scholarly journals Inflammation in Post-Traumatic Stress Disorder (PTSD): A Review of Potential Correlates of PTSD with a Neurological Perspective

Antioxidants ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 107 ◽  
Author(s):  
Tammy D. Kim ◽  
Suji Lee ◽  
Sujung Yoon
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Inflammatory Markers ◽  
Stress Disorder ◽  
Inflammatory Responses ◽  
Brain Regions ◽  
Post Traumatic Stress ◽  
Psychosocial Burden ◽  
Trauma Types ◽  
Post Traumatic

Post-traumatic stress disorder (PTSD) is a chronic condition characterized by symptoms of physiological and psychosocial burden. While growing research demonstrated signs of inflammation in PTSD, specific biomarkers that may be representative of PTSD such as the detailed neural correlates underlying the inflammatory responses in relation to trauma exposure are seldom discussed. Here, we review recent studies that explored alterations in key inflammatory markers in PTSD, as well as neuroimaging-based studies that further investigated signs of inflammation within the brain in PTSD, as to provide a comprehensive summary of recent literature with a neurological perspective. A search was conducted on studies published from 2009 through 2019 in PubMed and Web of Science. Fifty original articles were selected. Major findings included elevated levels of serum proinflammatory cytokines in individuals with PTSD across various trauma types, as compared with those without PTSD. Furthermore, neuroimaging-based studies demonstrated that altered inflammatory markers are associated with structural and functional alterations in brain regions that are responsible for the regulation of stress and emotion, including the amygdala, hippocampus, and frontal cortex. Future studies that utilize both central and peripheral inflammatory markers are warranted to elucidate the underlying neurological pathway of the pathophysiology of PTSD.

scholarly journals Genetic and Neuroimaging Approaches to Understanding Post-Traumatic Stress Disorder

2020 ◽  
Vol 21 (12) ◽  
pp. 4503
Author(s):  
Sabah Nisar ◽  
Ajaz A. Bhat ◽  
Sheema Hashem ◽  
Najeeb Syed ◽  
Santosh K. Yadav ◽  
...  
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Memory Function ◽  
Deep Understanding ◽  
Brain Regions ◽  
Post Traumatic Stress ◽  
Brain Areas ◽  
Social Burden ◽  
Post Traumatic

Post-traumatic stress disorder (PTSD) is a highly disabling condition, increasingly recognized as both a disorder of mental health and social burden, but also as an anxiety disorder characterized by fear, stress, and negative alterations in mood. PTSD is associated with structural, metabolic, and molecular changes in several brain regions and the neural circuitry. Brain areas implicated in the traumatic stress response include the amygdala, hippocampus, and prefrontal cortex, which play an essential role in memory function. Abnormalities in these brain areas are hypothesized to underlie symptoms of PTSD and other stress-related psychiatric disorders. Conventional methods of studying PTSD have proven to be insufficient for diagnosis, measurement of treatment efficacy, and monitoring disease progression, and currently, there is no diagnostic biomarker available for PTSD. A deep understanding of cutting-edge neuroimaging genetic approaches is necessary for the development of novel therapeutics and biomarkers to better diagnose and treat the disorder. A current goal is to understand the gene pathways that are associated with PTSD, and how those genes act on the fear/stress circuitry to mediate risk vs. resilience for PTSD. This review article explains the rationale and practical utility of neuroimaging genetics in PTSD and how the resulting information can aid the diagnosis and clinical management of patients with PTSD.

Inflammatory markers in post-traumatic stress disorder: a systematic review, meta-analysis, and meta-regression

2015 ◽  
Vol 2 (11) ◽  
pp. 1002-1012 ◽  
Author(s):  
Ives Cavalcante Passos ◽  
Mirela Paiva Vasconcelos-Moreno ◽  
Leonardo Gazzi Costa ◽  
Maurício Kunz ◽  
Elisa Brietzke ◽  
...  
Keyword(s):  
Systematic Review ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Inflammatory Markers ◽  
Stress Disorder ◽  
Meta Analysis ◽  
Post Traumatic Stress ◽  
Post Traumatic ◽  
Meta Regression

scholarly journals DNA methylation of Nuclear Factor of Activated T Cells 1 mediates the prospective relation between exposure to different traumatic event types and post-traumatic stress disorder

2021 ◽  
Author(s):  
James R. Occean ◽  
Agaz H. Wani ◽  
Janelle Donglasan ◽  
Allison E. Aiello ◽  
Sandro Galea ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Nuclear Factor ◽  
Post Traumatic Stress ◽  
Activated T Cells ◽  
Cpg Site ◽  
Trauma Types ◽  
Post Traumatic

The mechanisms through which exposure to differing trauma types become biologically embedded to shape the risk for subsequent post-traumatic stress disorder (PTSD) is unclear. DNA methylation (5-mC), particularly in stress-relevant genes, may play a role in this relationship. We conducted path analysis using generalized structural equation modeling to investigate whether blood-derived 5-mC in Nuclear Factor of Activated T Cells 1 (NFATC1) mediated the prospective association between each of five different trauma types (assaultive violence, other injury or shocking experience, learning of trauma to loved one, sudden, unexpected death of a close friend or relative, and other) and lifetime PTSD. All five trauma types were significantly associated with reduced methylation at NFATC1 CpG site, cg17057218. Three of the five trauma types were significantly associated with increased methylation at NFATC1 CpG site, cg22324981. Moreover, methylation at cg17057218 significantly mediated 23-34% of the total effect for three of the five trauma types, while methylation at cg22324981 mediated 36-53% of the total effect for two of the five trauma types. These CpG sites were differentially associated with transcription factor binding sites and chromatin state signatures. NFATC1 5-mC may be a potential mechanism in the relationship between some trauma types and prospective risk for PTSD.

Inflammatory Markers and Post Traumatic Stress Disorder (PTSD)

2013 ◽  
Vol 23 (9) ◽  
pp. 594
Author(s):  
E.C. McCanlies ◽  
K. Sarkisian ◽  
J.K. Gu ◽  
A. Mnatsakanova ◽  
M.E. Andrew ◽  
...  
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Inflammatory Markers ◽  
Stress Disorder ◽  
Post Traumatic Stress ◽  
Post Traumatic

Executive Function in Post-Traumatic Stress Disorder

2018 ◽  
Author(s):  
Jennifer Newman ◽  
Charles R. Marmar
Keyword(s):  
Executive Function ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Brain Connectivity ◽  
Brain Regions ◽  
Future Research ◽  
Neurocognitive Deficits ◽  
Post Traumatic Stress ◽  
Post Traumatic

This chapter discusses the role of executive function in post-traumatic stress disorder (PTSD), which is far from fully understood. Deficits are subtle and findings are often inconsistent. Impairments have been related to worsening of psychological symptoms, functioning, and quality of life. They can also negatively impact treatment. Functional imaging shows that neurocognitive deficits in PTSD may be related to an imbalance in brain connectivity, where emotion processing is enhanced and control is reduced. Structural findings show abnormalities in brain regions involved in higher-level functions. However, findings are often discrepant. Factors related to these inconclusive results are considered, including developmental course, premorbid functioning, and comorbidities such as traumatic brain injury, depression, substance use, attention deficit hyperactivity disorder, health behaviors, and medical concerns. Treatment implications, limitations of this work, and future directions are presented. The aim of future research is to advance scientific understanding of PTSD, neurocognitive impairments, and related conditions, with the goal of improving outcomes for those who encounter trauma.

scholarly journals Is PTSD-Phenotype Associated with HPA-Axis Sensitivity?: The Endocannabinoid System in Modulating Stress Response in Rats

2021 ◽  
Vol 22 (12) ◽  
pp. 6416
Author(s):  
Dor Danan ◽  
Doron Todder ◽  
Joseph Zohar ◽  
Hagit Cohen
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Endocannabinoid System ◽  
Brain Regions ◽  
Post Traumatic Stress ◽  
Behavioral Reactions ◽  
Behavioral Disruption ◽  
Post Traumatic ◽  
Arachidonoyl Glycerol

Endocannabinoids play a role in adaptation to stress and regulate the release of glucocorticoids in stressed and unstressed conditions. We recently found that basal corticosterone pulsatility may significantly impact the vulnerability for developing post-traumatic-stress-disorder (PTSD), suggesting that the endocannabinoid system may contribute to its development. To examine this, we exposed rats to predator scent stress (PSS). Behavioral reactions were recorded seven days post-PSS. Cerebrospinal fluid (CSF) was collected from anesthetized rats shortly after PSS exposure to determine the levels of 2-arachidonoyl glycerol (2-AG) and anandamide (AEA). To correlate between endocannabinoids and corticosterone levels, rats were placed in metabolic cages for urine collection. To assess the levels of endocannabinoids in specific brain regions, rats’ brains were harvested one day after behavioral analysis for staining and fluorescence quantification. Moreover, 2-AG was elevated in the CSF of PTSD-phenotype rats as compared with other groups and was inversely correlated with corticosterone urinary secretion. Eight days post-PSS exposure, hippocampal and hypothalamic 2-AG levels and hippocampal AEA levels were significantly more reduced in the PTSD-phenotype group compared to other groups. We posit that maladaptation to stress, which is propagated by an abnormal activation of endocannabinoids, mediates the subsequent stress-induced behavioral disruption, which, later, reduces neuronal the expression of endocannabinoids, contributing to PTSD symptomology.

scholarly journals Post-traumatic stress disorder and declarative memory functioning: a review

2011 ◽  
Vol 13 (3) ◽  
pp. 346-351 ◽  
Keyword(s):  
Risk Factor ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Declarative Memory ◽  
Memory Deficits ◽  
Brain Regions ◽  
Post Traumatic Stress ◽  
Memory Dysfunction ◽  
Post Traumatic

Declarative memory dysfunction is associated with post-traumatic stress disorder (PTSD). This paper reviews this literature and presents two frameworks to explain the nature of this dysfunction: that memory deficits are a product of neurobiological abnormalities caused by PTSD and/or that pre-existing memory deficits serve as a risk factor for the development of PTSD following trauma exposure. Brain regions implicated in declarative memory deficits include the hippocampus and prefrontal cortex, and imaging and biochemistry studies as they relate to memory dysfunction are described. Prospective and twin studies provide support for a risk factor model.

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