| Project/Area Number |
24500877
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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 |
Applied health science
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| Research Institution | Hyogo Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
FUJIWARA Noriko 兵庫医科大学, 医学部, 准教授 (10368532)
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| Research Collaborator |
YOSHIHARA Daisaku 兵庫医科大学, 医学部, 助教 (00567266)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 酸化ストレス / SOD1 / 神経伝達 / 行動学 / モノアミン / SOD / 加齢 / 行動 |
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| Outline of Final Research Achievements |
Reactive oxygen species (ROS) are generated by a multitude of biochemical reactions and cellular functions in all cells. The excess reactive oxygen species (ROS) could lead to damage to DNA, proteins and lipid, and this damage accumulates over time. Oxidative stress caused by accumulated ROS is thought to cause neurotransmitter disorders associated with those diseases may induce learning disabilities, memory deficits and depression. However, little is known whether oxidative stress induces neurotransmitter disorders. Cu/Zn-superoxide dismutase (SOD1) is an anti-oxidative enzyme and protects cells against oxidative stress. The effects of SOD1 deficiency on brain functions and tissue contents of monoamines were tested. We found that SOD1 KO mice exhibited some abnormal behaviors in shuttle box learning tests and alterations in brain monoamine metabolism compared with wild-type mice. These data suggest that oxidative stress affects monoamine metabolism and neurotransmission.
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