The mechanism of axonal degeneration caused by demyelination in B7-2 KO NOD mouse
| Project/Area Number |
26461292
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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 |
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| Co-Investigator(Kenkyū-buntansha) |
飯島 正博 名古屋大学, 医学系研究科, 寄附講座講師 (40437041)
小池 春樹 名古屋大学, 医学系研究科, 准教授 (80378174)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥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 / 動物モデル（animal model） / B7-2ノックアウト / non-obesity diabetic / CIDP / モデルマウス / B7-2ノックアウトマウス / non-obesity diabetes / マクロファージ / TAG-1 / ランビエ絞輪部 / イオンチャンネル / TAG-1ノックアウトマウス / 軸索障害 / B7-2 NOD ノックアウトマウス / TAG-1 ノックアウトマウス / 脱髄性ニューロパチー / 予後不良因子 / 治療反応性 |
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| Outline of Final Research Achievements |
In chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), development of axonal degeneration is known as a characteristic of refractory to immune therapy and long-term poor prognosis.
An animal model of CIDP, non-obese diabetic (NOD) mouse characterized by spontaneous chronic autoimmune neuropathy is known and we confirmed the histopathological findings of NOD mouse. Mild inflammatory cell infiltration was observed from around 20 weeks of age in NOD mouse, and exhibited highly inflammatory cell infiltration with active demyelination. After the infiltration of inflammatory cells declined, secondary axonal degeneration was observed.
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Report
(4 results)
Research Products
(23 results)
