Evidence map›Paper›PMID 27271499›Full record

SynthesisMolecular psychiatry2016

Postmortem evidence of cerebral inflammation in schizophrenia: a systematic review.

M O Trépanier, K E Hopperton, R Mizrahi, N Mechawar, R P Bazinet

Open access · bronzeAbstract readSystematic Review
PubMed Full text at PMC Publisher
In one paragraph

Synthesis in Molecular psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 209 papers, 15 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
209citing papers in PubMed, 15 pooled it
12.9field-weighted citation impact, top 1% of its field
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

209 citing papers in PubMed, 15 syntheses or guidelines pooled it, 354 citations in OpenAlex.

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  4. White-matter free-water diffusion MRI in schizophrenia: a systematic review and meta-analysis.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022
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149 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

5 authors at 3 institutions in 1 country.

M O TrépanierDepartment of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, ON, Canada.
K E HoppertonDepartment of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, ON, Canada.
R MizrahiResearch Imaging Centre, Centre for Addiction and Mental Health, Toronto, ON, Canada.
N MechawarMcGill Group for Suicide Studies, Douglas Mental Health University Institute, Montreal, QC, Canada.
R P BazinetDepartment of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, ON, Canada.
University of Toronto · CACentre for Addiction and Mental Health · CADouglas Mental Health University Institute · CA

Funding

CIHR 303157
6 · The paper itself

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.

Indexed as

AstrocytesAutopsyBrainCytokinesFemaleGlial Fibrillary Acidic ProteinHumansInflammationMaleMicrogliaNeurogliaNeuroimmunomodulationSchizophreniaCytokinesGlial Fibrillary Acidic Protein

Identifiers

PMID27271499
PMCPMC4960446
OpenAlexW2415131480

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.