| Project/Area Number |
18K15518
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 52030:Psychiatry-related
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| Research Institution | Ehime University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2018: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 間歇型一酸化炭素中毒 / 成体海馬神経細胞新生 / ミクログリア / 神経栄養因子 / 認知機能 / アセチルコリン / 神経幹細胞 / 海馬神経細胞新生 / グリア細胞 / 神経前駆細胞 / アストロサイト / 細胞・組織 |
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| Outline of Final Research Achievements |
Carbon monoxide (CO) poisoning has acute and delayed stages. Delayed CO poisoning, a few weeks after recovery from the acute stage,causes neuropsychiatric symptoms such as cognitive impairment, and its pathophysiology and treatment remain unclear. Adult neurogenesis is occured in the dentate gyrus (DG) of hippocampus, and plays important roles in the cognitive function. We investigated the effects of CO exposure on the DG in this rat model.
Model rats showed significant cognitive impairment 7 days after CO exposure. Immunohistochemistry showed that compared to the control, cell numbers of neural precursor cells in the DG and cell numbers of microglia in the hippocampus were significantly less 21 days after CO exposure. Furthermore, mRNA expression of neurotrophic factors, which are neurogenic factors in neurogenesis, was significantly decreased in the hippocampus.
Dysregulated adult neurogenesis and glial changes in delayed CO poisoning were associated with delayed cognitive impairment.
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| Academic Significance and Societal Importance of the Research Achievements |
一酸化炭素(以下CO)は無色、無味、無臭、非刺激性でありながら、極めて毒性の強い気体であり、我が国の薬毒物死の原因の中では最多となっている。なお、CO中毒による死亡者の大半が自殺によるものであるため、CO中毒は社会的にも重要な問題でもあり、有効な治療法の確立が望まれる。しかし、数週間後、突然認知機能低下などで発症する間歇型CO中毒は、その病態生理など依然不明である。
今回、間歇型CO中毒の認知機能低下の病態生理において、成体海馬神経細胞新生の関与および神経栄養因子に対する影響を示すことができた。今後これらの結果を元に間歇型CO中毒による認知機能低下の予防や治療法の開発に寄与する可能性がある。
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