| Project/Area Number |
15K15085
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
Kazuhiko Tsuruya 九州大学, 医学研究院, 准教授 (20372740)
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| Research Collaborator |
Naoki Haruyama
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 認知症 / 慢性腎不全 / MTH1 / OGG1 / 8-オキソグアニン / 8-オキシグアニン |
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| Outline of Final Research Achievements |
Increased oxidative stress in brains of patients with chronic kidney disease (CKD), which frequently occurs in elderly people, has been implicated as one of the causes for dementia. Neurodegeneration of hippocampal CA3 region has been reported in brain of CKD model mouse generated by ligation of left renal artery and partial removal of right kidney. In this study, we examined whether oxidative damage in nucleic acids play a role for developing the brain dysfunction in this CKD model using mice lacking genes for defense and repair of oxidative damage in nucleic acids. As a result, neither cognitive dysfunction nor degenerative lesions of the brain were recognized in this CKD model, and even in mice lacking genes for defense and repair of oxidative damage in nucleic acids, CKD did not enhance brain dysfunction. From the results, we concluded that brain dysfunction is not induced in this CKD model mouse.
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