scholarly journals Gene Expression Differences Between Young Adults Based on Trauma History and Post-traumatic Stress Disorder

2021 ◽  
Vol 12 ◽  
Author(s):  
Kaitlin E. Bountress ◽  
Vladimir Vladimirov ◽  
Gowon McMichael ◽  
Z. Nathan Taylor ◽  
Gary Hardiman ◽  
...  
Keyword(s):  
Gene Expression ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Gene Network ◽  
Stress Disorder ◽  
Trauma Exposure ◽  
Differentially Expressed ◽  
Post Traumatic Stress ◽  
Network Analyses ◽  
Post Traumatic

Background: The purpose of this study was to identify gene expression differences associated with post-traumatic stress disorder (PTSD) and trauma exposure (TE) in a three-group study design comprised of those with and without trauma exposure and PTSD.Methods: We conducted gene expression and gene network analyses in a sample (n = 45) composed of female subjects of European Ancestry (EA) with PTSD, TE without PTSD, and controls.Results: We identified 283 genes differentially expressed between PTSD-TE groups. In an independent sample of Veterans (n = 78) a small minority of these genes were also differentially expressed. We identified 7 gene network modules significantly associated with PTSD and TE (Bonferroni corrected p ≤ 0.05), which at a false discovery rate (FDR) of q ≤ 0.2, were significantly enriched for biological pathways involved in focal adhesion, neuroactive ligand receptor interaction, and immune related processes among others.Conclusions: This study uses gene network analyses to identify significant gene modules associated with PTSD, TE, and controls. On an individual gene level, we identified a large number of differentially expressed genes between PTSD-TE groups, a minority of which were also differentially expressed in the independent sample. We also demonstrate a lack of network module preservation between PTSD and TE, suggesting that the molecular signature of PTSD and trauma are likely independent of each other. Our results provide a basis for the identification of likely disease pathways and biomarkers involved in the etiology of PTSD.

scholarly journals Paranoia in patients attending child and adolescent mental health services

2021 ◽  
pp. 000486742098141
Author(s):  
Jessica C Bird ◽  
Emma C Fergusson ◽  
Miriam Kirkham ◽  
Christina Shearn ◽  
Ashley-Louise Teale ◽  
...  
Keyword(s):  
Mental Health ◽  
Health Services ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Post Traumatic Stress ◽  
Network Analyses ◽  
Self Harm ◽  
Post Traumatic ◽  
Peer Difficulties

Objective: Paranoia may be particularly prevalent during adolescence, building on the heightened social vulnerabilities at this age. Excessive mistrust may be corrosive for adolescent social relationships, especially in the context of mental health disorders. We set out to examine the prevalence, symptom associations, and persistence of paranoia in a cohort of young people attending child and adolescent mental health services. Method: A total of 301 patients (11–17 years old) completed measures of paranoia, affect, peer difficulties and behavioural problems. Clinicians also rated each participant’s psychiatric symptoms. Patterns of association were examined using linear regressions and network analyses. In total, 105 patients repeated the measures several months later. Results: Most of the adolescents had affective disorders ( n = 195), self-harm/suicidality ( n = 82), or neurodevelopmental conditions ( n = 125). Few had suspected psychosis ( n = 7). Rates of paranoia were approximately double compared with previous reports from the general population. In this patient sample, 35% had at least elevated paranoia, 15% had at least moderate paranoia, and 6% had high paranoia. Paranoia had moderate associations with clinician-rated peer difficulties, self-harm, and trauma, and small associations with clinician-rated social anxiety, depression, generalised anxiety, and educational problems. Network analyses showed paranoia had the strongest unique relationship with peer difficulties. Paths from peer difficulties to anxiety, self-harm, post-traumatic stress disorder symptoms, and behavioural problems were all via paranoia. Both self-harm and post-traumatic stress disorder were solely associated with paranoia in the network. Paranoia remained persistent for three-quarters and was associated with greater psychological problems over time. Conclusion: Paranoia is relatively common and persistent across a range of clinical presentations in youth. When paranoia occurs alongside emotional problems, important peer interactions may be adversely affected. Wider consideration of paranoia in adolescent patients is needed.

scholarly journals Microglial deletion and inhibition alleviate behavior of post-traumatic stress disorder in mice

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Shuoshuo Li ◽  
Yajin Liao ◽  
Yuan Dong ◽  
Xiaoheng Li ◽  
Jun Li ◽  
...  
Keyword(s):  
Gene Expression ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Microglial Activation ◽  
Stress Disorder ◽  
Critical Role ◽  
Post Traumatic Stress ◽  
Minocycline Treatment ◽  
Post Traumatic ◽  
Shock Exposure

Abstract Background Alteration of immune status in the central nervous system (CNS) has been implicated in the development of post-traumatic stress disorder (PTSD). However, the nature of overall changes in brain immunocyte landscape in PTSD condition remains unclear. Methods We constructed a mouse PTSD model by electric foot-shocks followed by contextual reminders and verified the PTSD-related symptoms by behavior test (including contextual freezing test, open-field test, and elevated plus maze test). We examined the immunocyte panorama in the brains of the naïve or PTSD mice by using single-cell mass cytometry. Microglia number and morphological changes in the hippocampus, prefrontal cortex, and amygdala were analyzed by histopathological methods. The gene expression changes of those microglia were detected by quantitative real-time PCR. Genetic/pharmacological depletion of microglia or minocycline treatment before foot-shocks exposure was performed to study the role of microglia in PTSD development and progress. Results We found microglia are the major brain immune cells that respond to PTSD. The number of microglia and ratio of microglia to immunocytes was significantly increased on the fifth day of foot-shock exposure. Furthermore, morphological analysis and gene expression profiling revealed temporal patterns of microglial activation in the hippocampus of the PTSD brains. Importantly, we found that genetic/pharmacological depletion of microglia or minocycline treatment before foot-shock exposure alleviated PTSD-associated anxiety and contextual fear. Conclusion Our results demonstrated a critical role for microglial activation in PTSD development and a potential therapeutic strategy for the clinical treatment of PTSD in the form of microglial inhibition.

scholarly journals An epistasis between dopaminergic and oxytocinergic systems confers risk of post-traumatic stress disorder in a traumatized Chinese cohort

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Kunlin Zhang ◽  
Gen Li ◽  
Li Wang ◽  
Chengqi Cao ◽  
Ruojiao Fang ◽  
...  
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Trauma Exposure ◽  
Environment Interaction ◽  
Post Traumatic Stress ◽  
Ptsd Diagnosis ◽  
Psychiatric Syndrome ◽  
Chinese Cohort ◽  
Post Traumatic

AbstractPost-traumatic stress disorder (PTSD) is a psychiatric syndrome that occurs after trauma exposure. Neurotransmitters such as dopamine and oxytocin have been reported to be involved in neuropathology of PTSD. Previous studies indicated that the dopamine–oxytocin interaction may contribute to behavioral disorders. Thus, exploring the epistasis (gene–gene interaction) between oxytocinergic and dopaminergic systems might be useful to reveal the genetic basis of PTSD. In this study, we analyzed two functional single nucleotide polymorphisms (SNPs), rs2268498 for oxytocinergic gene OXTR and rs1801028 for dopaminergic gene DRD2 based on putative oxytocin receptor–dopamine receptor D2 (OTR–DR2) heterocomplex in a Chinese cohort exposed to the 2008 Wenchuan earthquake (156 PTSD cases and 978 controls). Statistical analyses did not find any single variant or gene–environment interaction (SNP × earthquake-related trauma exposure) associated with provisional PTSD diagnosis or symptoms. An OXTR–DRD2 interaction (rs2268498 × rs1801028) was identified to confer risk of provisional PTSD diagnosis (OR = 9.18, 95% CI = 3.07–27.46 and P = 7.37e-05) and further subset analysis indicated that rs2268498 genotypes controlled the association directions of rs1801028 and rs1801028 genotypes also controlled the association directions of rs2268498. Rs2268498 × rs1801028 is also associated with PTSD symptoms (P = 0.043). Our study uncovered a genetic and putative function-based contribution of dopaminergic–oxytocinergic system interaction to PTSD.

Integrated analysis profiles of long non–coding RNAs reveal potential biomarkers across brain regions in post–traumatic stress disorder

2020 ◽  
Author(s):  
Yaoyao Bian ◽  
Lili Yang ◽  
Zhongli Wang ◽  
Wen Li ◽  
Qing Wang ◽  
...  
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Expression Profiles ◽  
Differentially Expressed ◽  
Integrated Analysis ◽  
Post Traumatic Stress ◽  
Post Traumatic ◽  
Non Coding Rnas ◽  
Potential Biomarkers

Abstract Background Post–traumatic stress disorder (PTSD) is characterized by impaired fear extinction, excessive anxiety and depression. However, underlying mechanisms, especially the function roles of long non–coding RNAs (lncRNAs) involved in PTSD is still unclear. We argued that the lncRNAs, co–expressed mRNAs, as well as the associated pathways, are altered and may thus serve as potential biomarkers and key pathways related to PTSD.Methods The gene expression profiles of GSE68077 was downloaded from the GEO database, and the differentially expressed lncRNAs and mRNAs were identified. Gene ontology (GO) and Kyto Encyclopedia of Genes and Genomes pathway (KEGG) enrichment analysis were performed. Subsequently, protein–protein interaction (PPI) network was analyzed, and module analysis of the differentially expressed mRNAs was performed with Cytoscape software. Finally, lncRNAs–mRNAs co–expression network was constructed and core pair lncRNAs involved in PTSD were mapped.Results A total of 45 differentially expressed lncRNAs and 726 differentially expressed mRNAs were obtained. Among of which, 17 lncRNAs and 86 mRNAs were inter–regulated, and most of the lncRNAs–mRNAs co–expression showed positive correlations. The lncRNAs–mRNAs co–expressed network suggested the potentially functional roles of lncRNAs, regulated mRNAs and related pathways in PTSD. By implication of the core pair network, lncRNA–NONMMUT010120.2 synergistically up–regulated Ppargc1a and down–regulated Cir1, Slc38a9, Atp6v0a2. Moreover, lncRNA–NONMMUT023440.2, NONMMUT034155.2, NONMMUT105407.1 and NONMMUT149972.1 were co–expressed with 10 co–expressed mRNAs, which indicated that lncRNAs involved in PTSD might work by regulating the co–expressed mRNAs.

Prevention of Post-Traumatic Stress Disorder

2018 ◽  
Author(s):  
Arieh Y. Shalev ◽  
Anna C. Barbano ◽  
Wei Qi ◽  
Charles R. Marmar
Keyword(s):  
Mental Disorders ◽  
Early Development ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Traumatic Events ◽  
Trauma Exposure ◽  
Post Traumatic Stress ◽  
Post Traumatic

Post-traumatic stress disorder (PTSD) follows an exposure to traumatic events and as such its onset and early development are better charted then those of most other mental disorders. It is not surprising, therefore, that major efforts have been dedicated to preventing its occurrence before, during and after trauma exposure. This chapter discusses the rationale, desirability, feasibility and outcome of interventions designed to prevent PTSD. Several efficient interventions have been documented. Barriers to their early implementations, however, greatly reduce their effectiveness and require urgent attention.

scholarly journals Optogenetic sleep enhancement improves fear-associated memory processing following trauma exposure in rats

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Christopher J. Davis ◽  
William M. Vanderheyden
Keyword(s):  
Sleep Duration ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Trauma Exposure ◽  
Dark Phase ◽  
Post Traumatic Stress ◽  
Memory Processing ◽  
Optogenetic Stimulation ◽  
Post Traumatic

Abstract Sleep disturbances are commonly found in trauma-exposed populations. Additionally, trauma exposure results in fear-associated memory impairments. Given the interactions of sleep with learning and memory, we hypothesized that increasing sleep duration following trauma exposure would restore overall function and improve trauma-induced fear-associated memory dysfunction. Here, we utilized single prolonged stress, a validated rodent model of post-traumatic stress disorder, in combination with optogenetic activation of hypothalamic melanin-concentrating hormone containing cells to increase sleep duration. The goal of this work was to ascertain if post-trauma sleep increases are sufficient to improve fear-associated memory function. In our laboratory, optogenetic stimulation after trauma exposure was sufficient to increase REM sleep duration during both the Light and Dark Phase, whereas NREM sleep duration was only increased during the Dark Phase of the circadian day. Interestingly though, animals that received optogenetic stimulation showed significantly improved fear-associated memory processing compared to non-stimulated controls. These results suggest that sleep therapeutics immediately following trauma exposure may be beneficial and that post-trauma sleep needs to be further examined in the context of the development of post-traumatic stress disorder.

scholarly journals Mediating role of avoidance of trauma disclosure and social disapproval in ICD-11 post-traumatic stress disorder and complex post-traumatic stress disorder: cross-sectional study in a Lithuanian clinical sample

BJPsych Open ◽  
2021 ◽  
Vol 7 (6) ◽  
Author(s):  
Monika Kvedaraite ◽  
Odeta Gelezelyte ◽  
Thanos Karatzias ◽  
Neil P. Roberts ◽  
Evaldas Kazlauskas
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Clinical Sample ◽  
Trauma Exposure ◽  
Traumatic Experiences ◽  
Post Traumatic Stress ◽  
Mediating Role ◽  
Post Traumatic ◽  
The Relationship

Background ICD-11 includes a new diagnosis of complex post-traumatic stress disorder (CPTSD), resulting predominantly from reoccurring or prolonged trauma. Previous studies showed that lack of social support is among the strongest predictors of PTSD, but social factors have been sparsely studied in the context of the ICD-11 definition of PTSD and CPTSD. Aims To analyse the factor structure of the International Trauma Questionnaire (ITQ) in a Lithuanian clinical sample and to evaluate the mediating role of social and interpersonal factors in the relationship between trauma exposure and ICD-11 PTSD and CPTSD. Method The sample comprised 280 adults from out-patient mental health centres (age, years: mean 39.48 (s.d. = 13.35); 77.5% female). Trauma-related stress symptoms were measured with the ITQ. Social disapproval was measured with the Social Acknowledgment Questionnaire (SAQ) and trauma disclosure using the Disclosure of Trauma Questionnaire (DTQ). Results ICD-11 PTSD and CPTSD prevalence among the participants in this study was 13.9% and 10.0% respectively. Results indicated that avoidance of trauma disclosure mediated the relationship between trauma exposure and PTSD as well as CPTSD, whereas social disapproval mediated only the relationship between trauma exposure and CPTSD. Conclusions The findings suggest that disclosure of traumatic experiences and support from closest friends and family members might mitigate the effects of traumatic experiences, potentially reducing the risk of developing CPTSD.

Alcohol abuse in subjects developing or not post-traumatic stress disorder after trauma exposure

2017 ◽  
Vol 27 ◽  
pp. S1018-S1019
Author(s):  
F. Fiori ◽  
F. Vellante ◽  
F. Sarchione ◽  
M. Brunetti ◽  
G. Martinotti ◽  
...  
Keyword(s):  
Alcohol Abuse ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Trauma Exposure ◽  
Post Traumatic Stress ◽  
Post Traumatic

scholarly journals Transcriptional Control of Monocyte Gene Expression in Post-Traumatic Stress Disorder

2011 ◽  
Vol 30 (2-3) ◽  
pp. 123-132 ◽  
Author(s):  
Aoife O’Donovan ◽  
Bing Sun ◽  
Steve Cole ◽  
Hans Rempel ◽  
Maryann Lenoci ◽  
...  
Keyword(s):  
Gene Expression ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Transcriptional Control ◽  
Target Genes ◽  
Stress Disorder ◽  
Post Traumatic Stress ◽  
Down Regulation ◽  
Increased Risk ◽  
Post Traumatic

Post-traumatic stress disorder (PTSD) confers an increased risk for disorders with an inflammatory etiology. PTSD-related dysregulation of the sympathetic nervous system (SNS) and hypothalamic-pituitary adrenal (HPA) axis and associated alterations in inflammatory activity may contribute to this increased risk. However, little is known about convergent SNS, HPA and inflammatory signaling at the level of the immune cell transcriptome in PTSD. To explore such signaling, we examined the prevalence of specific transcription factor binding motifs in the promoter regions of differentially expressed genes in monocytes from individuals with PTSD and matched controls. Participants included 49 men (24 PTSD+ and 25 trauma-exposed controls) and 18 women (10 PTSD+ and 8 controls). Men with PTSD showed up-regulation of target genes for the NF-κB/Rel family of transcription factors, which convey inflammatory signals, up-regulation of target genes for CREB/ATF transcription factors, which convey adrenergic signals from the SNS, and down-regulation of target genes for the glucocorticoid receptor, which conveys glucocorticoid signals from the HPA axis. Women with PTSD also showed significant up-regulation of target genes for NF-κB and non-significant down-regulation of target genes for GR, but significant down-regulation of target genes for CREB/ATF. Altered transcriptional control of monocyte gene expression could contribute to exaggerated inflammatory activity in PTSD.

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