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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.

Author information

1
Molecular Neuroscience Research Center, Shiga University of Medical Science, Otsu, Japan.
2
Department of Fundamental Nursing, Shiga University of Medical Science, Otsu, Japan.
3
Northeastern Industrial Research Center of Shiga Prefecture, Nagahama, Japan.
4
Otsuka Pharmaceutical Co., Ltd, Kawauchi-cho, Japan.
5
Molecular Neuroscience Research Center, Shiga University of Medical Science, Otsu, Japan. Electronic address: kinchan@belle.shiga-med.ac.jp.

Abstract

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.

KEYWORDS:

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

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