| Project/Area Number |
22590927
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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 | Hamamatsu University School of Medicine |
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Principal Investigator |
KONO Satoshi 浜松医科大学, 医学部附属病院, 講師 (40397386)
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| Co-Investigator(Kenkyū-buntansha) |
MIJAJIMA Hiroaki 浜松医科大学, 医学部, 教授 (90221613)
鈴木 万幾子 浜松医科大学, 医学部附属病院, 医員 (60549278)
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| Co-Investigator(Renkei-kenkyūsha) |
SUZUKI Makiko 浜松医科大学, 医学部附属病院, 医員 (60549278)
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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 |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2012: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2010: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | ビタミン B1 / ウエルニッケ様脳症 / SLC19A3 遺伝子 / チアミントランスポーター / ビタミンB1 / SLC19A3遺伝子 |
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| Research Abstract |
An aim of this study is clarify molecular pathological mechanism of Wernicke’s-like encephalopathy which we first identified in 2009. Wernicke -like encephalopathy is autosomal recessive inherited neurological disease due to SLC19A3 gene mutation encoding thiamine transporter 2. Clinical characters of this disease are similar to Wernicke encephalopathy caused by thiamin deficiency. SLC19A3 transgenic mice was generated to investigate brain glucose metabolism using positron emission tomography(PET) and biochemical thiamine metabolism in primary neuronal cell culture system. Homozygous transgenic mice with a mutation in SLC19A3 gene were dead at a late embryonic stage. There was no difference in brain glucose metabolism between the heterozygous mice and wild mice. In the process of investigation, we report some novel findings in the functional brain analysis and molecular cellular model in hereditary neurological disease including amyotrophic lateral sclerosis, Parkinson’s disease and et al. Functional brain imaging in heterozygous mice under thiamin deficiency and biochemical analysis of brain tissues in homozygous mice are in progress.
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