| Project/Area Number |
22590928
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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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 |
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| Co-Investigator(Kenkyū-buntansha) |
IIJIMA Masahiro 名古屋大学, 大学院・医学系研究科, COE特任助教 (40437041)
KOIKE Haruki 名古屋大学, 大学院・医学系研究科, 病院助教 (80378174)
SOBUE Gen 名古屋大学, 大学院・医学系研究科, 教授 (20148315)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 脱髄性ニューロパチー / 軸索障害 / Axon-myelin interaction / 治療反応性 / イオンチャネル / 脱髄 / 末梢神経 / チャネル / axon-glial interaction / TAG-1 / CIDP / 慢性炎症性脱髄性多発ニューロパチー(CIDP) / Intravenous immunoglobulin(IVIg) / 軸索機能障害 / 一塩基多型(single nucleotide polymorphism,SNP) |
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| Research Abstract |
The association between axon-myelin interaction and functional several molecules which are distributed from node of Ranvie to juxtaparanode is well recognized. In this study, we analyzed immunohistochemically the distribution and expression of those molecules, including sodium channel, TAG-1, CNTN1, Caspr and Caspr2, using by teased-fiber preparation in patients with demyelinating neuropathies. The expression of sodium channel in demyelinating neuropathies showed markedly decrease compared with normal control although no morphological changes are observed in light microscopic study. In addition, we confirmed that homologous TAG-1 knockout mice resulted in significant ateliosis. These results may suggest that several molecules which is associated with axon-myelin interaction, including TAG-1, express their function in the development phase and play an important role in repair after demyelination.
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