ABSTRACT: PTSD - Posttraumatic stress disorder. 33 samples taken from PMBCs of survivors of psychological trauma, in two time points: in ER, few hours after the truma, and four months later. Some of the patients devepled chronic PTSD (17 samples) and others recovered and set to be the Control group (16 samples). This is the normalized active genes: 4512 probes from U95A chip. The raw data is available in series GSE845. Samples are labeled with 3 tags: P/C for PTSD or Control, ER/M4 - for time point of sample, D/ND for Decrement or Non-decrement symptoms over time. (e.g. sample 23C-M4-D-Norm was taken 4 months after trauma from patient 23 which belongs to the control group and showed decrease in symptoms) . Samples include the expression value, the GeneBank accession number and Affymetrix indication of valid calls. Keywords = PTSD Keywords = Normalized Keywords = PMBC Keywords: other
Project description:PTSD - Posttraumatic stress disorder. 33 samples taken from PMBCs of survivors of psychological trauma, in two time points: in ER, few hours after the truma, and four months later. Some of the patients devepled chronic PTSD (17 samples) and others recovered and set to be the Control group (16 samples). This is the raw data consists of 12,600 probes from U95A chip. Samples are labeled with 3 tags: P/C for PTSD or Control, ER/M4 - for time point of sample, D/ND for Decrement or Non-decrement symptoms over time. (e.g. sample 23C-M4-D was taken 4 months after trauma from patient 23 which belongs to the control group and showed decrease in symptoms) . Samples include the expression value, the GeneBank accession number and Affymetrix indication of valid calls. Keywords: other
Project description:PTSD - Posttraumatic stress disorder. 33 samples taken from PMBCs of survivors of psychological trauma, in two time points: in ER, few hours after the truma, and four months later. Some of the patients devepled chronic PTSD (17 samples) and others recovered and set to be the Control group (16 samples). This is the normalized active genes: 4512 probes from U95A chip. The raw data is available in series GSE845. Samples are labeled with 3 tags: P/C for PTSD or Control, ER/M4 - for time point of sample, D/ND for Decrement or Non-decrement symptoms over time. (e.g. sample 23C-M4-D-Norm was taken 4 months after trauma from patient 23 which belongs to the control group and showed decrease in symptoms) . Samples include the expression value, the GeneBank accession number and Affymetrix indication of valid calls.
Project description:Post-Traumatic Stress Disorder is a mental health condition that may develop after exposure to a traumatic event. The diagnosis of PTSD is based on clinical signs and symptoms; there is increasing evidence that biological markers aid in the diagnosis of PTSD. In a Dutch military cohort, we compared blood-based transcriptomic profiles of individuals susceptible and resilient to developing PTSD symptoms after combat-trauma exposure. Whole blood samples were collected from susceptible (n=20) and resilient (n=20) military personnel deployed to Afghanistan, 6 months after returning from military deployment.
Project description:Military service members often return from deployment with a multiplicity of injuries, including mild traumatic brain injury, depression, and sleep disorders, which obsures diagnosis of PTSD symptoms and complicates treatment of PTSD. In order to understand the biological mechanisms underlying PTSD, gene expression profiles of military service members with and without PTSD were compared. Additionally, gene expression was examined based on intrusion symptoms, a distinct subtype of PTSD symptoms, and on improvement of PTSD symptoms at a three month follow up. RNA was extracted from blood samples and hybridized to the HG-U133_Plus_2 Affymetrix chip.
Project description:The gene expression approach has provided promising insights into the pathophysiology of PTSD. However, few studies used hypothesis-free transcriptome-wide expression approach. Transcriptome-wide expression study using RNA sequencing (RNA-Seq) of whole blood was conducted in 324 World Trade Center responders (201 with never, 81 current and 42 past PTSD). The current and never PTSD samples were randomly split to form both discovery (N=195) and replication (N=87) cohorts. Differentially expressed genes identified in RNA-Seq were used in pathway analysis and to create a polygenic expression score. There were 448 differentially expressed genes in the discovery cohort, of which 99 remained significant in the replication cohort, and 5 (FKBP5, NDUFA1, CCDC85B, SNORD54, SNORD46) showed >1.2-fold difference in expression consistently between the discovery and replication cohorts. Several enriched biological pathways were found, including glucocorticoid receptor signaling and immunity-related pathways, but were not significant following FDR correction. The gene expression score achieved sensitivity of 0.917 and specificity of 0.508 for identifying PTSD cases in the replication cohort. It was similar in current and past PTSD, with both groups scoring higher than trauma-exposed controls. We confirmed the role of FKBP5 in PTSD and identified four additional differentially expressed genes that may constitute biomarkers for this condition. Together with the pathway analysis results, these findings point to HPA-axis and immune dysregulation as key biological processes underpinning PTSD. A novel polygenic expression aggregate that differentiates PTSD patients from trauma-exposed controls might be a useful screening tool for research and clinical practice, if replicated in other populations.
Project description:Prenatal exposure to maternal stress and depression has been identified as a risk factor for adverse behavioral and neurodevelopmental outcomes in early childhood. However, the molecular mechanisms through which maternal psychopathology shapes offspring development remain poorly understood. We analyzed transcriptome-wide gene expression profiles of 149 UCB samples from neonates born to mothers with prenatal PTSD (n=20), depression (n=31) and PTSD with comorbid depression (PTSD/Dep; n=13), compared to neonates born to carefully matched trauma exposed controls without meeting PTSD criteria (TE; n=23) and healthy mothers (n=62). We also evaluated physiological and developmental measures in these infants at birth, six months and twenty-four months. A multistep analytic approach was used that specifically sought to: 1) identify dysregulated genes, molecular pathways and discrete groups of co-regulated gene modules in UCB associated with prenatal maternal psychopathologies; and 2) to determine the impact of perinatal PTSD and depression on early childhood development outcomes.
Project description:A social-stress mouse model, involving exposure of an intruder (male C57BL/6) mouse to a resident aggressor (male SJL) mouse followed by exposure to trauma reminders with post-trauma periods, was used to simulate features of human PTSD. Transcriptome changes in blood, brain regions and spleen, and DNA methylome changes in hemi-brain of aggressor-exposed and control C57BL/6 mice were assayed at one, 10 and 42 days of post-trauma periods. Assessments of activation patterns for differentially expressed transcripts (overlapping among hemi-brain, blood and spleen), and differentially methylated promoter regions showed increased activations of inflammatory pathways, and inhibited pathways related to neurogenesis and synaptic plasticity at longer post-trauma days. In amygdala, hippocampus and medial pre-frontal cortext, these pathways were activated at earlier post-trauma periods. But at longer post-trauma periods, neurogenesis and synaptic plasticity were inhibited while lower level of activated inflammation persisted in hippocampus and medial pre-frontal cortex. Pathways implicated in diabetes, insulin signaling, metabolic disorder, mitochondrial dysfunctions, circadian disruption, oxidative stress and inhibited telomere maintenance were significantly enriched. Identification of brain – blood overlapping molecular signatures provide increased confidence in using blood as brain surrogate sample for clinical translation. Our findings suggest that stress-induced inflammation triggers impaired neurogenesis, cognitive decline, and chronic pain (physical complaints in PTSD patients). Signaling pathways implicated in neurogenesis and synaptic plasticity seem to be mediating the effect of neuroinflammation in the development and maintenance of behavioral manifestations of PTSD. While inflammation seems to be directly involved in tissue damage triggering, exacerbating or maintaining the somatic comorbid pathologies of PTSD.
Project description:Analysis of transcript abundance estimates as a function of child soldier status, PTSD symptoms, and psychological resilience. Gene expression profiling was conducted on dried blood spot (DBS) samples collected from community dwelling adolescents and young adults in Nepal. Approximatley half of the sample were former child soldiers in the Nepal People's War and the other half were demographically similiar civilian non-combatants. In addition to basic demographic characteristics (age, sex, ethnic minority status, social caste status, education level), participants were also assessed on syptoms of post-traumatic stress (PTS, assessed by a culturally adapted version of The Child PTSD Symptom Scale; Kohrt BA, et al. (2011) Validation of cross-cultural child mental health and psychosocial research instruments: adapting the Depression Self-Rating Scale and Child PTSD Symptom Scale in Nepal. BMC Psychiatry 11(1):e127, with higher values indicating greater PTSD symptoms) and psychological resilience (assessed by a culturally adapted version of the Resilience Scale; Wagnild GM & Young HM (1993) Development and psychometric evaluation of the Resilience Scale. Journal of Nursing Measurement, with higher values indicating greater resilience). Dichotomous variables were coded 0=no/absent and 1=yes/present. Valid gene expression data are available for 254 samples.
Project description:Post-traumatic stress disorder is a concerning psycho behavioral disorder thought to emerge from the complex interaction between genetic and environmental factors. For soldiers exposed to combat, the risk of developing this disorder is two-fold and diagnosis is often late, when much sequela has set in. To be able to identify and diagnose in advance those at “risk” of developing PTSD, would greatly taper the gap between late sequelae and treatment. Therefore, this study sought to test the hypothesis that the transcriptome can be used to track the development of PTSD in this unique and susceptible cohort of individuals. Gene expression levels in peripheral blood samples from 85 Canadian infantry soldiers (n = 58 subjects negative for PTSD symptoms and n = 27 subjects with PTSD symptoms) were determined by RNA sequencing technology following their return from deployment to Afghanistan. Count-based gene expression quantification, normalization and differential analysis (with thorough correction for confounders) revealed significant differences in two genes, LRP8 and GOLM1 . These preliminary results provide a proof-of-principle for the diagnostic utility of blood-based gene expression profiles for tracking symptoms of post-traumatic stress disorder in soldiers returning from tour. It is also the first to report transcriptome-wide expression profiles alongside a post-traumatic symptom checklist.