Evidence map›Paper›PMID 27626494›Full record

ArticleOncotarget2016

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

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
  2. Biology · 2026
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  11. The Effects ofInternational journal of molecular sciences · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 2 countries.

Yan KongDepartment of Biochemistry and Molecular Biology, Medical School, Southeast University, Nanjing, Jiangsu, China.
Ke LiGladstone Institute of Cardiovascular Disease and Department of Pharmaceutical Chemistry, University of California, San Francisco, CA, USA.
Tingting FuMOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing University, Nanjing, China.
Chao WanState Education Ministry's Key Laboratory of Developmental Genes and Human Diseases, Institute of Life Sciences, Southeast University, China.
Dongdong ZhangState Education Ministry's Key Laboratory of Developmental Genes and Human Diseases, Institute of Life Sciences, Southeast University, China.
Hang SongState Education Ministry's Key Laboratory of Developmental Genes and Human Diseases, Institute of Life Sciences, Southeast University, China.
Yao ZhangState Education Ministry's Key Laboratory of Developmental Genes and Human Diseases, Institute of Life Sciences, Southeast University, China.
Na LiuState Education Ministry's Key Laboratory of Developmental Genes and Human Diseases, Institute of Life Sciences, Southeast University, China.
Zhenji GanMOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing University, Nanjing, China.
Liudi YuanDepartment of Biochemistry and Molecular Biology, Medical School, Southeast University, Nanjing, Jiangsu, China.
Southeast University · CNModel Animal Research Center · CNGladstone Institutes · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

Disease Models, AnimalAlzheimer DiseaseAmyloid beta-PeptidesAnimalsAnimals, Genetically ModifiedAntioxidantsCell Cycle ProteinsCyclin BDrosophila melanogasterDrosophila ProteinsGene Expression ProfilingGene OntologyHumansNeuroprotective AgentsQuercetinRNA InterferenceAmyloid beta-PeptidesAntioxidantsCell Cycle ProteinsCyclin BDrosophila ProteinsNeuroprotective AgentsQuercetinAlzheimer’s diseasecell cycleDNA replicationDrosophilaGerotargetquercetin

Identifiers

PMID27626494
PMCPMC5356514
OpenAlexW2516233270

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.