| First Author | Yanagisawa D | Year | 2015 |
| Journal | Neurobiol Aging | Volume | 36 |
| Issue | 1 | Pages | 201-10 |
| PubMed ID | 25179227 | Mgi Jnum | J:218307 |
| Mgi Id | MGI:5617284 | Doi | 10.1016/j.neurobiolaging.2014.07.041 |
| Citation | Yanagisawa D, et al. (2015) Curcumin derivative with the substitution at C-4 position, but not curcumin, is effective against amyloid pathology in APP/PS1 mice. Neurobiol Aging 36(1):201-10 |
| abstractText | Recent evidence supports the amyloid cascade hypothesis that a pathological change of amyloid beta (Abeta) in the brain is an initiating event in Alzheimer's disease (AD). Accordingly, modulating the abnormal Abeta 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 Abeta 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 Abeta aggregates; however, only FMeC1 significantly attenuated the cell toxicity of Abeta. These results indicate that FMeC1 may have potential for preventing AD. |
