Evidence map›Paper›PMID 28350400›Full record

SynthesisTranslational psychiatry2017

Immune involvement in the pathogenesis of schizophrenia: a meta-analysis on postmortem brain studies.

C F M G van Kesteren, H Gremmels, L D de Witte, E M Hol, A R Van Gool, P G Falkai, R S Kahn, I E C Sommer

Abstract readMeta-AnalysisSystematic Review
In one paragraph

Synthesis in Translational psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 192 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
192citing papers in PubMed, 8 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

192 citing papers in PubMed, 8 syntheses or guidelines pooled it.

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  12. Functional genomic profiling of schizophrenia-associated genes reveals key microglial regulators.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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132 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

C F M G van KesterenDepartment of Psychiatry, Brain Center Rudolf Magnus Institute, University Medical Center Utrecht, Utrecht, The Netherlands.
H GremmelsDepartment of Nephrology and Hypertension, University Medical Center Utrecht, Utrecht, The Netherlands.
L D de WitteDepartment of Psychiatry, Brain Center Rudolf Magnus Institute, University Medical Center Utrecht, Utrecht, The Netherlands.
E M HolDepartment of Translational Neuroscience, Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht, The Netherlands.
A R Van GoolDepartment of Psychiatry, Yulius Mental Health Organization, Barendrecht, The Netherlands.
P G FalkaiDepartment of Psychiatry and Psychotherapy, Ludwig Maximilian University, Munich, Germany.
R S KahnDepartment of Psychiatry, Brain Center Rudolf Magnus Institute, University Medical Center Utrecht, Utrecht, The Netherlands.
I E C SommerDepartment of Psychiatry, Brain Center Rudolf Magnus Institute, University Medical Center Utrecht, Utrecht, The Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although the precise pathogenesis of schizophrenia is unknown, genetic, biomarker and imaging studies suggest involvement of the immune system. In this study, we performed a systematic review and meta-analysis of studies investigating factors related to the immune system in postmortem brains of schizophrenia patients and healthy controls. Forty-one studies were included, reporting on 783 patients and 762 controls. We divided these studies into those investigating histological alterations of cellular composition and those assessing molecular parameters; meta-analyses were performed on both categories. Our pooled estimate on cellular level showed a significant increase in the density of microglia (P=0.0028) in the brains of schizophrenia patients compared with controls, albeit with substantial heterogeneity between studies. Meta-regression on brain regions demonstrated this increase was most consistently observed in the temporal cortex. Densities of macroglia (astrocytes and oligodendrocytes) did not differ significantly between schizophrenia patients and healthy controls. The results of postmortem histology are paralleled on the molecular level, where we observed an overall increase in expression of proinflammatory genes on transcript and protein level (P=0.0052) in patients, while anti-inflammatory gene expression levels were not different between schizophrenia and controls. The results of this meta-analysis strengthen the hypothesis that components of the immune system are involved in the pathogenesis of schizophrenia.

Indexed as

AstrocytesAutopsyBrainCase-Control StudiesCell CountHumansInflammationMicrogliaOligodendrogliaSchizophreniaTemporal LobeTranscriptome

Identifiers

PMID28350400
PMCPMC5404615

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.