| Project/Area Number |
17K11576
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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 |
Emergency medicine
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| Research Institution | Ehime University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
西原 佑 愛媛大学, 医学部附属病院, 講師 (50568912)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | microglia / neurotrophic factor / carbon monoxide / delayed encephalopathy / マイクログリア / 一酸化炭素 / 神経保護因子 / 遅発性脳症 / アポトーシス / 一酸化炭素中毒 / 神経細胞 / ミエリン / 脳・神経 |
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| Outline of Final Research Achievements |
Carbon monoxide (CO) causes a delayed neurologic syndrome called delayed encephalopathy (DE). Rats were randomly assigned to three groups; the air group, the CO group (exposed to CO), and the low O2 group (exposed to low concentration of O2). The impairment of memory function was observed only in the CO group. The demyelination in the CO group was more severe and continued longer than that in the low O2 group. Moreover, decrease in microglial cells were observed in the CO group, however, on the other hand, microglial cells were activated in the low O2 group. mRNAs of several neurotrophic factors expressed by microglia were decreased in the CO group but increased in the low O2 group. Conclusively, CO-induced DE displayed distinctive pathological features from simple hypoxic insults; prolonged demyelination accompanying a significant decrease in microglial cells. The decreased neurotrophic factor expression in microglial cells may be one of causes of CO-induced DE.
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| Academic Significance and Societal Importance of the Research Achievements |
我々の行った研究で得られた知見は、これまでの報告とは全く異なる新しいものであった。特に、マイクログリアの活性化によって脱髄が引き起こされることが問題の一つとされていたこれまでの報告と比べ、マイクログリアは活性化するどころか、逆に減少し、おそらくはそれに伴うと考えれらる神経保護因子の減少は、今後の治療方法が大きく変わる可能性がある。例えば、マイクログリアの活性化を抑制することを目的とする治療方針から、マイクログリアの生存を助けることを目的とする、もしくは、減少した神経保護因子を補う事を目的とする治療方針への転換などが考えられ、社会的に大きな意義を持つものと考えられる。
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