Role of Inflammation in Psychiatric Disease (2015)

Role of Inflammation in Psychiatric Disease

This chapter is built on increasing evidence that individuals diagnosed with a wide range of currently recognized psychiatric diseases show significant increases in peripheral inflammatory biomarkers and CNS markers of immune activation, while simultaneously evincing reduced effectiveness of immune elements important for protection against pathogens. From this foundational assumption, a number of central unanswered questions regarding the relationship of immunity to emotional and cognitive functioning and behavior are explored. Tentative conclusions are reached that in addition to being impacted by mental events, immune activity may contribute to the development of a wide range of psychiatric disorders, and may tend to promote different disorders at different stages of the life course.

  • Evidence That the Immune System is Involved in Psychiatric Disease Pathogenesis
  • Behavioral Abnormalities Associated with Immune Activation
  • Long-Term Behavioral Abnormalities Associated with Immune Activation Prenatally or in Early Life
  • Mechanisms by which Immune Activation (Inflammation) Produces Behavioral Disturbance
  • Effects of Inflammation on Neuroendocrine Mechanisms
  • Effects of Inflammation on Brain Biochemical Pathways Relevant to Psychiatric Disease
    – Monoamine Neurotransmitter Function
  • Mechanisms of Inflammatory Effects on Monoamine Metabolism
    – Indoleamine 2,3-Dioxygenase
    – Mitogen-Activated Protein Kinase
    -Tetrahydrobiopterin
    – Glutamate and γ-Aminobutyric Acid
  • Effects of Inflammation on Functional Brain Neurocircuitry
    – Basal Ganglia
    – Anterior Cingulate Cortex
  • Evidence that Patterns of CNS Activity Associated with Psychiatric Disease Affect Immune Functioning in Health-Relevant Ways
  • Psychosocial Stress and Promotion of the Proinflammatory Phenotype
  • Stress Outflow Mechanisms by Which Psychosocial Stress Affects Immunity
    – Hypothalamic–Pituitary–Adrenal Axis
    – Autonomic Nervous System
  • Evidence that Environmental Factors that Promote Psychiatric Morbidity May Do So By Altering Immune Function
  • Role of Disrupted Human–Microbial and Human–Parasitic Relationships in the Development of Psychiatric Disease
  • Evidence that Psychiatric Conditions Are Associated with Alterations in Peripheral and CNS Immune Activity

Inflammation impairs social cognitive processing: a randomized controlled trial of endotoxin

Neuropsychiatric disorders (e.g., autism, schizophrenia) are partially characterized by social cognitive deficits, including impairments in the ability to perceive others’ emotional states, which is an aspect of social cognition known as theory of mind (ToM). There is also evidence that inflammation may be implicated in the etiology of these disorders, but experimental data linking inflammation to deficits in social cognition is sparse. Thus, we examined whether exposure to an experimental inflammatory challenge led to changes in ToM. One hundred and fifteen (n=115) healthy participants were randomly assigned to receive either endotoxin, which is an inflammatory challenge, or placebo. Participants completed a social cognition task, the Reading the Mind in the Eyes (RME) test, at baseline and at the peak of inflammatory response for the endotoxin group. The RME test, a validated measure of ToM, evaluates how accurately participants can identify the emotional state of another person by looking only at their eyes. We found that endotoxin (vs. placebo) led to decreases in performance on the RME test from baseline to the peak of inflammatory response, indicating that acute inflammation can lead to decreases in the ability to accurately and reliably comprehend emotional information from others. Given that deficits in ToM are implicated in neuropsychiatric disorders, including those which may have an inflammatory basis, these results may have implications for understanding the links between inflammation, social cognition, and neuropsychiatric disorders.

IL-6, IL-18, sIL-2R, and TNFα proinflammatory markers in depression and schizophrenia patients who are free of overt inflammation

See also:

A role for the microbiome in schizophrenia?

Stage specific and prophylactic treatments?

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