Evidence map›Paper›PMID 34326892›Full record

ArticleComputational and mathematical methods in medicine2021

Identification of the Hub Genes in Alzheimer's Disease.

Huiwen Gui, Qi Gong, Jun Jiang, Mei Liu, Huanyin Li

Open access · hybridAbstract read
In one paragraph

Article in Computational and mathematical methods in medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.5field-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

14 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. From correlation to causation: cell-type-specific gene regulatory networks in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
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  5. Review
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  11. Mechanism of GAPDH Redox Signaling by HInternational journal of molecular sciences · 2022
    Article
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  13. Article
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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

5 authors at 2 institutions in 1 country.

Huiwen GuiDepartment of Neurology, Minhang Branch, Zhongshan Hospital, Fudan University, 170 Xinsong Road, 201199 Shanghai, China.
Qi GongDepartment of Neurology, Minhang Branch, Zhongshan Hospital, Fudan University, 170 Xinsong Road, 201199 Shanghai, China.
Jun JiangState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai 200438, China.
Mei LiuDepartment of General Practice, Minhang Branch, Zhongshan Hospital, Fudan University, 170 Xinsong Road, 201199 Shanghai, China.ORCID https://orcid.org/0000-0002-1090-7672
Huanyin LiDepartment of Neurology, Minhang Branch, Zhongshan Hospital, Fudan University, 170 Xinsong Road, 201199 Shanghai, China.ORCID https://orcid.org/0000-0002-2058-5259
Fudan University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeAlzheimer's disease (AD) is considered to be the most common neurodegenerative disease and also one of the major fatal diseases affecting the elderly, thus bringing a huge burden to society. Therefore, identifying AD-related hub genes is extremely important for developing novel strategies against AD. MATERIALS AND

methodsHere, we extracted the gene expression profile GSE63061 from the National Center for Biotechnology Information (NCBI) GEO database. Once the unverified gene chip was removed, we standardized the microarray data after quality control. We utilized the Limma software package to screen the differentially expressed genes (DEGs). We conducted Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses of DEGs. Subsequently, we constructed a protein-protein interaction (PPI) network using the STRING database.

resultWe screened 2169 DEGs, comprising 1313 DEGs with upregulation and 856 DEGs with downregulation. Functional enrichment analysis showed that the response of immune, the degranulation of neutrophils, lysosome, and the differentiation of osteoclast were greatly enriched in DEGs with upregulation; peptide biosynthetic process, translation, ribosome, and oxidative phosphorylation were dramatically enriched in DEGs with downregulation. 379 nodes and 1149 PPI edges were demonstrated in the PPI network constructed by upregulated DEGs; 202 nodes and 1963 PPI edges were shown in the PPI network constructed by downregulated DEGs. Four hub genes, including GAPDH, RHOA, RPS29, and RPS27A, were identified to be the newly produced candidates involved in AD pathology.

conclusionGAPDH, RHOA, RPS29, and RPS27A are expected to be key candidates for AD progression. The results of this study can provide comprehensive insight into understanding AD's pathogenesis and potential new therapeutic targets.

Indexed as

Gene Regulatory NetworksAlzheimer DiseaseComputational BiologyDatabases, GeneticGene Expression Regulation, NeoplasticGene OntologyGlyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating)HumansProtein Interaction MapsrhoA GTP-Binding ProteinRibosomal ProteinsSoftwareUbiquitinsGAPDH protein, humanGlyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating)rhoA GTP-Binding ProteinRHOA protein, humanRibosomal ProteinsRPS27a protein, humanUbiquitins

Identifiers

PMID34326892
PMCPMC8302378
OpenAlexW3185966651

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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.