Genome Wide DNA Methylation in the Neuronal Fraction of the Prefrontal Cortex from Depressed, Suicide, and Normal Control Subjects
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA659746 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We analyzed the levels of DNA methylation in DNA purified from BA9 of 21 depressed suicide completers and 21 healthy controls, using the Infinium® MethylationEPICBeadChip. The goal of the study was to determine which genes were differentially methylated in neurons between the two groups. We identified1,236 differentially methylated CpGs with a p ≤ 0.001. Gene Ontology and Ingenuity Pathway Analysis were performed to determine classes of genes and pathways associated with the suicide completers.
2022-08-26 | GSE156996 | GEO
Project description:A total of 36 postmortem brain samples (23 suicide completers, 13 control sudden death) were collected. We evaluated the proteome profile in the prefrontal cortex (Brodmann area 9, 10) with TMT-based quantification using LC-MS/MS. Several bioinformatics tools were used to elucidate biological mechanisms related to suicide. Subgroup analysis was conducted to find common differentially expressed proteins (DEPs) among various clinically different groups. Among the 9801 proteins identified in our dataset, 295 proteins were differentially expressed between suicide completers and sudden death subjects. Various bioinformatics analysis revealed that suicide completion is predominately enriched in synaptic functions and synaptogenesis especially in endocannabinoid and GABA signaling pathway. Our finding presents the largest protein pools related to suicide completion, and suggests that newly emerging neurotransmitter systems such as endocannabinoid system and synaptogenesis processes may have an impact upon the biological cascade leading to suicide.
2022-05-20 | PXD029845 | Pride
Project description:We compared the gene expression profile in the dorsolateral prefrontal area of subjects with dual diagnosis who died by suicide to the transcriptome of subjects with mood disorders and subjects with substance use disorder who died by suicide.
2019-12-02 | GSE125681 | GEO
Project description:Background: Major Depressive Disorder (MDD) represents a major social and economic health issue and constitutes a major risk factor for MDD suicide. The molecular pathology of suicidal depression remains poorly understood, although it has been hypothesized that regulatory genomic processes are involved in the pathology of both MDD and suicidality. Methods: Genome-wide patterns of DNA methylation were assessed in depressed MDD suicide completers (n=20) and compared to non-psychiatric, sudden-death controls (n=20) using tissue from two cortical brain regions (Brodmann Area 11 (BA11) and Brodmann Area 25 (BA25)). Analyses focussed on identifying differentially methylated regions (DMRs) associated with suicidal depression, and epigenetic variation was explored in the context of polygenic risk scores for major depression and MDD suicide. Weighted gene co-methylation network analysis was used to identify modules of co-methylated loci associated with depressed MDD suicide completers and polygenic burden for MDD and MDD suicide attempt. Results: We identified a DMR upstream of the PSORS1C3 gene, subsequently validated using bisulfite-pyrosequencing and replicated in a second set of MDD suicide samples, which is characterized by significant hypomethylation in both cortical brain regions in MDD MDD suicide cases. We also identified discrete modules of co-methylated loci associated with polygenic risk burden for MDD suicide attempt, but not major depression. MDD suicide-associated co-methylation modules were enriched among gene networks implicating biological processes relevant to depression and suicidality, including nervous system development and mitochondria function. Conclusions: Our data suggest there are coordinated changes in DNA methylation associated with MDD suicide that may offer novel insights into the molecular pathology associated with depressed MDD suicide completers.
2016-11-01 | GSE88890 | GEO
Project description:Epigenome analysis of depressed and control subjects.
| PRJNA515256 | ENA
Project description:Genome wide DNA methylation profiling of depressed (n=489) and control subjects (n=210) that were recruited at the Max Planck Institute of Psychiatry (MPIP). The Illumina Infinium 450k Human DNA methylation Beadchip was used to obtain DNA methylation profiles based whole blood samples.
2019-01-16 | GSE125105 | GEO
Project description:BackgroundRecent studies suggest that alterations in expression of genes, including those which regulate neural and structural plasticity, may be crucial in the pathogenesis of depression. MicroRNAs (miRNAs) are newly discovered regulators of gene expression that have recently been implicated in a variety of human diseases, including neuropsychiatric diseases.Methodology/principal findingsThe present study was undertaken to examine whether the miRNA network is altered in the brain of depressed suicide subjects. Expression of miRNAs was measured in prefrontal cortex (Brodmann Area 9) of antidepressant-free depressed suicide (n = 18) and well-matched non-psychiatric control subjects (n = 17) using multiplex RT-PCR plates. We found that overall miRNA expression was significantly and globally down-regulated in prefrontal cortex of depressed suicide subjects. Using individual tests of statistical significance, 21 miRNAs were significantly decreased at p = 0.05 or better. Many of the down-regulated miRNAs were encoded at nearby chromosomal loci, shared motifs within the 5'-seeds, and shared putative mRNA targets, several of which have been implicated in depression. In addition, a set of 29 miRNAs, whose expression was not pairwise correlated in the normal controls, showed a high degree of co-regulation across individuals in the depressed suicide group.Conclusions/significanceThe findings show widespread changes in miRNA expression that are likely to participate in pathogenesis of major depression and/or suicide. Further studies are needed to identify whether the miRNA changes lead to altered expression of prefrontal cortex mRNAs, either directly (by acting as miRNA targets) or indirectly (e.g., by affecting transcription factors).
| S-EPMC3302855 | biostudies-literature
Project description:Genome wide DNA methylation profiling of depressed (n=324) and control subjects (n=209) that were recruited at the Max Planck Institute of Psychiatry (MPIP). The Illumina Infinium 450k Human DNA methylation Beadchip was used to obtain DNA methylation profiles based whole blood samples.
2019-03-14 | GSE128235 | GEO
Project description:Analysis of gene-expression changes in depressed subjects with bipolar disorder compared to healthy controls. Results provide information on pathways that may be involved in the pathogenesis of bipolar depression. Total RNA isolated from PAXgene blood RNA tubes from 20 depressed subjects with bipolar disorder and 15 healthy controls.
2010-08-27 | E-GEOD-23848 | biostudies-arrayexpress
Project description:Abnormalities of neuroinflammation have been implicated in the pathogenesis of depression and suicide. This is primarily based on the observation that cytokines, which are major inflammatory molecules and play an important role in depression and suicide, are increased in both serum and in postmortem brain of depressed and suicidal subjects. Another class of immune mediators are chemokines which are primarily involved in chemotactic properties and trafficking of immune cells in the central nervous system (CNS). Chemokines also play an important role in CNS function. Whereas chemokines have been studied in the serum of depressed and suicidal patients, their role in brain of depressed or suicidal subjects is relatively unexplored. We studied the gene expression of several chemokines in the prefrontal cortex (PFC) obtained from depressed suicidal (DS) and normal control (NC) subjects. We determined the mRNA expression of several chemokines belonging to CXCL and CCL groups of chemokines using qPCR array technique and qPCR gene expression validation in 24 DS and 24 NC subjects. The postmortem brain samples were obtained from the Maryland Brain Collection. We found that the mRNA expression of chemokines CXCL1, CXCL2, CXCL3 and CCL2 was significantly decreased in the PFC of DS compared with NC subjects. No significant change was observed in CXCL5, CXCL6, CXCL10, CCL8 and CCL19 between DS and NC subjects. Since many of the chemokines are involved in mediating certain important CNS functions, such as neurotrophic effect, neurogenesis, anti-apoptotic growth factor release, modulation of synaptic transmission, brain development and neuronal loss, decreased levels of chemokines can reduce these functions which may be involved in the pathophysiology of depression.
| S-EPMC8231709 | biostudies-literature