Neuroinflammation in schizophrenia especially focused on the role of microglia
Abstract
An accumulating body of evidence point to the significance of neuroinflammation and immunogenetics also in schizophrenia. Recent genome-wide studies in schizophrenia suggest immune involvement in schizophrenia. Microglia are the resident macrophage of the brain and major players in innate immunity in the CNS. They 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 is closely associated with microglial activation. We and other researchers have shown the inhibitory effects of some typical or atypical antipsychotics on the release of inflammatory cytokines and free radicals from activated microglia, both of which are not only directly toxic to neurons but also cause a decrease in neurogenesis as well as white matter abnormalities in the brains of the patients with schizophrenia. The treatment through the inhibition of microglial activation may shed new light on the therapeutic strategy of schizophrenia.
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Alterations in peripheral inflammatory profile are observed in several neurodevelopmental disorders including ADHD.
“Alterations in the peripheral inflammatory profile are observed in several neurodevelopmental disorders (Kim et al., 2016; Landaas et al., 2010; Monji et al., 2013; Vargas et al., 2005), including ADHD”
From Neuroinflammation as a risk factor for attention deficit hyperactivity disorder (2019) · cites this paper as Monji et al., 2013
A number of neuropsychiatric disorders including ASD, schizophrenia, depression, anxiety, and bipolar disorder have been associated with exposure to increased peripheral and/or central inflammatory response during perinatal development.
“a number of neuropsychiatric disorders including ASD (Vargas et al., 2005), schizophrenia (Monji et al., 2013), depression (Kim et al., 2016), anxiety, and bipolar disorder (Landaas et al., 2010) have also been associated with exposure to an increased peripheral and/or central inflammatory response during perinatal development.”
From Neuroinflammation as a risk factor for attention deficit hyperactivity disorder (2019) · cites this paper as Monji et al., 2013
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- Authors
- Monji, A., Kato, T. A., Mizoguchi, Y., Horikawa, H., Seki, Y., Kasai, M., Yamauchi, Y., Yamada, S., & Kanba, S.
- Affiliations
- Saga University (JP)
- Kyushu University (JP)
- Corresponding author
- Monji, Akira
- Venue
- Progress in Neuro-Psychopharmacology and Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2013-04
- Volume
- 42
- Pages
- 115-121
- ISSN
- 0278-5846 (ISSN-L)
- OpenAlex
- W1972578501
- Cited by
- 314
- References
- 130
- Citations by year
- 2026: 7 · 2025: 15 · 2024: 13 · 2023: 24 · 2022: 18 · 2021: 36 · 2020: 22 · 2019: 21 · 2018: 32 · 2017: 36 · 2016: 17 · 2015: 23 · 2014: 20 · 2013: 18 · 2012: 12
- FWCI
- 0.83
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Progress in Neuro-Psychopharmacology and Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Japan Society for the Promotion of Science (24650227)
- 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, neuroinflammation, microglia, microglial activation, innate immunity, inflammatory cytokines, free radicals, antipsychotic drugs, neurogenesis, white matter abnormalities, immunogenetics, neuroprotection
- MeSH terms
- Animals, Encephalitis, Free Radicals, Humans, Schizophrenia, Antipsychotic Agents, Cytokines, Microglia
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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