| Project/Area Number | 13680838 |
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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 |
Neurochemistry/Neuropharmacology
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
INABA Akira Tokyo Medical and Dental University, Laboratory Meidine, RESEARCH ASSOCIATE, 医学部附属病院, 助手 (10282766)
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| Co-Investigator(Kenkyū-buntansha) |
YOKOTA Takanori Tokyo Medical and Dental University, Neurology, RESEARCH ASSOCIATE, 医学部附属病院, 講師 (90231688)
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| Project Period (FY) |
2001 – 2003
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| Project Status |
Completed(Fiscal Year 2003)
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| Budget Amount *help |
¥3,100,000 (Direct Cost : ¥3,100,000)
Fiscal Year 2003 : ¥600,000 (Direct Cost : ¥600,000)
Fiscal Year 2002 : ¥1,200,000 (Direct Cost : ¥1,200,000)
Fiscal Year 2001 : ¥1,300,000 (Direct Cost : ¥1,300,000)
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| Keywords | vitamin E. / aTTP / ALS. / SOD1 / Oxidative stress / lipid peroxidation / αTTP / SOD1 / 脊髄小脳変性症 / 運動ニューロン疾患 / G93Aトランスジェニックマウス / aTTP KOマウス / SOD / α-tocopherol / 運動ニューロン / 筋萎縮性側索硬化症 / G93A トランスジェニックマウス |
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| Research Abstract |
1) MDA and HNE modifications in the brain of aTTP null mouse were increased and improved by vitamin E supplementation.
2) HNE-modified protein is SOD. This modification disturbed the radical scavenge function of SOD, resulting in enhance the oxidative stress by vitamin E deficiency.
3) Dopamine content in the striatum of aTTP null mouse was decreased after administration of MPTP, indicating dopamine decrease in Parkinson disease is related to oxidative stress.
4) Onset of symptom in G93ASOD1 TgM crossed with aTTP null mouse is accelerated with more marked degeneration of anterior horn cell, indicating pathophysiology of ALS is affected by oxidative stress,
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