| Project/Area Number |
25460349
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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 |
General pharmacology
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| Research Institution | Nagasaki International University (2014-2015)
Fukuoka University (2013) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
YAMAUCHI Atsushi 福岡大学, 薬学部, 准教授 (90341453)
KOGA Mitsuhisa 福岡大学, 薬学部, 助教 (60570801)
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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 |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | CD147 / 白質 / 大脳白質 / 白質障害 / シクロフィリンA / オリゴデンドロサイト / 脳血管性認知症 |
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| Outline of Final Research Achievements |
Ischemic white matter lesions are the characteristic pathological changes in subcortical ischemic vascular dementia , a common form of vascular dementia. Demyelination of the central nervous system leads to progressive cognitive and motor dysfunction. CD147, a membrane glycoprotein of the immunoglobulin superfamily, is highly upregulated during dynamic cellular events including tissue remodelling. In this study, we studied expression of CD147 and a novel involvement of CD147 in white matter lesion animal model, cuprizone-induced demyelination. Mice were fed a diet containing 0.2% cuprizone for 5 weeks. Cuprizon treatment induces severe demyelination and microglial activation. We also found CD147 levels to be upregulated in the brain of cuprizone-induced demyelination mouse. These results provide new insights suggesting CD147 is a potential therapeutic target to inhibit white matter lesions.
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