| Project/Area Number |
24500404
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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 |
Nerve anatomy/Neuropathology
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| Research Institution | Asahikawa Medical College |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
BANDO Yoshio 旭川医科大学, 医学部, 准教授 (20344575)
TANAKA Tatsuhide 旭川医科大学, 医学部, 助教 (80567032)
MURAKAMI Koichi 旭川医科大学, 医学部, 助教 (90400085)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 脱髄 / オリゴデンドロサイト / 多発性硬化症 / EAE / プロテアーゼ / 電子顕微鏡 / カリクレイン / 走査型電子顕微鏡 |
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| Outline of Final Research Achievements |
The objective of the current study was to elucidate the mechanism of demyelination from the change of myelin condition and the function of the protease of oligodendrocytes. In experimental autoimmune allergic encephalitis, changes of the condition of myelin occurred earlier than previously thought. The involvement of KLK6 was also suggested. In contrast, demyelination by cuprizone administration was caused by different mechanism with less involvement of KLK6. KLK6 was also partially involved in demyelination after spinal cord injury. From the study of cultured oligodendrocytes, KLK6 may play a role during demyelination rather than development of oligodendrocytes.
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