| Project/Area Number |
15K09332
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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 | Tohoku University |
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Principal Investigator |
MISU TATSURO 東北大学, 医学系研究科, 講師 (00396491)
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| Co-Investigator(Renkei-kenkyūsha) |
Aoki Masashi 東北大学, 大学院医学系研究科, 教授 (70302148)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | アクアポリン4 / アストロサイト / 視神経脊髄炎 / 多発性硬化症 / 脱髄性疾患 / アストロサイトパチー / アクアポリン４ / 脱髄 / アクアポリン４抗体 |
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| Outline of Final Research Achievements |
We made a new high-affinity antibody against the extradomain of aquaporin-4(AQP4）and studied about its pathogenic roles in experimental rat models. We revealed that high-affinity IgG could make a diffuse astrocytophaty with extensively diffuse lesion lacking AQP4 compared with human IgG, suggesting the important role of antibody-related affinity in the pathogenesis of neuromyelitis optica (NMO). In addition, a rat model injected with AQP4-specific T cell lines and human-derived AQP4-IgG, we could make a new rat model with typical perivascular loss of AQP4 in cerebrum, periventriculum, spinal cord, retina, and optic chiasm with secondary demyelination and diffuse axonal damage, which is close to the pathological findings of tiffuse injury in NMO patients in post-mortem.
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