2013 Fiscal Year Final Research Report
Loss of the gene for a neuronal glutamate transporter-binding protein induces glutathione synthesis and better cognitive performances in mice.
| Project/Area Number |
23500454
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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 |
Neurochemistry/Neuropharmacology
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| Research Institution | Teikyo University |
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Principal Investigator |
AOYAMA KOJI 帝京大学, 医学部, 准教授 (00420943)
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| Project Period (FY) |
2011 – 2013
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| Keywords | グルタチオン / EAAC1 / GTRAP3-18 / 神経変性疾患 |
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| Research Abstract |
Glutathione (GSH) plays some important neuroprotective roles in the brain. The strategy to increase neuronal GSH level in the brain is a promising approach to the treatment of neurodegenerative diseases. To investigate the potential regulatory mechanism to increase neuronal GSH level in vivo, we generated GTRAP3-18-deficient (GTRAP3-18 KO) mice using a gene-targeting approach. Loss of the GTRAP3-18 gene resulted in increased neuronal GSH content and neuroprotection against oxidative stress. Moreover, GTRAP3-18 KO mice performed better in motor/spatial learning and memory tests than wild-type mice. These results indicate that the suppression of GTRAP3-18 increases neuronal resistance to oxidative stress and also facilitates cognitive function by increasing GSH content. The present study may provide a molecular basis for the development of treatments for neurodegenerative diseases.
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