Cytokines and schizophrenia: microglia hypothesis of schizophrenia
Abstract
The etiology of schizophrenia remains unclear, while there has been a growing amount of evidence for the neuroinflammation and immunogenetics, which are characterized by an increased serum concentration of several pro-inflammatory cytokines. Despite the fact that microglia comprise only <10% of the total brain cells, microglia respond rapidly to even minor pathological changes in the brain and may contribute directly to the neuronal degeneration by producing various pro-inflammatory cytokines and free radicals. In many aspects, the neuropathology of schizophrenia has recently been reported to be closely associatedwith microglial activation. Previous studies have shown the inhibitory effects of some typical/atypical antipsychotics on the release of inflammatory cytokines and free radicals from activated microglia, both of which have recently been known to cause a decrease in neurogenesis as well as white matter abnormalities in the brains of patients with schizophrenia. The microglia hypothesis of schizophrenia may shed new light on the therapeutic strategy for schizophrenia.
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Recent data from genome-wide association studies and analyses of postmortem human brain tissue have suggested that microglia and/or the complement cascade may also be involved in the development and pathogenesis of neurodevelopmental and psychiatric disorders.
“In addition to diseases associated with neurodegeneration, recent data from genome-wide association studies and analyses of postmortem human brain tissue have suggested that microglia and/or the complement cascade may also be involved in the development and pathogenesis of neurodevelopmental and psychiatric disorders (e.g., autism, obsessive compulsive disorder, schizophrenia, etc.) (Chen et al.,”
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- Authors
- Monji, A., Kato, T., & Kanba, S.
- Affiliations
- Kyushu University (JP)
- Corresponding author
- Monji, Akira
- Venue
- Psychiatry and Clinical Neurosciences
- Publisher
- Wiley
- Published
- 2009-05-14
- Volume
- 63
- Issue
- 3
- Pages
- 257-265
- ISSN
- 1323-1316 (ISSN-L)
- 1440-1819
- OpenAlex
- W2018838561
- Cited by
- 508
- References
- 9
- Citations by year
- 2026: 11 · 2025: 21 · 2024: 26 · 2023: 39 · 2022: 43 · 2021: 37 · 2020: 35 · 2019: 32 · 2018: 33 · 2017: 31 · 2016: 37 · 2015: 38 · 2014: 26 · 2013: 41 · 2012: 29
- FWCI
- 0.76
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Psychiatry and Clinical Neurosciences (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Keywords
- schizophrenia, microglia, neuroinflammation, inflammatory cytokines, microglial activation, immunogenetics, antipsychotic drugs, neurogenesis, white matter abnormalities, free radicals, neurodegeneration
- MeSH terms
- Animals, Humans, Inflammation, Schizophrenia, Antipsychotic Agents, Neuroimmunomodulation, Cytokines, Microglia, Models, Immunological, Neurogenesis
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