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Open AccessJournal ArticleDOI

Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond.

TLDR
The available data suggest that targeting inflammation may serve as a potential therapeutic target for treating fear- and anxiety-based disorders in the future, but the field must continue to characterize the specific role pro-inflammatory signaling in the maintenance of these unique psychiatric conditions.
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This article is published in Neuropsychopharmacology.The article was published on 2017-01-01 and is currently open access. It has received 425 citations till now. The article focuses on the topics: Phobias & Fear-potentiated startle.

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Imaging the Role of Inflammation in Mood and Anxiety-related Disorders

TL;DR: Neuroimaging effects of inflammation on reward and threat circuitry may be used as biomarkers of inflammation for future development of novel therapeutic strategies to better treat mood and anxiety-related disorders in patients with high inflammation.
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Developmental Trajectories of Early Life Stress and Trauma: A Narrative Review on Neurobiological Aspects Beyond Stress System Dysregulation

TL;DR: A narrative review of relevant evidence from mainly human research on the ten most acknowledged neurobiological allostatic pathways exerting enduring adverse effects of ELS even decades later shows most findings back a causal relation between ELS and psychobiological maladjustment in later life.
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Inflammation-related biomarkers in major psychiatric disorders: a cross-disorder assessment of reproducibility and specificity in 43 meta-analyses.

TL;DR: A cross-disorder study by systematically evaluating the meta-analysis results of inflammation-related factors in eight major psychiatric disorders, showing that well-powered case–control studies provided more consistent results than underpowered studies when one factor was meta-analysed by different researchers.
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Integrating Endocannabinoid Signaling and Cannabinoids into the Biology and Treatment of Posttraumatic Stress Disorder.

TL;DR: It is proposed that a state of endocannabinoid deficiency could represent a stress susceptibility endophenotype predisposing to the development of trauma- related psychopathology and provide biologically plausible support for the self-medication hypotheses used to explain high rates of cannabis use in patients with trauma-related disorders.
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Oxidative Stress, Inflammation, and Neuroprogression in Chronic PTSD.

TL;DR: Evidence for the involvement of oxidative stress and inflammation in chronic PTSD and the neurobiological consequences of these processes, including accelerated cellular aging and neuroprogression are reviewed.
References
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Journal ArticleDOI

Lifetime Prevalence and Age-of-Onset Distributions of DSM-IV Disorders in the National Comorbidity Survey Replication

TL;DR: Lifetime prevalence estimates are higher in recent cohorts than in earlier cohorts and have fairly stable intercohort differences across the life course that vary in substantively plausible ways among sociodemographic subgroups.
Journal ArticleDOI

Posttraumatic stress disorder in the National Comorbidity Survey.

TL;DR: Progress in estimating age-at-onset distributions, cohort effects, and the conditional probabilities of PTSD from different types of trauma will require future epidemiologic studies to assess PTSD for all lifetime traumas rather than for only a small number of retrospectively reported "most serious" traumAs.
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A Meta-Analysis of Cytokines in Major Depression

TL;DR: A meta-analysis of studies measuring cytokine concentration in patients with major depression reports significantly higher concentrations of the proinflammatory cytokines TNF-alpha and IL-6 in depressed subjects compared with control subjects, strengthening evidence that depression is accompanied by activation of the IRS.
Journal ArticleDOI

The empirical status of cognitive-behavioral therapy: a review of meta-analyses.

TL;DR: The 16 meta-analyses reviewed support the efficacy of CBT for many disorders and are consistent with other review methodologies that also provide support for the efficacy CBT.
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Dysregulation of the stress axis in the face of increased sympathetic tone and decreased parasympathetic activity characteristic of anxiety disorders could further augment inflammation and contribute to increased symptoms by having direct effects on brain regions critical for the regulation of fear and anxiety (such as the prefrontal cortex, insula, amygdala, and hippocampus).