Evidence map›Paper›PMID 28446202›Full record

ArticleAlzheimer's research & therapy2017

Analyzing the genes related to Alzheimer's disease via a network and pathway-based approach.

Yan-Shi Hu, Juncai Xin, Ying Hu, Lei Zhang, Ju Wang

Open access · goldAbstract read
In one paragraph

Article in Alzheimer's research & therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 3% 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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 111 citations in OpenAlex.

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  14. Single-cell genomics and regulatory networks for 388 human brains.bioRxiv : the preprint server for biology · 2024
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1 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

5 authors at 2 institutions in 1 country.

Yan-Shi HuSchool of Biomedical Engineering, Tianjin Medical University, Tianjin, 300070, China.
Juncai XinSchool of Biomedical Engineering, Tianjin Medical University, Tianjin, 300070, China.
Ying HuSchool of Biomedical Engineering, Tianjin Medical University, Tianjin, 300070, China.
Lei ZhangSchool of Computer Science and Technology, Tianjin University, Tianjin, 300072, China. lzhang@tju.edu.cn.
Ju WangSchool of Biomedical Engineering, Tianjin Medical University, Tianjin, 300070, China. wangju@tmu.edu.cn.ORCID http://orcid.org/0000-0002-6514-0923
Tianjin Medical University · CNTianjin University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOur understanding of the molecular mechanisms underlying Alzheimer's disease (AD) remains incomplete. Previous studies have revealed that genetic factors provide a significant contribution to the pathogenesis and development of AD. In the past years, numerous genes implicated in this disease have been identified via genetic association studies on candidate genes or at the genome-wide level. However, in many cases, the roles of these genes and their interactions in AD are still unclear. A comprehensive and systematic analysis focusing on the biological function and interactions of these genes in the context of AD will therefore provide valuable insights to understand the molecular features of the disease.

methodIn this study, we collected genes potentially associated with AD by screening publications on genetic association studies deposited in PubMed. The major biological themes linked with these genes were then revealed by function and biochemical pathway enrichment analysis, and the relation between the pathways was explored by pathway crosstalk analysis. Furthermore, the network features of these AD-related genes were analyzed in the context of human interactome and an AD-specific network was inferred using the Steiner minimal tree algorithm.

resultsWe compiled 430 human genes reported to be associated with AD from 823 publications. Biological theme analysis indicated that the biological processes and biochemical pathways related to neurodevelopment, metabolism, cell growth and/or survival, and immunology were enriched in these genes. Pathway crosstalk analysis then revealed that the significantly enriched pathways could be grouped into three interlinked modules-neuronal and metabolic module, cell growth/survival and neuroendocrine pathway module, and immune response-related module-indicating an AD-specific immune-endocrine-neuronal regulatory network. Furthermore, an AD-specific protein network was inferred and novel genes potentially associated with AD were identified.

conclusionBy means of network and pathway-based methodology, we explored the pathogenetic mechanism underlying AD at a systems biology level. Results from our work could provide valuable clues for understanding the molecular mechanism underlying AD. In addition, the framework proposed in this study could be used to investigate the pathological molecular network and genes relevant to other complex diseases or phenotypes.

Indexed as

Alzheimer DiseaseBrainComputer SimulationGene Expression ProfilingGene Regulatory NetworksGenetic Association StudiesGenetic Predisposition to DiseaseHumansMetabolic Flux AnalysisMetabolic Networks and PathwaysModels, GeneticNerve Tissue ProteinsSignal TransductionNerve Tissue ProteinsAlzheimer’s diseaseFunctional enrichment analysisNetwork analysisPathway crosstalk

Identifiers

PMID28446202
PMCPMC5406904
OpenAlexW2608472446

What OpenQuestion holds

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LicenceCC BY
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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.