in the Dgcr8(+/-) mice compared with control wild-type mice. These findings suggest that the role of an epigenetic regulatory mechanism of neural stem cells in cognitive function and in the development of schizophrenia.
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