| Project/Area Number |
23592593
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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 |
Ophthalmology
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| Research Institution | Nippon Medical School |
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Principal Investigator |
KAMEYA SHUHEI 日本医科大学, 医学部, 准教授 (30302269)
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| Co-Investigator(Kenkyū-buntansha) |
SUZUKI Yuko 独立行政法人国立精神・神経医療研究センター, 遺伝子疾患治療研究部, 室長 (00342931)
YAMAKI Kunihiko 日本医科大学, 医学部, 教授 (20125751)
TAKAHASHI Hisatomo 日本医科大学, 医学部, 助教 (10445801)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | neuromyelitis optica / alpha1-syntrophin / 視神経脊髄炎 / α1-syntrophin |
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| Research Abstract |
The purpose of the study was to analyse the mechanisms causing neuromyelitis optica (NMO). We used alpha1-syntrophin deficient mice to analyse the disease, since alpha1-syntrophin directly interact to aquaporin-4 (AQP4) which is important for the ethiology of NMO. We have performed histological analysis of optic nerve of wild type and alpha1-syntrophin deficient mice. There was no hisiological difference in optic nerve of these mice. We have performed immunohistological analysis of optic nerve of these mice. We used anti-AQP4, anti-Neurofilament, and anti-MBP antibodies. There were no difference of immunostaining by those antibodies in these mice. We tried to cause experimental autoimmune enchephalomyelitis (EAE) to these mice. We performed the procedure to cause EAE to these mice as previously reported, however we could not obtain mice with EAE. We examined optic nerve of these mice 14 days after immunaization, However there were no pathophysiological differeneces between these mice.
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