LncRNA and mRNA expression data in peripheral blood sampled from patients with Obsessive-Compulsive Disorder
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE78104 | GEO | 2018/08/30
REPOSITORIES: GEO
Similar Datasets
Project description:Neurogenetics of Obsessive-Compulsive Disorder
| PRJNA588485 | ENA
Project description:Neurogenetics of Obsessive-Compulsive Disorder
| PRJNA588486 | ENA
Project description:Anorexia nervosa (AN), bulimia nervosa (BN), and obsessive-compulsive disorder (OCD) are complex psychiatric disorders with shared obsessive features, thought to arise from the interaction of multiple genes of small effect with environmental factors. Potential candidate genes for AN, BN, and OCD have been identified through clinical association and neuroimaging studies; however, recent genome-wide association studies of eating disorders (ED) so far have failed to report significant findings. Additionally, few if any studies have interrogated postmortem brain tissue for evidence of eQTLs associated with candidate genes, which has particular promise as an approach to elucidating molecular mechanisms of association. We therefore selected single nucleotide polymorphisms (SNPs) based on candidate gene studies for AN, BN, and OCD from the literature, and examined the association of these SNPs with gene expression across the lifespan in prefrontal cortex of a non-psychiatric control cohort (N=268). Several risk-predisposing SNPs were significantly associated with gene expression among control subjects. We then measured gene expression in the prefrontal cortex of cases previously diagnosed with obsessive psychiatric disorders, e.g., eating disorders (ED; N=15), and obsessive-compulsive disorder/obsessive-compulsive personality disorder or tics (OCD/OCPD/Tic; N=16), and non-psychiatric controls (N=102) and identified 6 and 286 genes that were differentially expressed between ED compared to controls and OCD cases compared to controls, respectively (FDR < 5%). However, none of the clinical risk SNPs were among the eQTLs and none were significantly associated with gene expression within the broad obsessive cohort, suggesting larger sample sizes or other brain regions may be required to identify candidate molecular mechanisms of clinical association in postmortem brain datasets. Gene expression data from the dorsolateral prefrontal cortex (DLPFC) from postmortem tissue on 133 subjects - 15 eating disorder (ED) patients, 16 obessive compulsive disorder (OCD) patients, and 102 non-psychiatric controls - run on the Illumina HumanHT-12 v3 microarray
2014-08-08 | E-GEOD-60190 | biostudies-arrayexpress
Project description:Background: Obsessive-compulsive disorder (OCD) is characterized by intrusive thoughts and repetitive actions, that presents the involvement of the cortico-striatal areas. The contribution of environmental risk factors to OCD development suggests that epigenetic mechanisms may contribute to its pathophysiology. DNA methylation changes and gene expression were evaluated in post-mortem brain tissues of the cortical (anterior cingulate gyrus and orbitofrontal cortex) and ventral striatum (nucleus accumbens, caudate nucleus and putamen) areas from eight OCD patients and eight matched controls. Results: There were no differentially methylated CpG (cytosine-phosphate-guanine) sites (DMSs) in any brain area, nevertheless gene modules generated from CpG sites and protein-protein-interaction (PPI) showed enriched gene modules for all brain areas between OCD cases and controls. All brain areas but nucleus accumbens presented a predominantly hypomethylation pattern for the differentially methylated regions (DMRs). Although there were common transcriptional factors that targeted these DMRs, their targeted differentially expressed genes were different among all brain areas. The protein-protein interaction network based on methylation and gene expression data reported that all brain areas were enriched for G-protein signaling pathway, immune response, apoptosis and synapse biological processes but each brain area also presented enrichment of specific signaling pathways. Finally, OCD patients and controls did not present significant DNA methylation age differences. Conclusions: DNA methylation changes in brain areas involved with OCD, especially those involved with genes related to synaptic plasticity and the immune system could mediate the action of genetic and environmental factors associated with OCD.
2021-10-15 | GSE148021 | GEO
Project description:Anorexia nervosa (AN), bulimia nervosa (BN), and obsessive-compulsive disorder (OCD) are complex psychiatric disorders with shared obsessive features, thought to arise from the interaction of multiple genes of small effect with environmental factors. Potential candidate genes for AN, BN, and OCD have been identified through clinical association and neuroimaging studies; however, recent genome-wide association studies of eating disorders (ED) so far have failed to report significant findings. Additionally, few if any studies have interrogated postmortem brain tissue for evidence of eQTLs associated with candidate genes, which has particular promise as an approach to elucidating molecular mechanisms of association. We therefore selected single nucleotide polymorphisms (SNPs) based on candidate gene studies for AN, BN, and OCD from the literature, and examined the association of these SNPs with gene expression across the lifespan in prefrontal cortex of a non-psychiatric control cohort (N=268). Several risk-predisposing SNPs were significantly associated with gene expression among control subjects. We then measured gene expression in the prefrontal cortex of cases previously diagnosed with obsessive psychiatric disorders, e.g., eating disorders (ED; N=15), and obsessive-compulsive disorder/obsessive-compulsive personality disorder or tics (OCD/OCPD/Tic; N=16), and non-psychiatric controls (N=102) and identified 6 and 286 genes that were differentially expressed between ED compared to controls and OCD cases compared to controls, respectively (FDR < 5%). However, none of the clinical risk SNPs were among the eQTLs and none were significantly associated with gene expression within the broad obsessive cohort, suggesting larger sample sizes or other brain regions may be required to identify candidate molecular mechanisms of clinical association in postmortem brain datasets.
2014-08-08 | GSE60190 | GEO
Project description:Brain areas involved with obsessive-compulsive disorder present different DNA methylation modulation
| PRJNA622825 | ENA
Project description:The Affymetrix CytoScan HD 2.5M and Illumina HumanOmni2.5 arrays are high resolution SNP platform for studying copy number variations in the human genome. Both platforms have widely being used in both clinical and research settings for identifying causative variants as well as interrogating the genome for benign variants. We employed both platforms to investigate the risk factor CNVs in trios diagnosed with OCD. We genotyped 307 unrelated probands (including 174 complete parent-child trios; mean age of probands 7.9±3.5 years) and compared their genotypes to those of 3,861 population controls, in order to identify rare CNVs (<0.5% frequency) of at least 15 kb in size that might contribute to OCD. We uncovered de novo CNVs and Decipher Syndromes in probands. We have identified additional potentially risk factor CNVs impacting the coding sequencing of genes involved in brain functions.
2016-12-11 | GSE76437 | GEO
Project description:The Affymetrix CytoScan HD 2.5M and Illumina HumanOmni2.5 arrays are high resolution SNP platform for studying copy number variations in the human genome. Both platforms have widely being used in both clinical and research settings for identifying causative variants as well as interrogating the genome for benign variants. We employed both platforms to investigate the risk factor CNVs in trios diagnosed with OCD. We genotyped 307 unrelated probands (including 174 complete parent-child trios; mean age of probands 7.9±3.5 years) and compared their genotypes to those of 3,861 population controls, in order to identify rare CNVs (<0.5% frequency) of at least 15 kb in size that might contribute to OCD. We uncovered de novo CNVs and Decipher Syndromes in probands. We have identified additional potentially risk factor CNVs impacting the coding sequencing of genes involved in brain functions.
2016-12-11 | GSE76436 | GEO
Project description:Obsessive-compulsive disorder (OCD), a severe mental disease manifested in time-consuming repetition of behaviors, affects 1-3% of the human population. While highly heritable, complex genetics has hampered attempts to elucidate OCD etiology. Dogs suffer from naturally occurring compulsive disorders that closely model human OCD, manifested as an excessive repetition of normal canine behaviors that only partially responds to drug therapy. The limited diversity within dog breeds makes identifying underlying genetic factors easier. We use genome wide association of 87 Doberman Pinscher cases and 63 controls to identify genomic loci associated with OCD and sequence these regions in 8 affected dogs from high-risk breeds and 8 breed-matched controls. We find 119 variants in evolutionarily conserved sites that are specific to dogs with OCD. These case-only variants are significantly more common in high OCD risk breeds compared to breeds with no known psychiatric problems. Four genes, all with synaptic function, have the most case-only variation: neuronal cadherin (CDH2), catenin alpha2 (CTNNA2), ataxin-1 (ATXN1), and plasma glutamate carboxypeptidase (PGCP). Two different case-only variants targeted the same approximately 500-bp highly conserved regulatory element between the cadherin genes CDH2 and DSC3. We functionally test these variants in a human neuroblastoma cell line and show that they cause significant changes in gene expression, likely due to disrupted transcription factor binding. This work demonstrates how we can use the unique genetics of dog breeds, and mechanistic similarities between human and dog diseases, to find genes and regulatory pathways underlying complex psychiatric disorders. Affymetrix SNP arrays were performed according to the manufacturer's directions. Genome wide association analysis was performed for 87 doberman pinshcers OCD cases and 63 breed-matched controls.
2013-12-20 | E-GEOD-53488 | biostudies-arrayexpress
Project description:In vivo chemogenetic activation of astrocytes in the striatum via an engineered Gi-protein-coupled receptor was conducted in wild-type and SAPAP3 KO OCD mice. The resultant striatal tissue was extracted, homogenized in a detergent-free buffer, digested, and analyzed with LC/MS-MS.
2023-12-19 | MSV000093698 | MassIVE