| Project/Area Number |
23591679
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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 |
Psychiatric science
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| Research Institution | Sapporo Medical University |
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Principal Investigator |
UKAI Wataru 札幌医科大学, 医学部, 講師 (40381256)
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| Co-Investigator(Kenkyū-buntansha) |
HASHIMOTO Eri 札幌医科大学, 医学部, 准教授 (30301401)
TATENO Masaru 札幌医科大学, 医学部, 講師 (60464492)
YOSHINAGA Toshihiro 札幌医科大学, 医学部, 助教 (70404704)
KANETA Hiroo 札幌医科大学, 医学部, 研究員 (80581149)
ATAKA Koji 札幌医科大学, 医学部, 講師 (30563358)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 精神薬理学 / 統合失調症 / 認知機能 / 神経再生 / 神経新生 / 細胞移植 / 再生医療 / 神経分化 / 神経幹細胞 / 認知機能障害 / 社会性機能障害 / 抗精神病薬 / 社会認知機能 / 神経幹細胞移植 / 言語機能 / NG2細胞 |
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| Research Abstract |
The purpose of this study is to investigate the influence of antipsychotic on the neural circuit of verbal memory and theory of mind which has high impact on working and social function recoveries in schizophrenic patients and to link it to the development of the new regenerative strategy for psychiatric disease treatment. In the experiments using neural/glial stem cells derived from adult brain, it was revealed that all the tested atypical antipsychotics promoted NG2(+) cell differentiation to GABAergic interneuron inhibited by MK-801. As one of the candidate molecular mechanisms of this GABAergic interneurgenesis promotion by antipsychotics, we have indicated the involvement of HSP 90 expression change. These results suggested that the increase of adult GABAergic interneurogenesis through HSP90 expression change might be involved in the mechanisms of neural network repair in the schizophrenic brain and cognitive function recoveries by the atypical antipsychotic treatments.
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