Evidence map›Paper›PMID 28049760›Full record

ArticleSchizophrenia bulletin2017

A Study of TNF Pathway Activation in Schizophrenia and Bipolar Disorder in Plasma and Brain Tissue.

Eva Zsuzsanna Hoseth, Thor Ueland, Ingrid Dieset, Rebecca Birnbaum, Joo Heon Shin, Joel Edward Kleinman, Thomas Michael Hyde, Ragni Helene Mørch, Sigrun Hope, Tove Lekva and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in Schizophrenia bulletin, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 2 pooled it
1.4field-weighted citation impact, top 22% 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

49 citing papers in PubMed, 2 syntheses or guidelines pooled it, 77 citations in OpenAlex.

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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

19 authors at 3 institutions in 2 countries.

Eva Zsuzsanna HosethNORMENT, KG Jebsen Centre for Psychosis Research Building 49, Oslo University Hospital, Ullevål Kirkeveien 166, PO Box 4956 Nydalen 0424, Oslo, Norway.
Thor UelandResearch Institute for Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Ingrid DiesetNORMENT, KG Jebsen Centre for Psychosis Research Building 49, Oslo University Hospital, Ullevål Kirkeveien 166, PO Box 4956 Nydalen 0424, Oslo, Norway.
Rebecca BirnbaumLieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, MD.
Joo Heon ShinLieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, MD.
Joel Edward KleinmanLieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, MD.
Thomas Michael HydeLieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, MD.
Ragni Helene MørchNORMENT, KG Jebsen Centre for Psychosis Research Building 49, Oslo University Hospital, Ullevål Kirkeveien 166, PO Box 4956 Nydalen 0424, Oslo, Norway.
Sigrun HopeNORMENT, KG Jebsen Centre for Psychosis Research Building 49, Oslo University Hospital, Ullevål Kirkeveien 166, PO Box 4956 Nydalen 0424, Oslo, Norway.
Tove LekvaResearch Institute for Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Aurelija Judita AbraityteResearch Institute for Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Annika E MichelsenResearch Institute for Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Ingrid MelleNORMENT, KG Jebsen Centre for Psychosis Research Building 49, Oslo University Hospital, Ullevål Kirkeveien 166, PO Box 4956 Nydalen 0424, Oslo, Norway.
Lars Tjelta WestlyeNORMENT, KG Jebsen Centre for Psychosis Research Building 49, Oslo University Hospital, Ullevål Kirkeveien 166, PO Box 4956 Nydalen 0424, Oslo, Norway.
Torill UelandNORMENT, KG Jebsen Centre for Psychosis Research Building 49, Oslo University Hospital, Ullevål Kirkeveien 166, PO Box 4956 Nydalen 0424, Oslo, Norway.
Srdjan DjurovicDepartment of Medical Genetics, Oslo University Hospital, Oslo, Norway.
Pål AukrustResearch Institute for Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Daniel R WeinbergerLieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, MD.
Ole Andreas AndreassenNORMENT, KG Jebsen Centre for Psychosis Research Building 49, Oslo University Hospital, Ullevål Kirkeveien 166, PO Box 4956 Nydalen 0424, Oslo, Norway.
Oslo University Hospital · NOLieber Institute for Brain Development · USJohns Hopkins University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: A proinflammatory imbalance in the tumor necrosis factor (TNF) system may contribute to the pathogenesis of schizophrenia (SCZ) and bipolar disorders (BDs) and related comorbidities. We investigated the relative distribution of TNF-related molecules in blood and dorsolateral prefrontal cortex (DLPFC) in these disorders. Method: We measured plasma levels of TNF, soluble TNF receptor 1 (sTNFR1), soluble TNF receptor 2 (sTNFR2), and a disintegrin and metalloprotease-17 (ADAM17) using enzyme immunoassays and calculated the TNF/sTNFRs ratio (TNF/sTNFR1+sTNFR2) in a sample of 816 SCZ and BD spectrum patients and 624 healthy controls (HCs). TNF, TNFRSF1A (TNFR1), TNFRSF1B (TNFR2), and ADAM17 mRNA levels were determined in whole blood, and postmortem DLPFC obtained from an independent cohort (n = 80 SCZ, n = 44 BD, and n = 86 HC). Results: In peripheral blood, we show increased TNF-related measures in patients compared to HC, with an increased TNF/sTNFRs ratio (p = 6.00 × 10-5), but decreased TNF mRNA expression (p = 1 × 10-4), with no differences between SCZ and BD. Whole blood ADAM17 mRNA expression was markedly higher in BD vs SCZ patients (p = 1.40 × 10-14) and vs HC (p = 1.22 × 10-8). In postmortem DLPFC, we found no significant differences in mRNA expression of TNF pathway genes between any groups. Conclusions: SCZ and BD patients have increased plasma TNF pathway markers without corresponding increase in blood cell gene expression. ADAM17 expression in leukocytes is markedly different between the two disorders, while alterations in TNF-related gene expression in DLPFC are uncertain. Further studies are necessary to elucidate the aberrant regulation of the TNF pathway in severe mental disorders.

Indexed as

ADAM17 ProteinAdultBipolar DisorderFemaleGene ExpressionHumansMaleMiddle AgedPrefrontal CortexReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IIRNA, MessengerSchizophreniaSignal TransductionTumor Necrosis Factor-alphaADAM17 ProteinADAM17 protein, humanReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IIRNA, MessengerTNFRSF1A protein, humanTNFRSF1B protein, humanTumor Necrosis Factor-alphacytokinesDLPFCmRNApostmortemworking memory

Identifiers

PMID28049760
PMCPMC5515106
OpenAlexW2566625959

What OpenQuestion holds

Textmetadata
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.