The DOI matches its Crossref record; 168 of the 168 references it cites were found in a registry or an index.
The role of inflammation and microglial activation in the pathophysiology of psychiatric disorders
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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“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 .”
From Linking early-life NMDAR hypofunction and oxidative stress in schizophrenia pathogenesis (2016) · cites this paper as [90]
Citations
Cites
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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).”
Background
Metadata
- 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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