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Depression is currently the leading cause of disability around the world. We conducted an epigenome-wide association study (EWAS) in a sample of 58 depression score-discordant monozygotic twin pairs, aiming to detect specific epigenetic variants potentially related to depression and further integrate with gene expression profile data. Association between the methylation level of each CpG site and depression score was tested by applying a linear mixed effect model. Weighted gene co-expression network analysis (WGCNA) was performed for gene expression data. The association of DNA methylation levels of 66 CpG sites with depression score reached the level of  P  < 1 × 10 −4 . These top CpG sites were located at 34 genes, especially  PTPRN2 ,  HES5 ,  GATA2 ,  PRDM7 , and  KCNIP1 . Many ontology enrichments were highlighted, including Notch signaling pathway, Huntington disease, p53 pathway by glucose deprivation, hedgehog signaling pathway, DNA binding, and nucleic acid metabolic process. We detected 19 differentially methylated regions (DMRs), some of which were located at  GRIK2 ,  DGKA , and  NIPA2 . While integrating with gene expression data,  HELZ2 ,  PTPRN2 ,  GATA2 , and  ZNF624  were differentially expressed. In WGCNA, one specific module was positively correlated with depression score ( r  = 0.62,  P  = 0.002). Some common genes (including  BMP2 ,  PRDM7 ,  KCNIP1 , and  GRIK2 ) and enrichment terms (including complement and coagulation cascades pathway, DNA binding, neuron fate specification, glial cell differentiation, and thyroid gland development) were both identified in methylation analysis and WGCNA. Our study identifies specific epigenetic variations which are significantly involved in regions, functional genes, biological function, and pathways that mediate depression disorder.

Genome-wide DNA methylation and gene expression analyses in monozygotic twins identify potential biomarkers of depression