2011 Fiscal Year Final Research Report
A study on CNS oxidative stress-resistant mouse
| Project/Area Number |
21590291
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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 |
General pharmacology
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| Research Institution | Teikyo University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
AOYAMA Koji 帝京大学, 医学部, 講師 (00420943)
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| Project Period (FY) |
2009 – 2011
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| Keywords | GTRAP3-18 / EAAC1 / 神経細胞 / グルタチオン / 遺伝子破壊マウス / 神経変性疾患 |
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| Research Abstract |
To investigate the potential regulatory mechanism to increase neuronal GSH level in vivo, we generated GTRAP3-18-deficient(GTRAP3-18./.) mice using a gene-targeting approach. Disruption of the GTRAP3-18 gene resulted in increased EAAC1 expression in the plasma membrane, increased neuronal GSH content and neuroprotection against oxidative stress. In addition, GTRAP3-18./. mice performed better in motor/spatial learning and memory tests than wild-type mice. Therefore, the suppression of GTRAP3-18 increases neuronal resistance to oxidative stress by increasing GSH content and also facilitates cognitive function. The present results may provide a molecular basis for the development of treatments for neurodegenerative diseases.
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