Cytokines and schizophrenia: Microglia hypothesis of schizophrenia
Article first published online: 13 APR 2009
© 2009 The Authors. Journal compilation © 2009 Japanese Society of Psychiatry and Neurology
Psychiatry and Clinical Neurosciences
Volume 63, Issue 3, pages 257–265, June 2009
How to Cite
Monji, A., Kato, T. and Kanba, S. (2009), Cytokines and schizophrenia: Microglia hypothesis of schizophrenia. Psychiatry and Clinical Neurosciences, 63: 257–265. doi: 10.1111/j.1440-1819.2009.01945.x
- Issue published online: 14 MAY 2009
- Article first published online: 13 APR 2009
- Accepted 27 January 2009.
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.