| Project/Area Number |
25460341
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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 |
General pharmacology
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| Research Institution | Saitama Medical University |
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Principal Investigator |
Maruyama Kei 埼玉医科大学, 医学部, 教授 (30211577)
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| Co-Investigator(Kenkyū-buntansha) |
吉川 圭介 埼玉医科大学, 医学部, 講師 (10435860)
柳下 聡介 国立研究開発法人国立精神・神経医療研究センター, 神経研究所 疾病研究第五部, 室長 (30585592)
淡路 健雄 埼玉医科大学, 医学部, 准教授 (60297546)
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| Co-Investigator(Renkei-kenkyūsha) |
Kondo Ryuichiro 九州大学, 農学研究科, 教授 (80091370)
Kuniyoshi Shimizu 九州大学, 農学研究科, 教授 (20346836)
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| Project Period (FY) |
2013-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
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| Keywords | アルツハイマー病 / アミロイドβタンパク質 / タウタンパク質 / タウ / 天然化合物 / 野生型マウス / 生活習慣病 / 天然由来成分 |
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| Outline of Final Research Achievements |
According to the "amyloid hypothesis", Alzheimer disease is developed by the deposition of amyloid beta protein (Aβ), followed by the accumulation of hyperphosphorylated tau and neuronal cell death. The hypothesis has been predominant for over ten years, but it is need to be readjust. We have generated two non-transgenic models: one with an increased Aβ production, and one with an increased phosphorylated tau. The former, which was generated by treatment of a natural resourse-derived compound, did not show abnormal behavior during the research duration. The latter was also used as an experimental model for sleep-disordered breathing, and we have shown that this model showed common gene expression pattern to ageing.
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