DNA Methylation signatures in Panic Disorder
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE102468 | GEO | 2018/01/10
SECONDARY ACCESSION(S): PRJNA397785
REPOSITORIES: GEO
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Project description:We used a model to induce patient-derived microglia-like cells (iMGs) to clarify the molecular characteristics and function of Panic disorder patient-iMGs (PD-iMGs). We established iMGs from 14 PD patients and 10 healthy controls (non-psychiatric controls, HC). We analyzed the phenotype of the PD-iMGs by RNA sequencing. The PD-iMGs clustered together distinct from HC-iMGs. Gene set enrichment analysis revealed the involvement of cholesterol biosynthesis and steroid metabolism in PD-iMGs.
2022-09-30 | GSE212802 | GEO
Project description:There are currently no biological tests that differentiate patients with bipolar disorder (BPD) from healthy controls. While there is evidence that peripheral gene expression differences between patients and controls can be utilized as biomarkers for psychiatric illness, it is unclear whether current use or residual effects of antipsychotic and mood stabilizer medication drives much of the differential transcription. We therefore tested whether expression changes in first-episode, never-medicated bipolar patients, can contribute to a biological classifier that is less influenced by medication and could potentially form a practicable biomarker assay for BPD. We employed microarray technology to measure global leukocyte gene expression in first-episode (n=3) and currently medicated BPD patients (n=26), and matched healthy controls (n=25). Following an initial feature selection of the microarray data, we developed a cross-validated 10-gene model that was able to correctly predict the diagnostic group of the training sample (26 medicated patients and 12 controls), with 89% sensitivity and 75% specificity (p<0.001). The 10-gene predictor was further explored via testing on an independent test cohort consisting of three pairs of monozygotic twins discordant for BPD, plus the original enrichment sample cohort (the three never-medicated BPD patients and 13 matched control subjects), and a sample of experimental replicates (n=34). 83% of the independent test sample was correctly predicted, with a sensitivity of 67% and specificity of 100% (although this result did not reach statistical significance). Additionally, 88% of sample diagnostic classes were classified correctly for both the enrichment (p=0.015) and the replicate samples (p<0.001). Peripheral blood leukocytes (PBLs) from whole blood were collected from 26 patients with bipolar disorder who had previously received medication, three patients with bipolar disorder who were experiencing their first hospitalization and had not previously received medication, and 25 matched control subjects, for RNA extraction and hybridization on Affymetrix microarrays. Immediately after blood collection, blood samples were split into two (when a sufficient volume had been collected); an "1" and replicate "2" sample (thus two separate RNA extractions, cDNA and cRNA syntheses and array hybridizations were performed).
2013-06-25 | E-GEOD-46449 | biostudies-arrayexpress
Project description:Microglia-like cells derived from patients with panic disorder
| PRJNA877345 | ENA
Project description:Transcriptional profiling in the whole blood samples of healthy controls and major depression disorder (MDD) patients who have never been treated with depression medication. Samples included 20 healthy controls and 20 MDD patients who have never been treated with depression medication. Goal was to discover the differentially expressed genes.
2022-07-18 | GSE201332 | GEO
Project description:Effects of stressful life-events on DNA methylation in panic disorder and major depressive disorder
| PRJNA828020 | ENA
Project description:Background: Panic disorder (PD) is characterized by recurrent panic attacks and higher affection of women as compare to men. The lifetime prevalence of PD is about 2-3 % in the general population leading to tremendous distress and disability. Etiologically, genetic and environmental factors, such as stress, contribute to the onset and relapse of PD. In the present study, we investigated epigenome-wide DNA methylation (DNAm) in respond to a cumulative, stress-weighted life events score (wLE) in patients with PD and its boundary to major depressive disorder (MDD), frequently co-occurring with symptoms of PD. Methods: DNAm was assessed by the Illumina HumanMethylation450 BeadChip. In a meta-analytic approach, epigenome-wide DNAm changes in association with wLE were first analyzed in two PD cohorts (with a total sample size of 183 PD patients and 85 healthy controls) and lastly in 102 patients with MDD to identify possible overlapping and opposing effects of wLE on DNAm. Additionally, analysis of differentially methylated regions (DMRs) was conducted to identify regional clusters of association. Results: Two CpG-sites presented with p-values below 1x10-05 in PD: cg09738429 (p=6.40x10-06, located in an intergenic shore region in next proximity of PYROXD1) and cg03341655 (p=8.14x10-06, located in the exonic region of GFOD2). The association of DNAm at cg03341655 and wLE could be replicated in the independent MDD case sample indicating a diagnosis independent effect. Genes mapping to the top hits were significantly upregulated in brain and top hits have been implicated in the metabolic system. Additionally, two significant DMRs were identified for PD only on chromosome 10 and 18, including CpG-sites which have been reported to be associated with anxiety and other psychiatric phenotypes. Conclusion: This first DNAm analysis in PD reveals first evidence of small but significant DNAm changes in PD in association with cumulative stress-weighted life events. Most of the top associated CpG-sites are located in genes implicated in metabolic processes supporting the hypothesis that environmental stress contributes to health damaging changes by affecting a broad spectrum of systems in the body.
2022-04-22 | GSE200954 | GEO
Project description:Background: Panic disorder (PD) is characterized by recurrent panic attacks and higher affection of women as compare to men. The lifetime prevalence of PD is about 2-3 % in the general population leading to tremendous distress and disability. Etiologically, genetic and environmental factors, such as stress, contribute to the onset and relapse of PD. In the present study, we investigated epigenome-wide DNA methylation (DNAm) in respond to a cumulative, stress-weighted life events score (wLE) in patients with PD and its boundary to major depressive disorder (MDD), frequently co-occurring with symptoms of PD. Methods: DNAm was assessed by the Illumina HumanMethylation450 BeadChip. In a meta-analytic approach, epigenome-wide DNAm changes in association with wLE were first analyzed in two PD cohorts (with a total sample size of 183 PD patients and 85 healthy controls) and lastly in 102 patients with MDD to identify possible overlapping and opposing effects of wLE on DNAm. Additionally, analysis of differentially methylated regions (DMRs) was conducted to identify regional clusters of association. Results: Two CpG-sites presented with p-values below 1x10-05 in PD: cg09738429 (p=6.40x10-06, located in an intergenic shore region in next proximity of PYROXD1) and cg03341655 (p=8.14x10-06, located in the exonic region of GFOD2). The association of DNAm at cg03341655 and wLE could be replicated in the independent MDD case sample indicating a diagnosis independent effect. Genes mapping to the top hits were significantly upregulated in brain and top hits have been implicated in the metabolic system. Additionally, two significant DMRs were identified for PD only on chromosome 10 and 18, including CpG-sites which have been reported to be associated with anxiety and other psychiatric phenotypes. Conclusion: This first DNAm analysis in PD reveals first evidence of small but significant DNAm changes in PD in association with cumulative stress-weighted life events. Most of the top associated CpG-sites are located in genes implicated in metabolic processes supporting the hypothesis that environmental stress contributes to health damaging changes by affecting a broad spectrum of systems in the body.
2022-04-22 | GSE200956 | GEO
Project description:Social anxiety disorder (SAD) is a psychiatric disorder characterized by extensive fear in social situations. Multiple genetic and environmental factors are known to contribute to its pathogenesis. One of the main environmental risk factors is early life adversity (ELA). Evidence is emerging that epigenetic mechanisms such as DNA methylation might play an important role in the biological mechanisms underlying SAD and ELA. To investigate the relationship between ELA, DNA methylation, and SAD, we performed an epigenome-wide association study for SAD and ELA examining DNA from whole blood of a cohort of 143 individuals using DNA methylation arrays. We identified two differentially methylated regions (DMRs) associated with SAD located within the genes SLC43A2 and TNXB. As this was the first epigenome-wide association study for SAD, it is worth noting that both genes have previously been associated with panic disorder. Further, we identified two DMRs associated with ELA within the SLC17A3 promoter region and the SIAH3 gene and several DMRs that were associated with the interaction of SAD and ELA. Of these, the regions within C2CD2L and MRPL28 showed the largest difference in DNA methylation. Lastly, we found that two DMRs were associated with both the severity of social anxiety and ELA, however, neither of them was found to mediate the contribution of ELA to SAD later in life. Future studies are needed to replicate our findings in independent cohorts and to investigate the biological pathways underlying these effects.
2021-01-31 | GSE164056 | GEO
Project description:Epigenome analysis of autism spectrum disorder samples
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Project description:Anxiety disorders including panic disorders with or without agoraphobia are the most prevalent mental disorders. Exposure is a core technique within the framework of cognitive behavioral therapy to treat phobia- and anxiety-related symptoms. The primary aim of this study was to trace specific anxiety-related plasma gene expression changes of subjects with PD at three time points in order to identify biomarkers for acute anxiety states. In this intervention, the patient is exposed to highly feared and mostly avoided situations.
2018-09-15 | GSE119995 | GEO