Parallel molecular alteration between Alzheimer’s disease and major depressive disorder in the human brain dorsolateral prefrontal cortex: an insight from gene expression and methylation profile analyses

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dc.contributor.authorRastad, S.
dc.contributor.authorBarjaste, N.
dc.contributor.authorLanjanian, H.
dc.contributor.authorMoeini, A.
dc.contributor.authorKiani, F.
dc.contributor.authorMasoudi-Nejad, A.
dc.date.accessioned2024-05-19T14:33:18Z
dc.date.available2024-05-19T14:33:18Z
dc.date.issued2022
dc.departmentİstinye Üniversitesien_US
dc.description.abstractAlzheimer’s disease (AD) and major depressive disorder (MDD) are comorbid neuropsychiatric disorders that are among the leading causes of long-term dis-ability worldwide. Recent research has indicated the existence of parallel molecular mechanisms between AD and MDD in the dorsolateral prefrontal cortex (DLPFC). However, the premorbid history and molecular mechanisms have not yet been well characterized. In this study, differentially expressed gene (DEG), differentially co-expressed gene and protein–protein interaction (PPI) network propagation analyses were applied to gene expression data of postmortem DLPFC samples from human individuals diagnosed with and without AD or MDD (AD: cases = 310, control = 157; MDD: cases = 75, control = 161) to identify the main genes in the two disorders’ specific and shared biological pathways. Subsequently, the results were evaluated using another four assessment datasets (n1 = 230, n2 = 65, n3 = 58, n4 = 48). Moreover, the postmortem DLPFC methylation status of human subjects with AD or MDD was compared using 68 and 608 samples for AD and MDD, respectively. Eight genes (XIST, RPS4Y1, DDX3Y, USP9Y, DDX3X, TMSB4Y, ZFY and E1FAY) were common DEGs in DLPFC of subjects with AD or MDD. These genes play important roles in the nervous system and the innate immune system. Furthermore, we found HSPG2, DAB2IP, ARHGAP22, TXNRD1, MYO10, SDK1 and KRT82 as common differentially methylated genes in the DLPFC of cases with AD or MDD. Finally, as evidence of shared molecular mechanisms behind this comorbidity, we propose some genes as candidate biomarkers for both AD and MDD. However, more research is required to clarify the molecular mechanisms underlying the co-existence of these two important neuropsychiatric disorders. © 2023 The Author(s).en_US
dc.identifier.doi10.1266/ggs.22-00022
dc.identifier.endpage324en_US
dc.identifier.issn1341-7568
dc.identifier.issue6en_US
dc.identifier.pmid36928034en_US
dc.identifier.scopus2-s2.0-85153412689en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage311en_US
dc.identifier.urihttps://doi.org/10.1266/ggs.22-00022
dc.identifier.urihttps://hdl.handle.net/20.500.12713/4179
dc.identifier.volume97en_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherGenetics Society of Japanen_US
dc.relation.ispartofGenes and Genetic Systemsen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.snmz20240519_kaen_US
dc.subjectAlzheimer's Disease (Ad)en_US
dc.subjectDiffer-Entially Co-Expressed Genesen_US
dc.subjectDifferentially Expressed Genes (Degs)en_US
dc.subjectDifferentially Methylated Genesen_US
dc.subjectMajor Depressive Disorder (Mdd)en_US
dc.titleParallel molecular alteration between Alzheimer’s disease and major depressive disorder in the human brain dorsolateral prefrontal cortex: an insight from gene expression and methylation profile analysesen_US
dc.typeArticleen_US

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