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Article Publish Status: FREE
Abstract Title:

Quercetin ameliorates Aβ toxicity in Drosophila AD model by modulating cell cycle-related protein expression.

Abstract Source:

Oncotarget. 2016 Sep 10. Epub 2016 Sep 10. PMID: 27626494

Abstract Author(s):

Yan Kong, Ke Li, Tingting Fu, Chao Wan, Dongdong Zhang, Hang Song, Yao Zhang, Na Liu, Zhenji Gan, Liudi Yuan

Article Affiliation:

Yan Kong

Abstract:

Alzheimer's disease (AD) is a prevalent neurodegenerative disorder characterized byβ amyloid (Aβ) deposition and neurofibril tangles. It has been reported that a bioflavonoid, quercetin, could ameliorate AD phenotypes in C. elegans and mice. However, the mechanism underlying the ameliorative effect of quercetin is not fully understood yet. Drosophila models could recapitulate AD-like phenotypes, such as shortened lifespan, impaired locomotive ability as well as defects in learning and memory. So in this study, we investigated the effects of quercetin on AD in Drosophila model and explored the underlying mechanisms. We found quercetin could effectively intervene in AD pathogenesis in vivo. Mechanism study showed quercetin could restore the expression of genes perturbed by Aβ accumulation, such as those involved in cell cycle and DNA replication. Cyclin B, an important cell cycle protein, was chosen to test whether it participated in the AD ameliorative effects of quercetin. We found that cyclin B RNAi in the brain could alleviate AD phenotypes. Taken together, the current study suggested that the neuroprotective effects of quercetin were mediated at least partially by targeting cell cycle-related proteins.

Study Type : Insect Study

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Sayer Ji
Founder of GreenMedInfo.com

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