A Systematic Bioinformatics Workflow With Meta-Analytics Identified Potential Pathogenic Factors of Alzheimer’s Disease

Potential pathogenic factors, other than well-known , , and , can be further identified from transcriptomics studies of differentially expressed genes (DEGs) that are specific for Alzheimer's disease (AD), but findings are often inconsistent or even contradictory. Evidence corroboration by comb...

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Veröffentlicht in:Frontiers in neuroscience Jg. 14; S. 209
Hauptverfasser: Yuen, Sze Chung, Zhu, Hongmei, Leung, Siu-wai
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Switzerland Frontiers Research Foundation 13.03.2020
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ISSN:1662-453X, 1662-4548, 1662-453X
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Abstract Potential pathogenic factors, other than well-known , , and , can be further identified from transcriptomics studies of differentially expressed genes (DEGs) that are specific for Alzheimer's disease (AD), but findings are often inconsistent or even contradictory. Evidence corroboration by combining meta-analysis and bioinformatics methods may help to resolve existing inconsistencies and contradictions. This study aimed to demonstrate a systematic workflow for evidence synthesis of transcriptomic studies using both meta-analysis and bioinformatics methods to identify potential pathogenic factors. Transcriptomic data were assessed from GEO and ArrayExpress after systematic searches. The DEGs and their dysregulation states from both DNA microarray and RNA sequencing datasets were analyzed and corroborated by meta-analysis. Statistically significant DEGs were used for enrichment analysis based on KEGG and protein-protein interaction network (PPIN) analysis based on STRING. AD-specific modules were further determined by the DIAMOnD algorithm, which identifies significant connectivity patterns between specific disease-associated proteins and non-specific proteins. Within AD-specific modules, the nodes of highest degrees (>95th percentile) were considered as potential pathogenic factors. After systematic searches of 225 datasets, extensive meta-analyses among 25 datasets (21 DNA microarray datasets and 4 RNA sequencing datasets) identified 9,298 DEGs. The dysregulated genes and pathways in AD were associated with impaired amyloid-β (Aβ) clearance. From the AD-specific module, Fyn, and EGFR were the most statistically significant and biologically relevant. This meta-analytical study suggested that the reduced Aβ clearance in AD pathogenesis was associated with the genes encoding Fyn and EGFR, which were key receptors in Aβ downstream signaling.
AbstractList Potential pathogenic factors, other than well-known , , and , can be further identified from transcriptomics studies of differentially expressed genes (DEGs) that are specific for Alzheimer's disease (AD), but findings are often inconsistent or even contradictory. Evidence corroboration by combining meta-analysis and bioinformatics methods may help to resolve existing inconsistencies and contradictions. This study aimed to demonstrate a systematic workflow for evidence synthesis of transcriptomic studies using both meta-analysis and bioinformatics methods to identify potential pathogenic factors. Transcriptomic data were assessed from GEO and ArrayExpress after systematic searches. The DEGs and their dysregulation states from both DNA microarray and RNA sequencing datasets were analyzed and corroborated by meta-analysis. Statistically significant DEGs were used for enrichment analysis based on KEGG and protein-protein interaction network (PPIN) analysis based on STRING. AD-specific modules were further determined by the DIAMOnD algorithm, which identifies significant connectivity patterns between specific disease-associated proteins and non-specific proteins. Within AD-specific modules, the nodes of highest degrees (>95th percentile) were considered as potential pathogenic factors. After systematic searches of 225 datasets, extensive meta-analyses among 25 datasets (21 DNA microarray datasets and 4 RNA sequencing datasets) identified 9,298 DEGs. The dysregulated genes and pathways in AD were associated with impaired amyloid-β (Aβ) clearance. From the AD-specific module, Fyn, and EGFR were the most statistically significant and biologically relevant. This meta-analytical study suggested that the reduced Aβ clearance in AD pathogenesis was associated with the genes encoding Fyn and EGFR, which were key receptors in Aβ downstream signaling.
Potential pathogenic factors, other than well-known APP, APOE4, and PSEN, can be further identified from transcriptomics studies of differentially expressed genes (DEGs) that are specific for Alzheimer’s disease (AD), but findings are often inconsistent or even contradictory. Evidence corroboration by combining meta-analysis and bioinformatics methods may help to resolve existing inconsistencies and contradictions. This study aimed to demonstrate a systematic workflow for evidence synthesis of transcriptomic studies using both meta-analysis and bioinformatics methods to identify potential pathogenic factors. Transcriptomic data were assessed from GEO and ArrayExpress after systematic searches. The DEGs and their dysregulation states from both DNA microarray and RNA sequencing datasets were analyzed and corroborated by meta-analysis. Statistically significant DEGs were used for enrichment analysis based on KEGG and protein–protein interaction network (PPIN) analysis based on STRING. AD-specific modules were further determined by the DIAMOnD algorithm, which identifies significant connectivity patterns between specific disease-associated proteins and non-specific proteins. Within AD-specific modules, the nodes of highest degrees (>95th percentile) were considered as potential pathogenic factors. After systematic searches of 225 datasets, extensive meta-analyses among 25 datasets (21 DNA microarray datasets and 4 RNA sequencing datasets) identified 9,298 DEGs. The dysregulated genes and pathways in AD were associated with impaired amyloid-β (Aβ) clearance. From the AD-specific module, Fyn, and EGFR were the most statistically significant and biologically relevant. This meta-analytical study suggested that the reduced Aβ clearance in AD pathogenesis was associated with the genes encoding Fyn and EGFR, which were key receptors in Aβ downstream signaling.
Potential pathogenic factors, other than well-known APP, APOE4, and PSEN, can be further identified from transcriptomics studies of differentially expressed genes (DEGs) that are specific for Alzheimer's disease (AD), but findings are often inconsistent or even contradictory. Evidence corroboration by combining meta-analysis and bioinformatics methods may help to resolve existing inconsistencies and contradictions. This study aimed to demonstrate a systematic workflow for evidence synthesis of transcriptomic studies using both meta-analysis and bioinformatics methods to identify potential pathogenic factors. Transcriptomic data were assessed from GEO and ArrayExpress after systematic searches. The DEGs and their dysregulation states from both DNA microarray and RNA sequencing datasets were analyzed and corroborated by meta-analysis. Statistically significant DEGs were used for enrichment analysis based on KEGG and protein-protein interaction network (PPIN) analysis based on STRING. AD-specific modules were further determined by the DIAMOnD algorithm, which identifies significant connectivity patterns between specific disease-associated proteins and non-specific proteins. Within AD-specific modules, the nodes of highest degrees (>95th percentile) were considered as potential pathogenic factors. After systematic searches of 225 datasets, extensive meta-analyses among 25 datasets (21 DNA microarray datasets and 4 RNA sequencing datasets) identified 9,298 DEGs. The dysregulated genes and pathways in AD were associated with impaired amyloid-β (Aβ) clearance. From the AD-specific module, Fyn, and EGFR were the most statistically significant and biologically relevant. This meta-analytical study suggested that the reduced Aβ clearance in AD pathogenesis was associated with the genes encoding Fyn and EGFR, which were key receptors in Aβ downstream signaling.Potential pathogenic factors, other than well-known APP, APOE4, and PSEN, can be further identified from transcriptomics studies of differentially expressed genes (DEGs) that are specific for Alzheimer's disease (AD), but findings are often inconsistent or even contradictory. Evidence corroboration by combining meta-analysis and bioinformatics methods may help to resolve existing inconsistencies and contradictions. This study aimed to demonstrate a systematic workflow for evidence synthesis of transcriptomic studies using both meta-analysis and bioinformatics methods to identify potential pathogenic factors. Transcriptomic data were assessed from GEO and ArrayExpress after systematic searches. The DEGs and their dysregulation states from both DNA microarray and RNA sequencing datasets were analyzed and corroborated by meta-analysis. Statistically significant DEGs were used for enrichment analysis based on KEGG and protein-protein interaction network (PPIN) analysis based on STRING. AD-specific modules were further determined by the DIAMOnD algorithm, which identifies significant connectivity patterns between specific disease-associated proteins and non-specific proteins. Within AD-specific modules, the nodes of highest degrees (>95th percentile) were considered as potential pathogenic factors. After systematic searches of 225 datasets, extensive meta-analyses among 25 datasets (21 DNA microarray datasets and 4 RNA sequencing datasets) identified 9,298 DEGs. The dysregulated genes and pathways in AD were associated with impaired amyloid-β (Aβ) clearance. From the AD-specific module, Fyn, and EGFR were the most statistically significant and biologically relevant. This meta-analytical study suggested that the reduced Aβ clearance in AD pathogenesis was associated with the genes encoding Fyn and EGFR, which were key receptors in Aβ downstream signaling.
Abstract Potential pathogenic factors, other than well-known APP, APOE4 and PSEN, can be further identified from transcriptomics studies of differentially expressed genes (DEGs) that are specific for Alzheimer’s disease (AD), but findings are often inconsistent or even contradictory. Evidence corroboration by combining meta-analysis and bioinformatics methods may help to resolve existing inconsistencies and contradictions. This study aimed to demonstrate a systematic workflow for evidence synthesis of transcriptomic studies using both meta-analysis and bioinformatics methods to identify potential pathogenic factors. Transcriptomic data were assessed from GEO and ArrayExpress after systematic searches. The DEGs and their dysregulation states from both DNA microarray and RNA sequencing datasets were analyzed and corroborated by meta-analysis. Statistically significant DEGs were used for enrichment analysis based on KEGG and protein–protein interaction network (PPIN) analysis based on STRING. AD-specific modules were further determined by the DIAMOnD algorithm, which identifies significant connectivity patterns between specific disease-associated proteins and non-specific proteins. Within AD-specific modules, the nodes of highest degrees (> 95th percentile) were considered as potential pathogenic factors. After systematic searches of 225 datasets, extensive meta-analyses among 25 datasets (21 DNA microarray datasets and 4 RNA sequencing datasets) identified 9,298 DEGs. The dysregulated genes and pathways in AD were associated with impaired amyloid-β (Aβ) clearance. From the AD-specific module, Fyn and EGFR were the most statistically significant and biologically relevant. This meta-analytical study suggested that the reduced Aβ clearance in AD pathogenesis was associated with the genes encoding Fyn and EGFR, which were key receptors in Aβ downstream signaling.
Author Leung, Siu-wai
Zhu, Hongmei
Yuen, Sze Chung
AuthorAffiliation 2 School of Informatics, College of Science and Engineering, University of Edinburgh , Edinburgh , United Kingdom
1 State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau , Macao , China
AuthorAffiliation_xml – name: 1 State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau , Macao , China
– name: 2 School of Informatics, College of Science and Engineering, University of Edinburgh , Edinburgh , United Kingdom
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  givenname: Hongmei
  surname: Zhu
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– sequence: 3
  givenname: Siu-wai
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  fullname: Leung, Siu-wai
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Keywords meta-analysis
microarray analysis
Alzheimer’s disease
RNA sequence analysis
bioinformatics
Language English
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Edited by: Woon-Man Kung, Chinese Culture University, Taiwan
This article was submitted to Neurodegeneration, a section of the journal Frontiers in Neuroscience
Reviewed by: Chung-Feng Kao, National Chung Hsing University, Taiwan; Judith Potashkin, Rosalind Franklin University of Medicine and Science, United States
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crossref_primary_10_3389_fnins_2020_00209
PublicationCentury 2000
PublicationDate 2020-03-13
PublicationDateYYYYMMDD 2020-03-13
PublicationDate_xml – month: 03
  year: 2020
  text: 2020-03-13
  day: 13
PublicationDecade 2020
PublicationPlace Switzerland
PublicationPlace_xml – name: Switzerland
– name: Lausanne
PublicationTitle Frontiers in neuroscience
PublicationTitleAlternate Front Neurosci
PublicationYear 2020
Publisher Frontiers Research Foundation
Frontiers Media S.A
Publisher_xml – name: Frontiers Research Foundation
– name: Frontiers Media S.A
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Snippet Potential pathogenic factors, other than well-known , , and , can be further identified from transcriptomics studies of differentially expressed genes (DEGs)...
Abstract Potential pathogenic factors, other than well-known APP, APOE4 and PSEN, can be further identified from transcriptomics studies of differentially...
Potential pathogenic factors, other than well-known APP, APOE4, and PSEN, can be further identified from transcriptomics studies of differentially expressed...
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SubjectTerms Algorithms
Alzheimer's disease
Amyloid
Bioinformatics
Brain
Datasets
Dementia
Deoxyribonucleic acid
DNA
DNA microarrays
DNA sequencing
Drugs
Epidermal growth factor receptors
Fyn protein
Gene expression
Homeostasis
Hypotheses
Kinases
Meta-analysis
microarray analysis
Neurodegenerative diseases
Neuroscience
Neurotoxicity
Phosphorylation
Proteins
Ribonucleic acid
RNA
RNA sequence analysis
Statistical analysis
Studies
Transcriptomics
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Title A Systematic Bioinformatics Workflow With Meta-Analytics Identified Potential Pathogenic Factors of Alzheimer’s Disease
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