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Neurobiol Aging. 2015 Jan;36(1):201-10. doi: 10.1016/j.neurobiolaging.2014.07.041. Epub 2014 Aug 2.

Curcumin derivative with the substitution at C-4 position, but not curcumin, is effective against amyloid pathology in APP/PS1 mice.

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Molecular Neuroscience Research Center, Shiga University of Medical Science, Otsu, Japan.
Department of Fundamental Nursing, Shiga University of Medical Science, Otsu, Japan.
Northeastern Industrial Research Center of Shiga Prefecture, Nagahama, Japan.
Otsuka Pharmaceutical Co., Ltd, Kawauchi-cho, Japan.
Molecular Neuroscience Research Center, Shiga University of Medical Science, Otsu, Japan. Electronic address:


Recent evidence supports the amyloid cascade hypothesis that a pathological change of amyloid β (Aβ) in the brain is an initiating event in Alzheimer's disease (AD). 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 curcumin and 2 novel curcumin derivatives, FMeC1 and FMeC2, on AD pathology in APPswe/PS1dE9 double transgenic mice. Mice fed a chow diet that contained FMeC1 for 6 months showed a reduction in insoluble Aβ deposits and glial cell activity together with reduced cognitive deficits, compared to animals receiving a control diet or with curcumin or FMeC2 in their diet. Both curcumin and FMeC1 modulated the formation of Aβ aggregates; however, only FMeC1 significantly attenuated the cell toxicity of Aβ. These results indicate that FMeC1 may have potential for preventing AD.


APP/PS1 transgenic mice; Alzheimer's disease; amyloid-β; curcumin

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