| Project/Area Number |
25460479
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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 |
Experimental pathology
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| Research Institution | Okinawa National College of Technology (2015)
University of the Ryukyus (2013-2014) |
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Principal Investigator |
CHIBA SHUNMEI 沖縄工業高等専門学校, 生物資源工学科, 特命教授 (20367361)
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| Co-Investigator(Kenkyū-buntansha) |
TANIGUCHI Taizo 姫路獨協大学, 薬学部, 教授 (70346253)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 認知症 / 神経幹細胞 / リゾリン脂質 / 神経再生 / 治療 / LPAシグナル / 神経再生誘導 / 新規治療薬 / リゾリン脂質シグナル / 幹細胞 |
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| Outline of Final Research Achievements |
We analysed the effect of LPA signaling for an dementia model of mice. Homozygous transgenic mice were mated, and bred for in vivo experiment. 6 monthes mice started showing a memory disturbance, and the hippocampus of 12 monthes mice was degenerated. The extracted neural stem cells from mice were not expandale as well, but LPA improved proliferation. Ki16425, as a inhibitor of LPA1 signaling, could improved the phenomenon of dimentia in 12 monthes model mice. Though, we were now analysing the movement and changing of neural stem cells in the brain, LPA signaling, especially in LPA1 inhibiton could be a high-potential drug for dementia, like as Alzheimer`s.
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