Neuroprogression in post-traumatic stress disorder

2019 ◽  
pp. 107-128
Author(s):  
Ryan M. Cassidy ◽  
Ives Cavalcante Passos ◽  
Márcia Kauer-Sant’Anna
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Cognitive Impairments ◽  
Post Traumatic Stress ◽  
Stress Markers ◽  
Post Traumatic ◽  
The Brain ◽  
And Oxidative Stress

Post-traumatic stress disorder (PTSD) has a lifetime prevalence of 10–12% in women and 5–6% in men. Patients with PTSD are at greater risk for obesity, type 2 diabetes mellitus, atherosclerosis, and myocardial infarction. In addition, a subset of these patients develops cognitive impairments unattributable to age or disease comorbidity alone, with hippocampal and prefrontal cortex atrophy. This chapter aims to review the evidence for neuroprogression in PTSD. This concept has been proposed as the pathological rewiring of the brain that takes place in parallel with the clinical and neurocognitive deterioration in the course of some psychiatric disorders. We will also review the biological pathways underlying neuroprogression in PTSD, including changes in inflammatory cytokines, corticosteroids, neurotrophins, and oxidative stress markers.

Putative Blood Somatic Mutations in Post-Traumatic Stress Disorder-Symptomatic Soldiers: High Impact of Cytoskeletal and Inflammatory Proteins

2021 ◽  
Vol 79 (4) ◽  
pp. 1723-1734
Author(s):  
Shlomo Sragovich ◽  
Michael Gershovits ◽  
Jacqueline C.K. Lam ◽  
Victor O.K. Li ◽  
Illana Gozes
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Somatic Mutations ◽  
Stress Disorder ◽  
Ptsd Symptom ◽  
High Impact ◽  
Post Traumatic Stress ◽  
Blood Samples ◽  
Post Traumatic ◽  
The Brain

Background: We recently discovered autism/intellectual disability somatic mutations in postmortem brains, presenting higher frequency in Alzheimer’s disease subjects, compared with the controls. We further revealed high impact cytoskeletal gene mutations, coupled with potential cytoskeleton-targeted repair mechanisms. Objective: The current study was aimed at further discerning if somatic mutations in brain diseases are presented only in the most affected tissue (the brain), or if blood samples phenocopy the brain, toward potential diagnostics. Methods: Variant calling analyses on an RNA-seq database including peripheral blood samples from 85 soldiers (58 controls and 27 with symptoms of post-traumatic stress disorder, PTSD) was performed. Results: High (e.g., protein truncating) as well as moderate impact (e.g., single amino acid change) germline and putative somatic mutations in thousands of genes were found. Further crossing the mutated genes with autism, intellectual disability, cytoskeleton, inflammation, and DNA repair databases, identified the highest number of cytoskeletal-mutated genes (187 high and 442 moderate impact). Most of the mutated genes were shared and only when crossed with the inflammation database, more putative high impact mutated genes specific to the PTSD-symptom cohorts versus the controls (14 versus 13) were revealed, highlighting tumor necrosis factor specifically in the PTSD-symptom cohorts. Conclusion: With microtubules and neuro-immune interactions playing essential roles in brain neuroprotection and Alzheimer-related neurodegeneration, the current mutation discoveries contribute to mechanistic understanding of PTSD and brain protection, as well as provide future diagnostics toward personalized military deployment strategies and drug design.

scholarly journals Unique relations between post-traumatic stress disorder symptoms and patient functioning in type 2 diabetes

2017 ◽  
Vol 25 (5) ◽  
pp. 652-664
Author(s):  
Danielle Arigo ◽  
Vanessa Juth ◽  
Paula Trief ◽  
Kenneth Wallston ◽  
Jan Ulbrecht ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Diabetes Distress ◽  
Post Traumatic Stress ◽  
Glucose Testing ◽  
Blood Glucose Testing ◽  
Post Traumatic

This study examined reported post-traumatic stress disorder symptoms in adults with poorly controlled type 2 diabetes who had no history of psychiatric diagnosis or treatment ( n = 184, MHbA1c = 9.13%, standard deviation = 1.68). Participants reported moderate to severe intensity of post-traumatic stress disorder symptoms ( M = 19.17, SD = 17.58). Together, depressive and post-traumatic stress disorder symptoms accounted for 10–40 percent of the variance in type 2 diabetes outcomes; post-traumatic stress disorder symptoms were associated with elevated diabetes distress and more frequent exercise and self-blood glucose testing (unique R2 ~ 3%). Post-traumatic stress disorder symptoms may be overlooked in type 2 diabetes among patients without formal psychiatric diagnoses, and warrant increased attention.

Evidence of diffuse damage in frontal and occipital cortex in the brain of patients with post-traumatic stress disorder

2011 ◽  
Vol 33 (1) ◽  
pp. 59-68 ◽  
Author(s):  
Maricla Tavanti ◽  
Marco Battaglini ◽  
Federico Borgogni ◽  
Letizia Bossini ◽  
Sara Calossi ◽  
...  
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Occipital Cortex ◽  
Post Traumatic Stress ◽  
Post Traumatic ◽  
The Brain

scholarly journals Levels of biogenic amines in the brain of rats at experimental post-traumatic stress disorder development

2015 ◽  
Vol 96 (5) ◽  
pp. 806-810
Author(s):  
R V Deev ◽  
Yu M Shatrova ◽  
A I Sinitskiy ◽  
N S Molchanova ◽  
A K Yunusova ◽  
...  
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Acid Level ◽  
Stress Disorder ◽  
Aminobutyric Acid ◽  
Behavioral Activity ◽  
Gamma Aminobutyric Acid ◽  
Post Traumatic Stress ◽  
Post Traumatic ◽  
The Brain

Aim. To study the changes in levels of biogenic amines-neurotransmitters in the brain at experimental post-traumatic stress disorder development in rats. Methods. Post-traumatic stress disorder was modeled by keeping 48 outbred male rats in under constant and inescapable strong unconditioned stimulus. The control group included 16 intact animals, not exposed to stress influences. The levels of 3,4-dihydroxyphenylalanine, dopamine, norepinephrine, epinephrine and gamma-aminobutyric acid were determined by fluorometric methods. Behavioral activity of animals was evaluated on the day 3, 7, 10 and 14 by «open field» and «elevated plus maze» actinographs. Results. When comparing the concentrations of studied neurotransmitters in the brain of control animals with experimental groups, reflecting the development of post-traumatic stress disorder at the time, adrenaline and 3,4-dihydroxyphenylalanine levels were increased on the third day, level of norepinephrine was reduced on the seventh day, 3,4-dihydroxyphenylalanine, dopamine, norepinephrine levels were elevaled, gamma-aminobutyric acid level was reduced on the tenth day, gamma-aminobutyric acid level was increased on the fourteenth day after the stress. Conclusion. According to the results of the correlation analysis, the largest contribution to the development of behavioral disorders are made by altered brain level of gamma-aminobutyric acid at the time of post-traumatic stress disorder formation (tenth and fourteenth day). At the earlier stages (third and seventh day), the relationship of rats behavioral activity and altered 3,4-dihydroxyphenylalanine and norepinephrine brain levels was shown.

Hormonal Contraception and the Brain: Examining Cognition and Psychiatric Disorders

2019 ◽  
Vol 15 (2) ◽  
pp. 116-131
Author(s):  
Stephanie Laird ◽  
Luke J. Ney ◽  
Kim L. Felmingham ◽  
Andrea Gogos
Keyword(s):  
Bipolar Disorder ◽  
Anxiety Disorders ◽  
Psychiatric Disorders ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Oral Contraceptive Pill ◽  
Post Traumatic Stress ◽  
Post Traumatic ◽  
The Brain

Background: The combined oral contraceptive pill (OC), containing synthetic estrogens and progestins, is used by millions of women worldwide, yet little is known about its effects on cognition or on psychiatric disorders. The progestin component of OCs determines their androgenicity, i.e. whether the OC has androgen binding components with masculinising effects or antiandrogenic components with feminising effects. Objective: The present review discusses the literature surrounding OC use and cognition in healthy women. Given the important role that sex hormones play in psychiatric disorders, we also consider the influence of OCs on symptoms of schizophrenia, post-traumatic stress disorder, depression, bipolar disorder, anxiety disorders and indirectly, sleep quality. Results: Research has shown that while there are no differences between OC users and non-users, androgenic OCs enhance visuospatial ability and anti-androgenic OCs enhance verbal fluency. Little is known about OCs effects on other cognitive domains, such as memory and executive function. There is little research examining OC use in schizophrenia, post-traumatic stress disorder, bipolar disorder and anxiety disorders. There is some evidence that OC use is associated with depression, however the exact causality of this association remains to be verified. Conclusion: We maintain that future studies need to address several methodological limitations, such as separating OCs based on androgenicity to avoid the masking effects that occur when various OCs are considered as one group. As this review highlights several significant effects of OC use on the brain, the implications of OC use needs to be considered in future research.

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