We tested for significant associations of common genetic variants of NOTCH1-4 (investigated by microarray) and genomic methylation of saliva-derived DNA with lifetime PTSD risk in independent cohorts from Northern Uganda (N<sub>1</sub> = 924) and Rwanda (N<sub>2</sub> = 371), and investigated whether NOTCH-related gene sets were enriched for associations with lifetime PTSD risk.
We discovered that the modified single prolonged stress-exposure induced significant PTSD-like symptoms as well as mildly impaired hippocampal Cornu Ammonis 1 (CA1) subregion cytoarchitecture, but not dentate gyrus neurogenesis, together with a gradual inhibition of TrkA-CREB-ERK signalings in hippocampal CA1 subregion.
Our results suggest that ketamine exhibited an antidepressant effect in FST and facilitated the fear memory extinction via presynaptic-mediated synaptic plasticity, which may provide new strategy for treatment of PTSD.
More interestingly, the augmented initial neural and pressor responses to SHG were associated with greater awake systolic BP variability during ambulation in women with PTSD (MSNA BF: <i>r</i> = 0.55, MSNA TA: <i>r</i> = 0.62, and SBP: <i>r</i> = 0.69, all <i>P</i> < 0.05).
More interestingly, the augmented initial neural and pressor responses to SHG were associated with greater awake systolic BP variability during ambulation in women with PTSD (MSNA BF: <i>r</i> = 0.55, MSNA TA: <i>r</i> = 0.62, and SBP: <i>r</i> = 0.69, all <i>P</i> < 0.05).
More interestingly, the augmented initial neural and pressor responses to SHG were associated with greater awake systolic BP variability during ambulation in women with PTSD (MSNA BF: <i>r</i> = 0.55, MSNA TA: <i>r</i> = 0.62, and SBP: <i>r</i> = 0.69, all <i>P</i> < 0.05).
We found associations of lifetime PTSD risk with single nucleotide polymorphism (SNP) rs2074621 (NOTCH3) (p<sub>uncorrected</sub> = 0.04) in both cohorts, and with methylation of CpG site cg17519949 (NOTCH3) (p<sub>uncorrected</sub> = 0.05) in Rwandans.
These data demonstrate that a panic-prone state leads to specific reduction in mGluR2 function within the amygdala network and facilitates fear, and mGluR2 PAMs could be a targeted treatment for panic symptoms in PD and PTSD patients.
Posttraumatic stress disorder is associated with reduced vitamin D levels and functional polymorphisms of the vitamin D binding-protein in a population-based sample.
The primary outcome measure was severity of PTSD-symptoms (Harvard Trauma Questionnaire (HTQ)) and secondary outcome measures were depression and anxiety symptoms (Hopkins Symptom Checklist-25 (HSCL-25), Hamilton Depression and Anxiety rating scales (HAM-D, HAM-A)), somatisation (somatisation items of SCL-90 (SI-SCL-90)), quality of life (WHO-5-Well-being Index (WHO-5)) and functioning (Sheehan Disability Scale (SDS), Global Assessment of Functioning (GAF-F, GAF-S)).
Participants were 103 refugee men with PTSD symptoms from Arabic, Farsi or Tamil-speaking backgrounds who were randomly assigned to either receive an 11-module online stigma reduction intervention specifically designed for refugees ('Tell Your Story', TYS) or to a wait-list control (WLC) group.
We suggest that further investigations of plasticity and pharmacology of the PAG-amygdala network provide a promising target for understanding pathophysiological circuitry that underlies PTSD in humans and that dopaminergic and neurokininergic drugs may have a potential for the treatment of psychiatric disorders that are associated with a dysfunctional dPAG.
Instead, the results showed a decline in expression of the pro-inflammatory mediator IFN-γ and the cytotoxin granzyme B in CD8<sup>+</sup> subpopulations from Veterans with PTSD.
Higher severity of delirium as indicated by the total DRS-R98 score and the total DRS-R98 severity score were associated with higher severity of PTSD symptoms.
The concentration changes of miR-203a-3p in EV and miR-339-5p in EVD were confirmed in an independent validation cohort that consisted of 20 veterans (10 with and 10 without PTSD) using qPCR.
However, a significant interaction effect between GHRLrs696217 and HCRTR1 rs2271933 was found to predict the PTSD Checklist (PCL-5) total score (P = 0.007).
The aim of this study was to investigate the influence of single nucleotide polymorphisms (SNPs) in the neuropeptide S receptor 1 (NPSR1) and the glutamate decarboxylase 1(GAD1) gene on PTSD and its psychopathological aspects among individuals affected by the Balkan wars during the 90s.
HLA-B*58:01 (p = 0.035), HLA-C*07:01 (p = 0.035), HLA-DQA1*01:01 (p = 0.003), HLA-DQB1*05:01 (p = 0.009) and HLA-DPB1*17:01 (p = 0.017) were more common in PTSD cases, while HLA-A*02:01 (p = 0.026), HLA-DQA1*05:05 (p = 0.011) and HLA-DRB1*11:01 (p < 0.001) were more frequent in controls.
We suggest that further investigations of plasticity and pharmacology of the PAG-amygdala network provide a promising target for understanding pathophysiological circuitry that underlies PTSD in humans and that dopaminergic and neurokininergic drugs may have a potential for the treatment of psychiatric disorders that are associated with a dysfunctional dPAG.
The present study investigated whether angiotensin (Ang) II-elicited hypertensive response is sensitized in a model of PTSD and whether inhibition of angiotensin-converting enzyme (ACE) or tumor necrosis factor (TNF)-α prior to PTSD blocks this sensitization of Ang II hypertension.