Blood DNA methylation profiles from schizophrenia cases and controls
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE147221 | GEO | 2020/12/31
REPOSITORIES: GEO
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Project description:Genome-wide patterns of DNA methylation were quantified using the Illumina Infinium HumanMethylation450K BeadChip (“450K array”) in DNA samples isolated from blood for schizophrenia cases, first episode psychosis patients and controls. These samples were profiled as part of a wider study where they were meta-analysed with other cohorts.
2021-04-07 | GSE152027 | GEO
Project description:Genome-wide patterns of DNA methylation were quantified using the Illumina Infinium HumanMethylationEPIC BeadChip (“EPIC array”) in DNA samples isolated from blood for schizophrenia cases, first episode psychosis patients and controls. These samples were profiled as part of a wider study where they were meta-analysed with other cohorts.
2021-04-07 | GSE152026 | GEO
Project description:Microarray methylation (Infinium® HumanMethylation450 BeadChip from Illumina) was performed on gingival tissue samples from 11 periodontitis cases and 12 age-matched healthy individuals. Bisulphite converted DNA from the 23 samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchip
2015-07-01 | E-GEOD-53849 | biostudies-arrayexpress
Project description:Genome wide DNA methylation profiling of 65 congenital imprinting disorder samples, 45 BWS and 22 SRS. The Illumina Infinium HumanMethylation450 BeadChips was used to obtain DNA methylation profiles across approximately 485,000 CpGs in blood samples.
2021-05-01 | GSE166531 | GEO
Project description:Background: Schizophrenia is a severe, highly heritable, neuropsychiatric disorder characterized by episodic psychosis and altered cognitive function. Despite success in identifying genetic variants associated with schizophrenia, there remains uncertainty about the causal genes involved in disease pathogenesis and how their function is regulated. Insights into the functional complexity of the genome have focussed attention on the role of non-sequence-based genomic variation in health and disease. Although a better understanding of the molecular mechanisms underlying disease phenotypes is best achieved using an integrated functional genomics strategy, few studies have attempted to systematically integrate genetic and epigenetic epidemiological approaches. Results: We performed a multi-stage epigenome-wide association study (EWAS), quantifying genome-wide patterns of DNA methylation in a total of 1,801 individuals from three independent sample cohorts. We identified multiple differentially methylated positions (DMPs) and region (DMRs) associated with schizophrenia, independently of important confounders such as smoking, with consistent effects across the three independent cohorts. We also show that polygenic burden for schizophrenia is associated with epigenetic variation at multiple loci across the genome, independently of loci implicated in the analysis of diagnosed schizophrenia. Finally, we show how DNA methylation quantitative trait loci (mQTL) analyses can be used to annotate the extended genomic regions nominated by genetic studies of schizophrenia, with Bayesian co-localization analyses highlighting potential regulatory variation causally involved in disease. Conclusion: This study represents the first systematic integrated analysis of genetic and epigenetic variation in schizophrenia, introducing a methodological pipeline that can be used to inform EWAS analyses of other complex traits and diseases. We demonstrate the utility of using polygenic risk score (PRS) for identifying molecular variation associated with etiological variation, and mQTLs for refining the functional/regulatory variation associated with schizophrenia risk variants. Finally, we present strong evidence for the co-localization of genetic associations for schizophrenia and differential DNA methylation. 675 whole blood derived DNA samples (353 schizophrenia cases and 322 controls) representing phase 1 of our meta-analysis. Bisulfite converted DNA from these samples were hybridized to the Illumina Infinium 450k Human Methylation Beadchip v1.0.
2016-08-01 | E-GEOD-80417 | biostudies-arrayexpress
Project description:Genome wide DNA methylation profiling of normal and preeclampsia placental samples. Illumina Infinium HumanMethylation450 BeadChip (450K array) was used to obtain DNA methylation profiles in placental samples. Samples included 16 samples from healthy uncomplicated pregnancies and 8 samples from pregnancies affected by preeclampsia.
2016-04-12 | GSE75196 | GEO
Project description:Abstract Background: Schizophrenia is a severe, highly heritable, neuropsychiatric disorder characterized by episodic psychosis and altered cognitive function. Despite success in identifying genetic variants associated with schizophrenia, there remains uncertainty about the causal genes involved in disease pathogenesis and how their function is regulated. Insights into the functional complexity of the genome have focussed attention on the role of non-sequence-based genomic variation in health and disease. Although a better understanding of the molecular mechanisms underlying disease phenotypes is best achieved using an integrated functional genomics strategy, few studies have attempted to systematically integrate genetic and epigenetic epidemiological approaches. Results: We performed a multi-stage epigenome-wide association study (EWAS), quantifying genome-wide patterns of DNA methylation in a total of 1,801 individuals from three independent sample cohorts. We identified multiple differentially methylated positions (DMPs) and region (DMRs) associated with schizophrenia, independently of important confounders such as smoking, with consistent effects across the three independent cohorts. We also show that polygenic burden for schizophrenia is associated with epigenetic variation at multiple loci across the genome, independently of loci implicated in the analysis of diagnosed schizophrenia. Finally, we show how DNA methylation quantitative trait loci (mQTL) analyses can be used to annotate the extended genomic regions nominated by genetic studies of schizophrenia, with Bayesian co-localization analyses highlighting potential regulatory variation causally involved in disease. Conclusion: This study represents the first systematic integrated analysis of genetic and epigenetic variation in schizophrenia, introducing a methodological pipeline that can be used to inform EWAS analyses of other complex traits and diseases. We demonstrate the utility of using polygenic risk score (PRS) for identifying molecular variation associated with etiological variation, and mQTLs for refining the functional/regulatory variation associated with schizophrenia risk variants. Finally, we present strong evidence for the co-localization of genetic associations for schizophrenia and differential DNA methylation. 847 whole blood derived DNA samples (414 schizophrenia cases and 433 controls) representing phase 2 of our meta-analysis. Bisulfite converted DNA from these samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchip v1.0.
2016-08-01 | E-GEOD-84727 | biostudies-arrayexpress
Project description:Genome-wide patterns of DNA methylation were quantified using the Illumina Infinium HumanMethylation450 BeadChip (“450K array”) in DNA samples isolated from whole blood collected at age 18 from members of the Environmental Risk (E-Risk) Longitudinal Twin Study.
2018-01-15 | GSE105018 | GEO
Project description:We used the Illumina 450KMethylation BeadChip to measure DNA methylation at 485,512 loci across the genome for 40 postmortem brain samples. The purpose of our study was to identify differentially methylated regions (DMRs) associated with autism. Samples included 16 temporal cortex brain tissue samples (6 cases and 10 controls), 11 prefrontal cortex brain tissue samples (6 cases and 5 controls), and 13 cerebellum brain tissue samples (7 cases and 6 controls). We bisulfute converted DNA from the 40 brain tissue samples, processed, and hybridized them to the Illumina Infinium 450K HumanMethylation450 BeadChip as specificed by the manufacturer.
2013-12-12 | E-GEOD-53162 | biostudies-arrayexpress
Project description:Background: Schizophrenia is a severe neuropsychiatric disorder that is hypothesized to result from disturbances in early brain development, and there is mounting evidence to support a role for developmentally-regulated epigenetic variation in the molecular etiology of the disorder. Here, we describe a systematic study of schizophrenia-associated methylomic variation in the adult brain and its relationship to changes in DNA methylation across human fetal brain development. Results: We profile methylomic variation in matched prefrontal cortex and cerebellum brain tissue from schizophrenia patients and controls, identifying disease-associated differential DNA methylation at multiple loci, particularly in the prefrontal cortex, and confirming these differences in an independent set of adult brain samples. Our data reveal discrete modules of co-methylated loci associated with schizophrenia that are enriched for genes involved in neurodevelopmental processes and include loci implicated by genetic studies of the disorder. Methylomic data from human fetal cortex samples, spanning 23 to 184 days post-conception, indicates that disease-associated differentially methylated positions are significantly enriched for loci at which DNA methylation is dynamically altered during human fetal brain development. Conclusions: Our data support the hypothesis that schizophrenia has an important early neurodevelopmental component, and suggest that epigenetic mechanisms may mediate these effects. 33 post-mortem brain (prefrontal cortex) samples (18 schizophrenia cases and 15 controls) were obtained from Douglas Bell-Canada Brain Bank (DBCBB), Montreal, Canada. Bisulfite converted DNA from these samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchip v1.0.
2014-09-13 | E-GEOD-61380 | biostudies-arrayexpress