Evidence map›Paper›PMID 34336099›Full record

ArticleOxidative medicine and cellular longevity2021

Integrative Functional Genomic Analysis of Molecular Signatures and Mechanistic Pathways in the Cell Cycle Underlying Alzheimer's Disease.

Zhike Zhou, Jun Bai, Shanshan Zhong, Rongwei Zhang, Kexin Kang, Xiaoqian Zhang, Ying Xu, Chuansheng Zhao, Mei Zhao

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 15% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.

  1. Pooled it
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  3. Review
  4. Article
  5. Review
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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

9 authors at 4 institutions in 2 countries.

Zhike ZhouDepartment of Geriatrics, The First Affiliated Hospital, China Medical University, Shenyang, 110001 Liaoning, China.ORCID https://orcid.org/0000-0002-3571-8130
Jun BaiCancer Systems Biology Center, The China-Japan Union Hospital, Jilin University, Changchun, 130033 Jilin, China.
Shanshan ZhongDepartment of Neurology, The First Affiliated Hospital, China Medical University, Shenyang, 110001 Liaoning, China.
Rongwei ZhangDepartment of Geriatrics, The First Affiliated Hospital, China Medical University, Shenyang, 110001 Liaoning, China.
Kexin KangDepartment of Geriatrics, The First Affiliated Hospital, China Medical University, Shenyang, 110001 Liaoning, China.
Xiaoqian ZhangDepartment of Neurology, The First Affiliated Hospital, China Medical University, Shenyang, 110001 Liaoning, China.
Ying XuCancer Systems Biology Center, The China-Japan Union Hospital, Jilin University, Changchun, 130033 Jilin, China.
Chuansheng ZhaoDepartment of Neurology, The First Affiliated Hospital, China Medical University, Shenyang, 110001 Liaoning, China.ORCID https://orcid.org/0000-0002-4100-1259
Mei ZhaoDepartment of Cardiology, The Shengjing Affiliated Hospital, China Medical University, Shenyang, 110004 Liaoning, China.ORCID https://orcid.org/0000-0003-4204-9235
First Hospital of China Medical University · CNChina Medical University · CNJilin University · CNUniversity of Georgia · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveAlzheimer's disease (AD) is associated with cell cycle reentry of mature neurons that subsequently undergo degeneration. This study is aimed to identify key regulators of the cell cycle and their underlying pathways for developing optimal treatment of AD.

methodsRNA sequencing data were profiled to screen for differentially expressed genes in the cell cycle. Correlation of created modules with AD phenotype was computed by weight gene correlation network analysis (WGCNA). Signature genes for trophic factor receptors were determined using Pearson correlation coefficient (PCC) analysis.

resultsAmong the 13,679 background genes, 775 cell cycle genes and 77 trophic factor receptors were differentially expressed in AD versus nondementia controls. Four coexpression modules were constructed by WGCNA, among which the turquoise module had the strongest correlation with AD. According to PCC analysis, 10 signature trophic receptors most strongly interacting with cell cycle genes were filtered and subsequently displayed in the global regulatory network. Further cross-talking pathways of signature receptors, such as glutamatergic synapse, long-term potentiation, PI3K-Akt, and MAPK signaling pathways, were identified.

conclusionsOur findings highlighted the mechanistic pathways of signature trophic receptors in cell cycle perturbation underlying AD pathogenesis, thereby providing new molecular targets for therapeutic intervention in AD.

Indexed as

Alzheimer DiseaseCell CycleGene Expression ProfilingGenomicsHumans

Identifiers

PMID34336099
PMCPMC8290224
OpenAlexW3180824217

What OpenQuestion holds

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LicenceCC BY
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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.