| Project/Area Number |
24590370
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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 |
Pathological medical chemistry
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| Research Institution | Tohoku University |
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Principal Investigator |
NISHIJIMA Ichiko 東北大学, 東北メディカル・メガバンク機構, 講師 (70600394)
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| Co-Investigator(Renkei-kenkyūsha) |
KATSUOKA Fumiki 東北大学, 東北メディカル・メガバンク機構, 准教授 (30447255)
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) |
2012-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 脳神経疾患 / 発現制御 / モデル動物 / H46R変異SOD1遺伝子発現マウス / Nrf1遺伝子発現マウス / Nrf1遺伝子欠損マウス / 神経変性 / Nrf1 / プロテアソーム / 筋萎縮性側索硬化症 / モデルマウス / hSOD1 |
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| Outline of Final Research Achievements |
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease of motor neurons. Although defective ubiquitin-proteasome system is associated with neurodegenerative diseases commonly, the underlying molecular mechanisms are still unknown. To understand defense mechanisms using ubiquitin-proteasome system against progressive degeneration of neurons, we have analyzed Nrf1 activation in neurodegenerative disease condition using the compound transgenic mice carrying Nrf1 and mutant human SOD1 genes. The compound transgenic mice overexpressed Nrf1 and mutant human SOD1 have similar onset of neurodegeneration to mutant SOD1 transgenic mice. However, their degenerative progression was faster than mutant SOD1 transgenic mice. Our data indicate that Nrf1 activation may contribute acceleration of neurodegenerative disorders.
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