| Project/Area Number |
25461278
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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 |
Neurology
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| Research Institution | Nagoya University |
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Principal Investigator |
IIJIMA MASAHIRO 名古屋大学, 医学(系)研究科(研究院), 寄附講座講師 (40437041)
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| Co-Investigator(Kenkyū-buntansha) |
Sobue Gen 名古屋大学, 医学系研究科, 特任教授 (20148315)
Kawagashira Yuichi 名古屋大学, 医学部附属病院, 病院助教 (40569779)
Koike Haruki 名古屋大学, 医学系研究科, 准教授 (80378174)
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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: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 免疫介在性ニューロパチー / TAG-1 / 傍ランビエ絞輪部 / 脱髄 / 軸索障害 / 動物モデル / 免疫性疾患 / 脳神経疾患 / 軸索ー髄鞘間相互作用 / 自己免疫疾患 / 実験的自己免疫性神経炎（EAN） / 免疫性脱髄性ニューロパチー / 軸索－髄鞘相互作用 / B7-2ノックアウトNODマウス / 免疫グロブリン療法 / CIDP / 脱髄性ニューロパチー / 実験的自己免疫性神経炎 |
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| Outline of Final Research Achievements |
Interaction between axon and myelin sheath has a crucial role for the maintenance of the peripheral nervous system. We have clarified that TAG-1, which specifically distributes on juxtaparanode, ameliorates the remyelinating process depends on non-synonymous amino acids changes through SNPs. In this study, we produce an experimental autoimmune neuritis model by inducing myelin-origined peptides with complete Freund adjuvant. This mice showed inflammatory demyelination followed by severe axonal degeneration. TAG-1 could work as a trigger for remyelination after demyelination. In addition, dysfunction of juxtaparnodal molecules would bring severe irreversible pathogenesis as like axonal degeneration.
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