Evidence map›Paper›PMID 30124448›Full record

ArticleJournal of Alzheimer's disease : JAD2018

Application of Weighted Gene Co-Expression Network Analysis to Explore the Key Genes in Alzheimer's Disease.

Jia-Wei Liang, Zheng-Yu Fang, Yong Huang, Zhen-Yu Liuyang, Xiao-Lin Zhang, Jing-Lin Wang, Hui Wei, Jian-Zhi Wang, Xiao-Chuan Wang, Ji Zeng and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

63 citing papers in PubMed, 101 citations in OpenAlex.

  1. VDJ-REMIX: REpertoire Module Identification and eXploration.Bioinformatics (Oxford, England) · 2026
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  17. Whole-genome sequencing study in Koreans identifies novel loci for Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
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  19. Review
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3 more citing papers are in PubMed but not listed here.

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

11 authors at 2 institutions in 1 country.

Jia-Wei LiangDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Zheng-Yu FangDepartment of Rehabilitation Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Yong HuangDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Zhen-Yu LiuyangDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Xiao-Lin ZhangDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Jing-Lin WangDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Hui WeiDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Jian-Zhi WangDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Xiao-Chuan WangDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Ji ZengDepartment of Clinic Laboratory, Pu Ai Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Rong LiuDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Huazhong University of Science and Technology · CNTongji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWeighted co-expression network analysis (WGCNA) is a powerful systems biology method to describe the correlation of gene expression based on the microarray database, which can be used to facilitate the discovery of therapeutic targets or candidate biomarkers in diseases.

objectiveTo explore the key genes in the development of Alzheimer's disease (AD) by using WGCNA.

methodsThe whole gene expression data GSE1297 from AD and control human hippocampus was obtained from the GEO database in NCBI. Co-expressed genes were clustered into different modules. Modules of interest were identified through calculating the correlation coefficient between the module and phenotypic traits. GO and pathway enrichment analyses were conducted, and the central players (key hub genes) within the modules of interest were identified through network analysis. The expression of the identified key genes was confirmed in AD transgenic mice through using qRT-PCR.

resultsTwo modules were found to be associated with AD clinical severity, which functioning mainly in mineral absorption, NF-κB signaling, and cGMP-PKG signaling pathways. Through analysis of the two modules, we found that metallothionein (MT), Notch2, MSX1, ADD3, and RAB31 were highly correlated with AD phenotype. Increase in expression of these genes was confirmed in aged AD transgenic mice.

conclusionWGCNA analysis can be used to analyze and predict the key genes in AD. MT1, MT2, MSX1, NOTCH2, ADD3, and RAB31 are identified to be the most relevant genes, which may be potential targets for AD therapy.

Indexed as

Gene Regulatory NetworksAdducinsAlzheimer DiseaseCalmodulin-Binding ProteinsFemaleGene Expression ProfilingGenetic Predisposition to DiseaseHumansMaleMental Status ScheduleMetallothioneinMSX1 Transcription Factorrab GTP-Binding ProteinsReceptor, Notch2RNA, MessengerSystems BiologyADD3 protein, humanAdducinsCalmodulin-Binding ProteinsMetallothioneinMSX1 protein, humanMSX1 Transcription FactorNOTCH2 protein, humanRAB31 protein, humanrab GTP-Binding ProteinsReceptor, Notch2RNA, MessengerADD3Alzheimer’s diseasemetallothioneinMSX1neurofibrillary tanglesNotch2RAB31WGCNA

Identifiers

PMID30124448
PMCPMC6218130
OpenAlexW2886175913

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.