Research Papers: Gerotarget (Focus on Aging):

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

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

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Oncotarget. 2016; 7:67716-67731. https://doi.org/10.18632/oncotarget.11963

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Yan Kong1, Ke Li2, Tingting Fu3, Chao Wan4, Dongdong Zhang4, Hang Song4, Yao Zhang4, Na Liu4, Zhenji Gan3 and Liudi Yuan1,4

1 Department of Biochemistry and Molecular Biology, Medical School, Southeast University, Nanjing, Jiangsu, China

2 Gladstone Institute of Cardiovascular Disease and Department of Pharmaceutical Chemistry, University of California, San Francisco, CA, USA

3 MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing University, Nanjing, China

4 State Education Ministry’s Key Laboratory of Developmental Genes and Human Diseases, Institute of Life Sciences, Southeast University, China

Correspondence to:

Liudi Yuan, email:

Zhenji Gan, email:

Yan Kong, email:

Keywords: quercetin, Drosophila, Alzheimer’s disease, cell cycle, DNA replication, Gerotarget

Received: September 22, 2015 Accepted: September 01, 2016 Published: September 10, 2016


Alzheimer’s disease (AD) is a prevalent neurodegenerative disorder characterized by β 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.

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