{"title":"Screening of Crucial Differentially-Methylated/Expressed Genes for Alzheimer's Disease.","authors":"Haiyuan Qiu, Qiuyan Weng","doi":"10.1177/15333175221116220","DOIUrl":null,"url":null,"abstract":"<p><p><b>Background:</b> We aimed to make an integrated analysis of published transcriptome and DNA methylation dataset to ascertain the key differentially methylated and differentially expressed genes for Alzherimer's disease (AD). <b>Methods:</b> Two gene expression microarrays and 1 gene methylation microarray were downloaded for identification of differentially expressed genes and differentially methylated genes. Then, we used various biological information databases to annotate the functions of the differentially-methylated/expressed genes, and screen out key genes and important signaling pathways. Finally, we validate the differentially-methylated/expressed genes in the additional online datasets and in blood from AD patients.<b>Results:</b> A total of 8 hub hypomethylated-high expression genes were obtained, including Rac family small GTPase 2, FGR proto-oncogene, Src family tyrosine kinase, LYN proto-oncogene, Src family tyrosine kinase, protein kinase C delta, myosin IF, integrin subunit alpha 5, semaphorin 4D, and growth arrest specific protein 7. Some enriched signaling pathways of hypomethylated-high expression genes were identified, including regulation of actin cytoskeleton, chemokine signaling pathway, Fc gamma R-mediated phagocytosis, and axon guidance. <b>Conclusion:</b> Differentially-methylated/expressed genes are likely to be associated with AD.</p>","PeriodicalId":50816,"journal":{"name":"American Journal of Alzheimers Disease and Other Dementias","volume":null,"pages":null},"PeriodicalIF":2.7000,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10624077/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"American Journal of Alzheimers Disease and Other Dementias","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1177/15333175221116220","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background: We aimed to make an integrated analysis of published transcriptome and DNA methylation dataset to ascertain the key differentially methylated and differentially expressed genes for Alzherimer's disease (AD). Methods: Two gene expression microarrays and 1 gene methylation microarray were downloaded for identification of differentially expressed genes and differentially methylated genes. Then, we used various biological information databases to annotate the functions of the differentially-methylated/expressed genes, and screen out key genes and important signaling pathways. Finally, we validate the differentially-methylated/expressed genes in the additional online datasets and in blood from AD patients.Results: A total of 8 hub hypomethylated-high expression genes were obtained, including Rac family small GTPase 2, FGR proto-oncogene, Src family tyrosine kinase, LYN proto-oncogene, Src family tyrosine kinase, protein kinase C delta, myosin IF, integrin subunit alpha 5, semaphorin 4D, and growth arrest specific protein 7. Some enriched signaling pathways of hypomethylated-high expression genes were identified, including regulation of actin cytoskeleton, chemokine signaling pathway, Fc gamma R-mediated phagocytosis, and axon guidance. Conclusion: Differentially-methylated/expressed genes are likely to be associated with AD.
期刊介绍:
American Journal of Alzheimer''s Disease and other Dementias® (AJADD) is for professionals on the frontlines of Alzheimer''s care, dementia, and clinical depression--especially physicians, nurses, psychiatrists, administrators, and other healthcare specialists who manage patients with dementias and their families. This journal is a member of the Committee on Publication Ethics (COPE).