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Updated: May 26, 2026

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
Published on: January 30, 2014
Neuroinflammation in schizophrenia especially focused on the role of microglia
Akira Monji1, Takahiro A Kato, Yoshito Mizoguchi
1Department of Psychiatry, Faculty of Medicine, Saga University Hospital, Nabeshima 5-1-1, Saga 849-8501, Japan. amonji@hf.rim.or.jp
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.
Insights
Neuroinflammation and microglia activation play key roles in schizophrenia. Antipsychotic drugs can inhibit these processes, offering new therapeutic strategies for schizophrenia treatment.
Area of Science:
- Neuroscience
- Immunology
- Psychiatry
Background:
- Schizophrenia is increasingly linked to neuroinflammation and immunogenetics.
- Genome-wide studies highlight immune system involvement in schizophrenia.
- Microglia, the brain's immune cells, are central to neuroinflammation.
Purpose of the Study:
- To explore the role of microglial activation in schizophrenia neuropathology.
- To investigate the impact of antipsychotics on microglial inflammatory responses.
- To assess the potential of targeting microglial activation as a therapeutic strategy for schizophrenia.
Main Methods:
- Review of existing evidence on neuroinflammation in schizophrenia.
- Analysis of studies on microglial activation and its mediators (cytokines, free radicals).
- Examination of the effects of typical and atypical antipsychotics on activated microglia.
Main Results:
- Microglial activation is closely associated with schizophrenia neuropathology.
- Activated microglia produce neurotoxic inflammatory cytokines and free radicals.
- Antipsychotics demonstrate inhibitory effects on inflammatory mediators released by activated microglia.
- These inflammatory processes contribute to neuronal degeneration, reduced neurogenesis, and white matter abnormalities in schizophrenia.
Conclusions:
- Inhibition of microglial activation presents a promising therapeutic avenue for schizophrenia.
- Understanding the interplay between microglia and antipsychotic drugs can refine treatment strategies.
- Targeting neuroinflammation offers a novel approach to managing schizophrenia.
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