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アルツハイマー病、他の認知症、老化 4
Alzheimer's Disease, Other Dementia, Aging 4

開催日 2014/9/12
時間 16:00 - 17:00
会場 Room I(311+312)
Chairperson(s) 古川 勝敏 / Katsutoshi Furukawa (東北大学加齢医学研究所老年医学分野 / Department of Geriatrics and Gerontology, Division of Brain Sciences, Institute of Development Aging and Cancer, Tohoku University, Jap)
遠山 育夫 / Ikuo Tooyama (滋賀医科大学分子神経科学研究センター / Molecular Neuroscience Research Center, Shiga University of Medical Science, Japan)

Effect of novel curcumin derivatives on amyloid pathology in APP/PS1 mice

  • O2-I-4-1
  • 柳沢 大治郎 / Daijiro Yanagisawa:1 Ibrahim Nor Faeizah / Nor Faeizah Ibrahim:1 Durani Lina Wati / Lina Wati Durani:1 田口 弘康 / Hiroyasu Taguchi:1 遠山 育夫 / Ikuo Tooyama:1 
  • 1:滋賀医科大学 / Shiga University of Medical Science, Japan 

Alzheimer's disease (AD) is characterized by a progression from episodic memory problems to a slow global decline in cognitive function. Recent studies on the progression of AD strongly support the amyloid cascade hypothesis that a pathological change in amyloid β (Aβ) in the brain is an initiating event. The abnormal changes in Aβ are believed to induce abnormal hyperphosphorylation of tau and tangle formation as well as neuronal loss, resulting eventually in cognitive impairment. Accordingly, modulating the abnormal Aβ aggregation is considered a potential therapeutic target in AD. Curcumin, a low molecular weight polyphenol derived from the well-known curry spice turmeric, has shown favorable effects on preventing or treating AD pathology. The present study investigated the effects of a novel curcumin derivative, FMeC1, which bears a substitution at the C-4 position, on AD pathology in a mouse model of AD. APPswe/PS1dE9 double transgenic mice were used as a mouse model of AD, and were fed a chow diet that contained FMeC1 for 6 months. The mice showed a reduction in insoluble Aβ and an attenuation of glial cell activity together with reduced cognitive deficits, compared to animals receiving a control diet or with curcumin in their diet. Both curcumin and FMeC1 modulated the formation of Aβ aggregates, however, only FMeC1 significantly attenuated the cell toxicity of Aβ in SH-SY5Y cells. These results indicate that FMeC1 may have potential for preventing AD.

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