Evidence map›Paper›PMID 20585325›Full record

ArticleMolecular psychiatry2011

Impaired glycolytic response in peripheral blood mononuclear cells of first-onset antipsychotic-naive schizophrenia patients.

M Herberth, D Koethe, T M K Cheng, N D Krzyszton, S Schoeffmann, P C Guest, H Rahmoune, L W Harris, L Kranaster, F M Leweke and 1 more

Open access · bronzeAbstract readComparative Study
PubMed Publisher
In one paragraph

Article in Molecular psychiatry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 2 pooled it
3.0field-weighted citation impact, top 9% 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

43 citing papers in PubMed, 2 syntheses or guidelines pooled it, 96 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Peripheral immune-cell bioenergetics in acute and stable schizophrenia.European archives of psychiatry and clinical neuroscience · 2026
    Article
  4. Review
  5. Review
  6. Article
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  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
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  15. Proteomics and Schizophrenia: The Evolution of a Great Partnership.Advances in experimental medicine and biology · 2022
    Article
  16. Serum Levels andFrontiers in psychiatry · 2022
    Article
  17. Review
  18. Article
  19. Article
  20. Article
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

11 authors at 3 institutions in 2 countries.

M HerberthInstitute of Biotechnology, University of Cambridge, Cambridge, UK.
D Koethe
T M K Cheng
N D Krzyszton
S Schoeffmann
P C Guest
H Rahmoune
L W Harris
L Kranaster
F M Leweke
S Bahn
University of Cambridge · GBCentral Institute of Mental Health · DEUniversity of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Little is known about the biological mechanisms underpinning the pathology of schizophrenia. We have analysed the proteome of stimulated and unstimulated peripheral blood mononuclear cells (PBMCs) from schizophrenia patients and controls as a potential model of altered cellular signaling using liquid-chromatography mass spectrometry proteomic profiling. PBMCs from patients and controls were stimulated for 72 h in vitro using staphylococcal enterotoxin B. In total, 18 differentially expressed proteins between first-onset, antipsychotic-naive patients and controls in the unstimulated and stimulated conditions were identified. Remarkably, eight of these proteins were associated with the glycolytic pathway and patient-control differences were more prominent in stimulated compared with unstimulated PBMCs. None of these proteins were altered in chronically ill antipsychotic-treated patients. Non-linear multivariate statistical analysis showed that small subsets of these proteins could be used as a signal for distinguishing first-onset patients from controls with high precision. Functional analysis of PBMCs did not reveal any difference in the glycolytic rate between patients and controls despite increased levels of lactate and the glucose transporter-1, and decreased levels of the insulin receptor in patients. In addition, subjects showed increased serum levels of insulin, consistent with the idea that some schizophrenia patients are insulin resistant. These results show that schizophrenia patients respond differently to PBMC activation and this is manifested at disease onset and may be modulated by antipsychotic treatment. The glycolytic protein signature associated with this effect could therefore be of diagnostic and prognostic value. Moreover, these results highlight the importance of using cells for functional discovery and show that it may not be sufficient to measure protein expression levels in static states.

Indexed as

AdultAntipsychotic AgentsBlood GlucoseEnterotoxinsFemaleGlucose Transporter Type 1HexokinaseHumansInsulinLactic AcidLeukocytes, MononuclearMaleProteomeProteomicsReceptor, InsulinSchizophreniaAntipsychotic AgentsBlood Glucoseenterotoxin B, staphylococcalEnterotoxinsGlucose Transporter Type 1HexokinaseInsulinLactic AcidProteomeReceptor, Insulin

Identifiers

PMID20585325
OpenAlexW1964047745

What OpenQuestion holds

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Read underepoch 390

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.