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Review
. 2016 Aug;21(8):1009-26.
doi: 10.1038/mp.2016.90. Epub 2016 Jun 7.

Postmortem Evidence of Cerebral Inflammation in Schizophrenia: A Systematic Review

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Free PMC article
Review

Postmortem Evidence of Cerebral Inflammation in Schizophrenia: A Systematic Review

M O Trépanier et al. Mol Psychiatry. .
Free PMC article

Abstract

Schizophrenia is a psychiatric disorder which has a lifetime prevalence of ~1%. Multiple candidate mechanisms have been proposed in the pathogenesis of schizophrenia. One such mechanism is the involvement of neuroinflammation. Clinical studies, including neuroimaging, peripheral biomarkers and randomized control trials, have suggested the presence of neuroinflammation in schizophrenia. Many studies have also measured markers of neuroinflammation in postmortem brain samples from schizophrenia patients. The objective of this study was to conduct a systematic search of the literature on neuroinflammation in postmortem brains of schizophrenia patients indexed in MEDLINE, Embase and PsycINFO. Databases were searched up until 20th March 2016 for articles published on postmortem brains in schizophrenia evaluating microglia, astrocytes, glia, cytokines, the arachidonic cascade, substance P and other markers of neuroinflammation. Two independent reviewers extracted the data. Out of 5385 articles yielded by the search, 119 articles were identified that measured neuroinflammatory markers in schizophrenic postmortem brains. Glial fibrillary acidic protein expression was elevated, lower or unchanged in 6, 6 and 21 studies, respectively, and similar results were obtained for glial cell densities. On the other hand, microglial markers were increased, lower or unchanged in schizophrenia in 11, 3 and 8 studies, respectively. Results were variable across all other markers, but SERPINA3 and IFITM were consistently increased in 4 and 5 studies, respectively. Despite the variability, some studies evaluating neuroinflammation in postmortem brains in schizophrenia suggest an increase in microglial activity and other markers such as SERPINA3 and IFITM. Variability across studies is partially explained by multiple factors including brain region evaluated, source of the brain, diagnosis, age at time of death, age of onset and the presence of suicide victims in the cohort.

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Figure 1
Figure 1
Systematic search results.

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References

    1. Tandon R, Keshavan MS, Nasrallah HA. Schizophrenia, ‘just the facts' what we know in 2008. 2. Epidemiology and etiology. Schizophr Res 2008; 102: 1–18. - PubMed
    1. van Os J, Kapur S. Schizophrenia. Lancet 2009; 374: 635–645. - PubMed
    1. Insel TR. Rethinking schizophrenia. Nature 2010; 468: 187–193. - PubMed
    1. Roussos P, Haroutunian V. Schizophrenia: susceptibility genes and oligodendroglial and myelin related abnormalities. Front Cell Neurosci 2014; 8: 5. - PMC - PubMed
    1. Karoutzou G, Emrich HM, Dietrich DE. The myelin-pathogenesis puzzle in schizophrenia: a literature review. Mol Psychiatry 2008; 13: 245–260. - PubMed

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