| Project/Area Number |
25461281
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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 |
Neurology
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| Research Institution | Kyushu University |
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Principal Investigator |
OKA SUGAKO 九州大学, 生体防御医学研究所, 研究員 (80467894)
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| Co-Investigator(Kenkyū-buntansha) |
KANG DONGCHON 九州大学, 医学系研究院 基礎医学部門, 教授 (80214716)
NAKABEPPU YUSAKU 九州大学, 生体防御医学研究所, 教授 (30180350)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | アルツハイマー病 / TFAM / インスリン抵抗性 / 糖尿病 / ミトコンドリア / DNA酸化障害 |
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| Outline of Final Research Achievements |
Diabetes is known to be a risk factor for Alzheimer’s disease (AD). However, we reported that microarray analysis of the hippocampus of an AD mouse model revealed the altered expression of diabetes-related genes. Moreover, we identified obesity and impaired glucose metabolism in AD model mice of a certain age. This vicious circle is considered to play a pivotal role in the development of AD, but the molecular mechanism remains unclear.
In the present study, we established AD model mice expressing human mitochondrial transcriptional factor A (hTFAM), and found that hTFAM expression effectively ameliorated the AD pathophysiology through the improvement of mitochondrial dysfunction. The expression of hTFAM also improved obesity and glucose tolerance in AD model mice. Our results provide new insights into the molecular mechanisms of the AD pathology, and potential new therapeutic strategies against AD.
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