Neuroinflammatory pathways in anxiety, posttraumatic stress, and obsessive compulsive disorders

Furtado, Melissa; Katzman, Martin A.

doi:10.1016/j.psychres.2015.05.036

Cited by 150 publications

(106 citation statements)

References 86 publications

(166 reference statements)

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“…In addition to the previously discussed effects of the HPA axis on cytokines, cytokines can influence HPA axis signaling and impair cellular processes by stimulating oxidative stress. The sequela that follows cytokine-induced changes in the HPA axis and central nervous system has been proposed to lead to the manifestation of PTSD symptoms [19]. This proposition is consistent with results of a study using the predator exposure animal model of PTSD that demonstrated elevated levels of pro-inflammatory cytokines and reactive oxygen species in the brain (hippocampus, amygdala, pre-frontal cortex) and in the periphery as a consequence of stressor exposure [20].…”

Section: Candidate Mechanisms Linking Ptsd and Immune Dysfunctionsupporting

confidence: 81%

Co-morbidity of PTSD and immune system dysfunction: opportunities for treatment

Neigh

Ali

2016

Current Opinion in Pharmacology

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Posttraumatic stress disorder (PTSD) is defined as a psychiatric disorder; however, PTSD co-occurs with multiple somatic manifestations. People living with PTSD commonly manifest dysregulations in the systems that regulate the stress response, including the hypothalamic-pituitary-adrenal (HPA) axis, and development of a pro-inflammatory state. Additionally, somatic autoimmune and inflammatory diseases and disorders have a high rate of co-morbidity with PTSD. Recognition and understanding of the compounding effect that these disease states can have on each other, evidenced from poorer treatment outcomes and accelerated disease progression in patients suffering from co-morbid PTSD and/or other autoimmune and inflammatory diseases, has the potential to lead to additional treatment opportunities.

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Section: Candidate Mechanisms Linking Ptsd and Immune Dysfunctionsupporting

confidence: 81%

Co-morbidity of PTSD and immune system dysfunction: opportunities for treatment

Neigh

Ali

2016

Current Opinion in Pharmacology

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“…Emerging evidence suggests that inflammation and activation of cell‐mediated immunity contribute to the risk of depression (Lotrich et al. 2011), anxiety disorders (Furtado and Katzman 2015), and bipolar disorder (Rosenblat and McIntyre 2015); thus, the inflammation associated with MS and with diseases such as diabetes (Spranger et al. 2003), chronic lung disease (Fahy 2015), or IBD, may promote psychiatric disorders in susceptible individuals.…”

Section: Discussionmentioning

confidence: 99%

Physical comorbidities increase the risk of psychiatric comorbidity in multiple sclerosis

et al. 2016

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BackgroundRisk factors for psychiatric comorbidity in multiple sclerosis (MS) are poorly understood.ObjectiveWe evaluated the association between physical comorbidity and incident depression, anxiety disorder, and bipolar disorder in a MS population relative to a matched general population cohort.MethodsUsing population‐based administrative data from Alberta, Canada we identified 9624 persons with MS, and 41,194 matches. Using validated case definitions, we estimated the incidence of depression, anxiety disorder, and bipolar disorder, and their association with physical comorbidities using Cox regression, adjusting for age, sex, socioeconomic status, and index year.ResultsIn both populations, men had a lower risk of depression and anxiety disorders than women, as did individuals who were ≥45 years versus <45 years at the index date. The risk of bipolar disorder declined with increasing age. The risks of incident depression (HR 1.92; 1.82–2.04), anxiety disorders (HR 1.52; 1.42–1.63), and bipolar disorder (HR 2.67; 2.29–3.11) were higher in the MS population than the matched population. These associations persisted essentially unchanged after adjustment for covariates including physical comorbidities. Multiple physical comorbidities were associated with psychiatric disorders in both populations.ConclusionPersons with MS are at increased risk of psychiatric comorbidity generally, and some physical comorbidities are associated with additional risk.

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“…Increased sEH expression has been observed with anorexia nervosa in human clinical patients which may be associated with depression and anxiety (Scott-Van Zeeland, et al, 2014; Shih, et al, 2016). Additionally, there may be a role neuroinflammation plays in the pathogenesis of anxiety, post-traumatic stress disorder and obsessive compulsive disorder (Furtado & Katzman, 2015) and thus an opportunity for sEH inhibition to improve mental health as well as physical ailment is very broad.…”

Section: Seh As a Target For Neurodegenerative Diseasesmentioning

confidence: 99%

Soluble epoxide hydrolase as a therapeutic target for pain, inflammatory and neurodegenerative diseases

Wagner

McReynolds

Schmidt

et al. 2017

Pharmacology & Therapeutics

225

204

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Eicosanoids are biologically active lipid signaling molecules derived from polyunsaturated fatty acids. Many of the actions of eicosanoid metabolites formed by cyclooxygenase and lipoxygenase enzymes have been characterized, however, the epoxy-fatty acids (EpFAs) formed by cytochrome P450 enzymes are newly described by comparison. The EpFA metabolites modulate a diverse set of physiologic functions that include inflammation and nociception among others. Regulation of EpFAs occurs primarily via release, biosynthesis and enzymatic transformation by the soluble epoxide hydrolase (sEH). Targeting sEH with small molecule inhibitors has enabled observation of the biological activity of the EpFAs in vivo in animal models, greatly contributing to the overall understanding of their role in the inflammatory response. Their role in modulating inflammation has been demonstrated in disease models including cardiovascular pathology and inflammatory pain, but extends to neuroinflammation and neuroinflammatory disease. Moreover, while the EpFA demonstrate activity against inflammatory pain, interestingly, this action extends to blocking chronic neuropathic pain as well. This review outlines the role of modulating sEH and the biological action of EpFA in models of pain and inflammatory diseases.

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Neuroinflammatory pathways in anxiety, posttraumatic stress, and obsessive compulsive disorders

Cited by 150 publications

References 86 publications

Co-morbidity of PTSD and immune system dysfunction: opportunities for treatment

Co-morbidity of PTSD and immune system dysfunction: opportunities for treatment

Physical comorbidities increase the risk of psychiatric comorbidity in multiple sclerosis

Soluble epoxide hydrolase as a therapeutic target for pain, inflammatory and neurodegenerative diseases

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