Basis Of Post-traumatic Stress Disorder Research Articles

Integrated analysis of proteomics, epigenomics and metabolomics data revealed divergent pathway activation patterns in the recent versus chronic post-traumatic stress disorder

Metabolomics, proteomics and DNA methylome assays, when done in tandem from the same blood sample and analyzed together, offer an opportunity to evaluate the molecular basis of post-traumatic stress disorder (PTSD) course and pathogenesis. We performed separate metabolomics, proteomics, and DNA methylome assays on blood samples from two well-characterized cohorts of 159 active duty male participants with relatively recent onset PTSD (<1.5 years) and 300 male veterans with chronic PTSD (>7 years). Analyses of the multi-omics datasets from these two independent cohorts were used to identify convergent and distinct molecular profiles that might constitute potential signatures of severity and progression of PTSD and its comorbid conditions. Molecular signatures indicative of homeostatic processes such as signaling and metabolic pathways involved in cellular remodeling, neurogenesis, molecular safeguards against oxidative stress, metabolism of polyunsaturated fatty acids, regulation of normal immune response, post-transcriptional regulation, cellular maintenance and markers of longevity were significantly activated in the active duty participants with recent PTSD. In contrast, we observed significantly altered multimodal molecular signatures associated with chronic inflammation, neurodegeneration, cardiovascular and metabolic disorders, and cellular attritions in the veterans with chronic PTSD. Activation status of signaling and metabolic pathways at the early and late timepoints of PTSD demonstrated the differential molecular changes related to homeostatic processes at its recent and multi-system syndromes at its chronic phase. Molecular alterations in the recent PTSD seem to indicate some sort of recalibration or compensatory response, possibly directed in mitigating the pathological trajectory of the disorder.

Animal models of post-traumatic stress disorder and novel treatment targets.

Understanding the neurobiological basis of post-traumatic stress disorder (PTSD) is fundamental to accurately diagnose this neuropathology and offer appropriate treatment options to patients. The lack of pharmacological effects, too often observed with the most currently used drugs, the selective serotonin reuptake inhibitors (SSRIs), makes even more urgent the discovery of new pharmacological approaches. Reliable animal models of PTSD are difficult to establish because of the present limited understanding of the PTSD heterogeneity and of the influence of various environmental factors that trigger the disorder in humans. We summarize knowledge on the most frequently investigated animal models of PTSD, focusing on both their behavioral and neurobiological features. Most of them can reproduce not only behavioral endophenotypes, including anxiety-like behaviors or fear-related avoidance, but also neurobiological alterations, such as glucocorticoid receptor hypersensitivity or amygdala hyperactivity. Among the various models analyzed, we focus on the social isolation mouse model, which reproduces some deficits observed in humans with PTSD, such as abnormal neurosteroid biosynthesis, changes in GABAA receptor subunit expression and lack of pharmacological response to benzodiazepines. Neurosteroid biosynthesis and its interaction with the endocannabinoid system are altered in PTSD and are promising neuronal targets to discover novel PTSD agents. In this regard, we discuss pharmacological interventions and we highlight exciting new developments in the fields of research for novel reliable PTSD biomarkers that may enable precise diagnosis of the disorder and more successful pharmacological treatments for PTSD patients.

Sex differences in learned fear expression and extinction involve altered gamma oscillations in medial prefrontal cortex

Sex differences in learned fear expression and extinction involve the medial prefrontal cortex (mPFC). We recently demonstrated that enhanced learned fear expression during auditory fear extinction and its recall is linked to persistent theta activation in the prelimbic (PL) but not infralimbic (IL) cortex of female rats. Emerging evidence indicates that gamma oscillations in mPFC are also implicated in the expression and extinction of learned fear. Therefore we re-examined our in vivo electrophysiology data and found that females showed persistent PL gamma activation during extinction and a failure of IL gamma activation during extinction recall. Altered prefrontal gamma oscillations thus accompany sex differences in learned fear expression and its extinction. These findings are relevant for understanding the neural basis of post-traumatic stress disorder, which is more prevalent in women and involves impaired extinction and mPFC dysfunction.

Drug could stop PTSD before it starts

Researchers investigating the genetic basis of posttraumatic stress disorder (PTSD) have found a drug that could stop the condition from developing if given shortly after a traumatic experience. Kerry Ressler, a psychiatrist at Yerkes National Primate Research Center in Atlanta, Georgia, wanted to

Cerebral basis of posttraumatic stress disorder following the Chernobyl disaster

Whether posttraumatic stress disorder (PTSD) following radiation emergency has psychopathological, neurocognitive, and neurophysiological peculiarities is at issue. The goal was to explore the features and cerebral basis of "radiation" PTSD in the survivors of the Chernobyl accident. Subjects and Methods The cross-sectional study included 241 people, 219 of whom have been diagnosed with PTSD according to the Diagnostic and Statistical Manual of Mental Disorders, 4th ed. (DSM-IV) criteria, among them 115 clean-up workers of the Chernobyl accident (34 with acute radiation sickness), 76 evacuees from the Chernobyl exclusion zone, 28 veterans of the war in Afghanistan, and 22 healthy unexposed individuals. Psychometric examinations, neurocognitive assessments, computerized electroencephalography, and cerebral vascular Doppler were used. "Radiation" PTSD includes "flashforward" phenomena and anticipating stress (projection of fear and danger to the future); somatoform disorders (depression, trait and state anxiety); and neurocognitive deficit (impaired memory and attention, auditory-verbal memory and learning, proactive and retroactive interference, cerebellar and stem symptoms, intellectual changes). The intima-media component, thickness of common carotid arteries, and common and left internal carotid arteries stenosis rates are increased in the liquidators. Changes of bioelectrical brain activity as a decrease of beta- and theta-power, together with an increase of alpha-power, were found in the Chernobyl accident survivors with PTSD. PTSD following radiation emergency is characterized by comorbidity of psychopathology, neurocognitive deficit, and cerebrovascular pathology with increased risk of cerebral atherosclerosis and stroke. The cerebral basis of this PTSD is proposed to be an abnormal communication between the pyramidal cells of the neocortex and the hippocampus, and deep brain structures. It is recommended that a system of emergency and long-term psychological and psychiatric care be organized for the survivors in Fukushima Daichi, Japan.

Posttraumatic Stress Disorder (Wiley Concise Guides to Mental Health)

The author is a psychologist in private practice in California, USA, and also an adjunct professor at Chapman University, Orange County. The Wiley Concise Guides to Mental Health are a series of texts covering topics such as substance use disorders, bipolar disorder and anxiety disorders. The aim of this paperback guide is to use clear language to provide an overview of the history, diagnosis, treatment, research, emerging trends and other critical information about post-traumatic stress disorder (PTSD). It describes its target audience as students, practising mental health professionals, emergency service providers, military personnel and others, who deal with traumatic situations and their aftermath. The book comprises 22 chapters organized in three sections. The first section deals with the theoretical and empirical foundations of PTSD, the second with its evaluation, assessment and treatment and the third section with more specialist areas such as PTSD in children, war, terrorism and torture. At the end of each chapter, there is a Quick Review where the content of the chapter is reiterated as a number of bullet points. The text is punctuated with case histories and boxed entries labelled as ‘alerts’ for professionals or lay people, where attention is drawn to ambiguous terminology or controversial material. The Quick Reviews provide very useful summaries and are an attractive feature of the text. The text is very readable and it fulfils the aim of the series editor to provide a condensed and comprehensive review of the topic. Although I assume that the book is targeted primarily at an American audience, it is easy to read, and there is little that is not relevant to a UK reader. I enjoyed dipping into the initial section, which explains clearly, and in depth, the theoretical basis of PTSD in terms of bio-psychosocial, cognitive and psychotherapeutic models. The most useful reference chapters for the occupational health physician are those on the assessment and treatment of PSTD. There is little mention, however, of PTSD in relation to work. Occupational health professionals who work with the emergency services or the military are likely to be disappointed if seeking practical advice on workplace management of the condition. I also doubt whether doctors in training, medical students, occupational medicine registrars or psychiatrists would choose it as a primary text on PTSD. But it covers much useful and interesting information, and it would be a good reference for the practising occupational health professional to keep in the library.

Does Filing a Post-Traumatic Stress Disorder Disability Claim Promote Mental Health Care Participation among Veterans?

This study examined the impact of participation in the Department of Veterans Affairs (VA) disability system on health care use by veterans filing disability claims on the basis of post-traumatic stress disorder (PTSD). VA administrative databases were used to examine health care use in 3-month intervals before, during, and after veterans' filing of PTSD disability claims. Subjects were all veterans using some VA health care who filed PTSD claims between 1997 and 1999 in a large Midwestern region. PTSD claimants used more medical and mental health services after filing a disability claim, compared with the preapplication period. Continuation of elevated mental health care use after claim determination occurred only for those veterans whose claims were approved. Use of VA mental health care before the disability examination was associated with an increased likelihood of claim approval. For veterans with PTSD, disability system participation may both promote and be promoted by receipt of mental health care.

Veterans seeking disability benefits for post-traumatic stress disorder: who applies and the self-reported meaning of disability compensation

Assumptions about the characteristics and motivations of individuals pursuing disability status are well known. However, policy, programming and interventions need to be based on information about the actual sociodemographic characteristics of disabled individuals, as well as their goals in seeking disability status. In this study, we focus on veterans seeking disability compensation for post-traumatic stress disorder (PTSD) from the United States Department of Veterans Affairs. We present information on their life circumstances and their self-reported reasons for valuing the obtainment of veterans’ disability status on the basis of PTSD. There was considerable variability in the background of veterans seeking disability status on the basis of PTSD. Of concern, only about half of these individuals were receiving any mental health treatment at the time of application. Most claimants reported seeking disability compensation for symbolic reasons, especially for acknowledgement, validation and relief from self-blame. Reasons having to do with improved finances were less frequently endorsed, although the importance of obtaining improved solvency through disability status decreased as income increased. The sense of investment in obtaining a sense of self-acceptance and acceptance from others through disability status varied by sociodemographic variables. Overall, findings suggest that individuals seeking disability benefits may have unmet mental health care needs, and that policy makers, investigators and providers should consider material benefit as one of many possible reasons for engaging in a disability compensation system.

Platelet serotonergic markers in posttraumatic stress disorder

The neurobiological basis of posttraumatic stress disorder (PTSD) is believed to involve alterations in different neurotransmitter systems, and recent studies elucidated the role of serotonin (5-hydroxytryptamine, 5-HT) in PTSD. The data on the role of 5-HT have been obtained using blood platelets as a peripheral model for central serotonergic neurons. The reports suggested that platelet 5-HT concentration and monoamine oxidase (MAO) activity might serve as biological, even trait, markers for particular mental disturbances. Since the data on the peripheral serotonergic markers in PTSD subjects are controversial, the aim of the study was to determine platelet 5-HT concentration and platelet MAO activity in war veterans with PTSD, war veterans who did not develop PTSD, and in war veterans who were prisoners of war and developed PTSD. Platelet 5-HT concentration and MAO activity did not differ significantly between war veterans with or without PTSD, and prisoners of war with PTSD. Clinician-Administered PTSD Scale (CAPS) scores did not differ between war veterans with PTSD and prisoners of war, but Montgomery–Asberg Depression Rating Scale (MADRS) scores were significantly higher in prisoners of war who developed PTSD than in war veterans with PTSD. There was no significant correlation between platelet 5-HT concentration or platelet MAO activity and CAPS or MADRS scores within these groups. Platelet 5-HT concentration was slightly higher and platelet MAO activity slightly lower in prisoners of war with PTSD, than in all other groups. These findings suggest that platelet 5-HT concentration and platelet MAO activity are not altered in three drug-free groups—war veterans who did or did not develop PTSD, or in prisoners of war with PTSD—and that these platelet serotonergic markers are not associated with symptoms of PTSD or comorbid depression.