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

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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

DOI 10.1016/j.neuroscience.2015.05.018

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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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Focal brain inflammation and autism
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Host-Pathogen Interactions: Subversion and Utilization of the NF-κB Pathway during Infection
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L-glutamate released from activated microglia downregulates astrocytic L-glutamate transporter expression in neuroinflammation: the ‘collusion’ hypothesis for increased extracellular L-glutamate concentration in neuroinflammation
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Valproate pretreatment protects dopaminergic neurons from LPS-induced neurotoxicity in rat primary midbrain cultures: role of microglia
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Evidence for morphological alterations in prefrontal white matter glia in schizophrenia and bipolar disorder
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Molecular mechanism and therapeutic modulation of high mobility group box 1 release and action: an updated review
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Aberrant NF-KappaB Expression in Autism Spectrum Condition: A Mechanism for Neuroinflammation
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Altered Peripheral and Central Inflammatory Responses in a Mouse Model of Autism
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Neuropathological and neuromorphometric abnormalities in bipolar disorder: View from the medial prefrontal cortical network
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Morphometric post-mortem studies in bipolar disorder: possible association with oxidative stress and apoptosis
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The Cytokine Model of Schizophrenia: Emerging Therapeutic Strategies
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Hypolocomotive behaviour associated with increased microglia in a prenatal immune activation model with relevance to schizophrenia
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Tryptophan breakdown is increased in euthymic overweight individuals with bipolar disorder: a preliminary report
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Myeloid dendritic cells frequencies are increased in children with autism spectrum disorder and associated with amygdala volume and repetitive behaviors
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Imipramine reverses alterations in cytokines and BDNF levels induced by maternal deprivation in adult rats
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Ketamine ameliorates depressive-like behaviors and immune alterations in adult rats following maternal deprivation
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Ketamine and imipramine in the nucleus accumbens regulate histone deacetylation induced by maternal deprivation and are critical for associated behaviors
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A New Pathophysiological Aspect of S100B in Schizophrenia: Potential Regulation of S100B by Its Scavenger Soluble RAGE
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Glial pathology is modified by age in mood disorders — A systematic meta-analysis of serum S100B in vivo studies
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Corticosteroids limit microglial activation occurring during acute stress
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Altered intracellular signaling cascades in peripheral blood mononuclear cells from BD patients
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“In addition, minocycline, which is a suppressor of activated microglia, has been shown to exert protective effects by reducing microglial activation, oxidative stress and inflammation (Réus et al., 2015).”
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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.
ORCID: Réus, G.Z.
Fries, G.R.
Stertz, L.
Badawy, M.
Passos, I.C.
Barichello, T.
Kapczinski, F.
Quevedo, J.
Venue: Neuroscience
Publisher: Elsevier BV
Published: 2015-08
Volume: 300
Pages: 141-154
ISSN: 0306-4522 (ISSN-L)
DOI: 10.1016/j.neuroscience.2015.05.018
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
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
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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The role of inflammation and microglial activation in the pathophysiology of psychiatric disorders

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