Cited by 595Tryptophan and brain disordersNeuroinflammation and Neurodegeneration MechanismsStress Responses and Cortisol

The role of inflammation and microglial activation in the pathophysiology of psychiatric disorders

Réus, G.Z., Fries, G.R., Stertz, L., Badawy, M., Passos, I.C., Barichello, T., Kapczinski, F., Quevedo, J.·2015·Neuroscience

Abstract

Psychiatric disorders, including major depressive disorder (MDD), bipolar disorder (BD) and schizophrenia, affect a significant percentage of the world population. These disorders are associated with educational difficulties, decreased productivity and reduced quality of life, but their underlying pathophysiological mechanisms are not fully elucidated. Recently, studies have suggested that psychiatric disorders could be considered as inflammatory disorders, even though the exact mechanisms underlying this association are not known. An increase in inflammatory response and oxidative stress may lead to inflammation, which in turn can stimulate microglia in the brain. Microglial activation is roused by the M1 phenotype, which is associated with an increase in interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). On the contrary, M2 phenotype is associated with a release of anti-inflammatory cytokines. Thus, it is possible that the inflammatory response from microglial activation can contribute to brain pathology, as well as influence treatment responses. This review will highlight the role of inflammation in the pathophysiology of psychiatric disorders, such as MDD, BD, schizophrenia, and autism. More specifically, the role of microglial activation and associated molecular cascades will also be discussed as a means by which these neuroinflammatory mechanisms take place, when appropriate.

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Crossref · 10.1016/j.neuroscience.2015.05.018

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  • Prenatal immune challenge by the viral mimetic PolyI:C causes a long-lasting sensitivity of the offspring to peri-pubertal stress and NMDAR antagonists.

    “Inflammation is also likely to be an aggravating factor in the effects of NMDAR hypofunction and oxidative stress: prenatal immune challenge by the viral mimetic Polyl:C causes a long-lasting sensitivity of the offspring to peri-pubertal stress and NMDAR antagonists 90 .”

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Authors
Réus, G. Z., Fries, G. R., Stertz, L., Badawy, M., Passos, I. C., Barichello, T., Kapczinski, F., & Quevedo, J.
Affiliations
  • Universidade do Extremo Sul Catarinense (BR)
  • Universidade Federal do Rio Grande do Sul (BR)
  • The University of Texas Health Science Center at Houston (US)
Corresponding author
Réus, G.Z.
Venue
Neuroscience
Publisher
Elsevier BV
Published
2015-08
Volume
300
Pages
141-154
ISSN
0306-4522 (ISSN-L)
OpenAlex
W297523562
Cited by
594
References
168
Citations by year
2026: 30 · 2025: 42 · 2024: 33 · 2023: 42 · 2022: 69 · 2021: 69 · 2020: 55 · 2019: 76 · 2018: 56 · 2017: 46 · 2016: 58 · 2015: 17
FWCI
3.32
Type
journal article
Language
en
Open access
closed
Locations
  • Neuroscience (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • CNPq
  • FAPESC
  • UNESC
  • ĹOréal/UNESCO/ABC Brazil Fellowship for Women in Science 2011
  • The University of Texas Medical School at Houston
Topics
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Keywords
neuroinflammation, microglial activation, mental illness, major depressive disorder, bipolar disorder, schizophrenia, autism spectrum disorder, M1/M2 microglial polarization, IL-1β, TNF-α, oxidative stress, anti-inflammatory cytokines, treatment response
MeSH terms
Animals, Mental Disorders, Brain, Humans, Inflammation, Microglia

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