Immunological subtypes of depression: insights from monocyte gene expression III
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE147584 | GEO | 2020/03/27
REPOSITORIES: GEO
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Project description:32 genes of a previously established inflammation-related gene signature were assessed in 197 patients with MDD and 151 controls collected during the EU-MOODINFLAME project. Monocyte gene expression data were related to age, gender, BMI, depression severity, Childhood Adversity (CA), and Suicide Risk (SR) data studycenter 1
2020-03-27 | GSE147582 | GEO
Project description:32 genes of a previously established inflammation-related gene signature were assessed in 197 patients with MDD and 151 controls collected during the EU-MOODINFLAME project. Monocyte gene expression data were related to age, gender, BMI, depression severity, Childhood Adversity (CA), and Suicide Risk (SR) data studycenter 2
2020-03-27 | GSE147583 | 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:Brain gene expression profiling studies of suicide and depression using oligonucleotide microarrays have often failed to distinguish these two phenotypes. Moreover, next generation sequencing approaches are more accurate in quantifying gene expression and can detect alternative splicing. Using RNA-seq, we examined whole-exome gene and exon expression in non-psychiatric controls (CON, N=29), DSM-IV major depressive disorder suicides (MDD-S, N=21) and MDD non-suicides (MDD, N=9) in the dorsal lateral prefrontal cortex (Brodmann Area 9) of sudden death medication-free individuals post mortem. Using small RNA-seq, we also examined miRNA expression (nine samples per group). DeSeq2 identified 35 genes differentially expressed between groups and surviving adjustment for false discovery rate (adjusted P<0.1). In depression, altered genes include humanin-like-8 (MTRNRL8), interleukin-8 (IL8), and serpin peptidase inhibitor, clade H (SERPINH1) and chemokine ligand 4 (CCL4), while exploratory gene ontology (GO) analyses revealed lower expression of immune-related pathways such as chemokine receptor activity, chemotaxis and cytokine biosynthesis, and angiogenesis and vascular development in (adjusted P<0.1). Hypothesis-driven GO analysis suggests lower expression of genes involved in oligodendrocyte differentiation, regulation of glutamatergic neurotransmission, and oxytocin receptor expression in both suicide and depression, and provisional evidence for altered DNA-dependent ATPase expression in suicide only. DEXSEq analysis identified differential exon usage in ATPase, class II, type 9B (adjusted P<0.1) in depression. Differences in miRNA expression or structural gene variants were not detected. Results lend further support for models in which deficits in microglial, endothelial (blood-brain barrier), ATPase activity and astrocytic cell functions contribute to MDD and suicide, and identify putative pathways and mechanisms for further study in these disorder
2017-07-18 | GSE101521 | GEO
Project description:We performed high-throughput snATAC-seq using the 10X Genomics Chromium platform on archived post-mortem dorsolateral prefrontal cortex (BA9) tissue in MDD subjects who died by suicide and neurotypical control subjects to identify cell-type specific differentially accessible chromatin regions. We further combined snATAC-seq with previously generated snRNA-seq data from the same subjects to generate high-resolution multi-modal accessibility and expression atlas of cortical cells. This identified accessible chromatin regions potentially regulating expression of genes. Further, MDD-associated genetic risk variants were examined for their allele-specific effects on chromatin accessibility and transcription factors binding sites in cell type speciifc manner, elucdiating target risk genes and pathways associated with MDD.
2025-01-21 | GSE246443 | GEO
Project description:Here we identified a set of genes with frequent expression changes in the postmortem brain of MDD subjectsand show that this gene set is genetically related to brain and organ illnesses frequently associated with MDD. Specifically, we performed a meta-analysis of eight gene array studies in three corticolimbic brain regions and identified ~450 genes frequentlyderegulated in MDD (n=103 subjects, 50.5%MDD). These âMetaA-MDDâ genes includepreviously-implicated neuroplasticity- and stress-related genes (CRH, BDNF, VGF), encompass multiple synaptic and signaling pathways, and suggests complex changes in cell structure and function. MetaA-MDD genes display low connectivity andhubnessin coexpression networks andare evenly distributed throughout the genome. However, MetaA-MDD genesare significantly over-represented in gene sets identified by the genome-wide association studies for brain disorders and organ diseases sharing clinical co-morbidity with MDD (e.g., cardiovascular, metabolic syndrome), but not for other diseases or body functions. Together, this study describes a robustmolecular characterization of altered brain function in MDD, and provides evidence for a shared genetic structure linking MDD andrelated illnesses, together biologically defining abroader dimensional definition ofa depressive-like syndrome. 14 pairs of human postmotem AMY samples of MDD patients and control
2016-07-03 | E-GEOD-44593 | biostudies-arrayexpress
Project description:Here we identified a set of genes with frequent expression changes in the postmortem brain of MDD subjectsand show that this gene set is genetically related to brain and organ illnesses frequently associated with MDD. Specifically, we performed a meta-analysis of eight gene array studies in three corticolimbic brain regions and identified ~450 genes frequentlyderegulated in MDD (n=103 subjects, 50.5%MDD). These “MetaA-MDD” genes includepreviously-implicated neuroplasticity- and stress-related genes (CRH, BDNF, VGF), encompass multiple synaptic and signaling pathways, and suggests complex changes in cell structure and function. MetaA-MDD genes display low connectivity andhubnessin coexpression networks andare evenly distributed throughout the genome. However, MetaA-MDD genesare significantly over-represented in gene sets identified by the genome-wide association studies for brain disorders and organ diseases sharing clinical co-morbidity with MDD (e.g., cardiovascular, metabolic syndrome), but not for other diseases or body functions. Together, this study describes a robustmolecular characterization of altered brain function in MDD, and provides evidence for a shared genetic structure linking MDD andrelated illnesses, together biologically defining abroader dimensional definition ofa depressive-like syndrome.
2016-01-01 | GSE44593 | GEO
Project description:We performed high-throughput snRNA-seq using the 10X Genomics Chromium platform on archived post-mortem dorsolateral prefrontal cortex (BA9) tissue in female MDD subjects who died by suicide and in female control subjects to identify cell-type specific differentially expressed genes. We further re-processed in parallel a previously generated snRNA-seq dataset in males with or without MDD to generate comparable differential expression results and compare the cell-type specific MDD-associated differences between the sexes.
2023-04-24 | GSE213982 | GEO
Project description:Major depressive disorder (MDD) is a clinically defined entity with little understanding as to the underlying pathological substrate. Biologically, MDD is characterized by disruption of neurotransmitters, especially serotonin and noradrenaline, which are the main targets of antidepressants. We previously demonstrated significant reduction of glial cell number in the cingulate and dorsolateral prefrontal cortical regions. Unfortunately, individuals living with HIV still have very high rates of MDD, despite the fact that mortality rates have fallen sharply with effective antiretroviral treatment. It is possible that in this treatment era, living with chronic HIV infection may result in long-term neuropathological changes that predispose to MDD. For example, it is known that HIV is associated with a range of inflammatory pathologies, neuronal loss, and dendrite-synaptic damage. In HIV, these neurodegenerative changes have been linked to neurocognitive impairments, however it is also possible that these changes potentiate MDD. In the current study, we sought to determine whether there are changes in gene expression in the MDD brain in the frontal cortex in HIV-context. We identify a large number of genes dysregulated at p<0.05 significance. Retrospective gene expression analysis of autopsy brain tissue. Four HIV/MDD subjects are identified and age-matched HIV patients without neuropsychiatric conditions are compared as controls.
2010-02-01 | E-GEOD-17440 | biostudies-arrayexpress