Evidence map›Paper›PMID 24569695›Full record

ArticleTranslational psychiatry2014

Markers of inflammation and stress distinguish subsets of individuals with schizophrenia and bipolar disorder.

S G Fillman, D Sinclair, S J Fung, M J Webster, C Shannon Weickert

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers, 11 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
118citing papers in PubMed, 11 pooled it
6.6field-weighted citation impact, top 2% 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

118 citing papers in PubMed, 11 syntheses or guidelines pooled it, 223 citations in OpenAlex.

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58 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 4 institutions in 2 countries.

S G Fillman1] Schizophrenia Research Institute, Sydney, NSW, Australia [2] Schizophrenia Research Laboratory, Neuroscience Research Australia, Sydney, NSW, Australia [3] School of Psychiatry, University of New South Wales, Sydney, NSW, Australia.
D Sinclair1] Schizophrenia Research Institute, Sydney, NSW, Australia [2] Schizophrenia Research Laboratory, Neuroscience Research Australia, Sydney, NSW, Australia [3] School of Psychiatry, University of New South Wales, Sydney, NSW, Australia [4] Department of Psychiatry, Neuropsychiatric Signaling Program, Center for Neurobiology and Behavior, University of Pennsylvania, Philadelphia, PA, USA.
S J Fung1] Schizophrenia Research Institute, Sydney, NSW, Australia [2] Schizophrenia Research Laboratory, Neuroscience Research Australia, Sydney, NSW, Australia [3] School of Psychiatry, University of New South Wales, Sydney, NSW, Australia.
M J WebsterLaboratory of Brain Research, Stanley Medical Research Institute, 9800 Medical Center Drive, Rockville, MD, USA.
C Shannon Weickert1] Schizophrenia Research Institute, Sydney, NSW, Australia [2] Schizophrenia Research Laboratory, Neuroscience Research Australia, Sydney, NSW, Australia [3] School of Psychiatry, University of New South Wales, Sydney, NSW, Australia.
UNSW Sydney · AUNeuroscience Research Australia · AUSchizophrenia Research Institute · AUStanley Medical Research Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Schizophrenia and bipolar disorder share a number of common features, both symptomatically and biologically. Abnormalities in the neuroimmune and the stress-signaling pathways have been previously identified in brains of individuals with both diseases. However, the possible relationship between abnormalities in stress and neuroimmune signaling within the cortex of people with psychotic illness has not been defined. To test the hypothesis that combined alterations in brain stress responsiveness and neuroimmune/inflammatory status are characteristic of some individuals suffering from major mental illness, we examined gene expression in the Stanley Array Cohort of 35 controls, 35 individuals with schizophrenia and 34 individuals with bipolar disorder. We used levels of 8 inflammatory-related transcripts, of which SERPINA3 was significantly elevated in individuals with schizophrenia (F(2,88)=4.137, P<0.05), and 12 glucocorticoid receptor signaling (stress) pathway transcripts previously examined, to identify two clusters of individuals: a high inflammation/stress group (n=32) and a low (n=68) inflammation/stress group. The high inflammation/stress group has a significantly greater number of individuals with schizophrenia (n=15), and a trend toward having more bipolar disorder individuals (n=11), when compared with controls (n=6). Using these subgroups, we tested which microarray-assessed transcriptional changes may be associated with high inflammatory/stress groups using ingenuity analysis and found that an extended network of gene expression changes involving immune, growth factors, inhibitory signaling and cell death factors also distinguished these groups. Our work demonstrates that some of the heterogeneity in schizophrenia and bipolar disorder may be partially explained by inflammation/stress interactions, and that this biological subtype cuts across Diagnostic and Statistical Manual of Mental Disorders (DSM)-defined categories.

Indexed as

Gene ExpressionAdultBiomarkersBipolar DisorderCerebral CortexCohort StudiesFemaleHumansInflammationMaleMiddle AgedSchizophreniaStress, PsychologicalYoung AdultBiomarkers

Identifiers

PMID24569695
PMCPMC3944638
OpenAlexW2081664670

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.