2017 Fiscal Year Final Research Report
Development of novel diagnostic and therapeutic methods on Alzheimer's disease by targeting amyloid oligomers
Project/Area Number |
26290022
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Partial Multi-year Fund |
Section | 一般 |
Research Field |
Neurochemistry/Neuropharmacology
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Research Institution | Shiga University of Medical Science |
Principal Investigator |
Tooyama Ikuo 滋賀医科大学, 神経難病研究センター, 教授 (20207533)
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Co-Investigator(Kenkyū-buntansha) |
椎野 顯彦 滋賀医科大学, 神経難病研究センター, 准教授 (50215935)
田口 弘康 滋賀医科大学, 神経難病研究センター, 特任教授 (90102912)
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Project Period (FY) |
2014-04-01 – 2017-03-31
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Keywords | 脳神経疾患 / アルツハイマー病 / 核磁気共鳴画像 / 診断 / 治療 / アミロイドオリゴマー |
Outline of Final Research Achievements |
The aim of this study is to find curcumin derivatives that have diagnostic and therapeutic potential for Alzheimer's disease (AD). We used, f-methyl-curcumin1 (FMeC1) and FMeC2. For MRI, FMeC1 or FMeC2 (200 mg/kg) was injected into the tail vein of six Tg2576, three APP/PS1 and six control mice. Then, amyloid imaging was employed using a 7.0 T MR scanner. For therapeutic experiments, 36 model mice and 12 wild mice were divided into four groups; control diet, curcumin, FMeC1 or FMeC2 group. FMeC1, or FMeC2 (500 ppm) for 6 months from 9-month-old. Behavioral tests were conducted from 14.5 months of age, and mice were sacrificed at 15 months of age for pathological analyses. FMeC1 but not FMeC2 successfully detected amyloid plaques in living mice. Only FMeC1 showed a significant improvement on cognitive function compared to control group (p < 0.05). In addition, FMeC1 reduced Aβ aggregation and glial cell activity (p < 0.05). FMeC1 is a potential diagnostic and therapeutic agent for AD.
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Free Research Field |
神経科学
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