Evidence map›Paper›PMID 24941246›Full record

ArticlePloS one2014

Assessment of cytochrome C oxidase dysfunction in the substantia nigra/ventral tegmental area in schizophrenia.

Matthew W Rice, Kristen L Smith, Rosalinda C Roberts, Emma Perez-Costas, Miguel Melendez-Ferro

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 17% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Review
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  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. In vitro effects of antipsychotics on mitochondrial respiration.Naunyn-Schmiedeberg's archives of pharmacology · 2019
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Psychiatric disorders biochemical pathways unraveled by human brain proteomics.European archives of psychiatry and clinical neuroscience · 2017
    Review
  17. Article
  18. Article
  19. Article
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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

5 authors at 1 institution in 1 country.

Matthew W RiceDepartment of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
Kristen L SmithDepartment of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
Rosalinda C RobertsDepartment of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
Emma Perez-CostasDepartment of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
Miguel Melendez-FerroDepartment of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
University of Alabama at Birmingham · US

Funding

NEUROPATHOLOGY OF DOPAMINE SYSTEMS IN SCHIZOPHRENIAR01MH066123 · NIMH · UNIVERSITY OF MARYLAND BALTIMORE · PI ROBERTS, ROSALINDA C · 2003 to 2015
$3.6M
NIMH NIH HHS MH066123NIMH NIH HHS R01 MH066123
6 · The paper itself

Abstract

Perturbations in metabolism are a well-documented but complex facet of schizophrenia pathology. Optimal cellular performance requires the proper functioning of the electron transport chain, which is constituted by four enzymes located within the inner membrane of mitochondria. These enzymes create a proton gradient that is used to power the enzyme ATP synthase, producing ATP, which is crucial for the maintenance of cellular functioning. Anomalies in a single enzyme of the electron transport chain are sufficient to cause disruption of cellular metabolism. The last of these complexes is the cytochrome c oxidase (COX) enzyme, which is composed of thirteen different subunits. COX is a major site for oxidative phosphorylation, and anomalies in this enzyme are one of the most frequent causes of mitochondrial pathology. The objective of the present report was to assess if metabolic anomalies linked to COX dysfunction may contribute to substantia nigra/ventral tegmental area (SN/VTA) pathology in schizophrenia. We tested COX activity in postmortem SN/VTA from schizophrenia and non-psychiatric controls. We also tested the protein expression of key subunits for the assembly and activity of the enzyme, and the effect of antipsychotic medication on subunit expression. COX activity was not significantly different between schizophrenia and non-psychiatric controls. However, we found significant decreases in the expression of subunits II and IV-I of COX in schizophrenia. Interestingly, these decreases were observed in samples containing the entire rostro-caudal extent of the SN/VTA, while no significant differences were observed for samples containing only mid-caudal regions of the SN/VTA. Finally, rats chronically treated with antipsychotic drugs did not show significant changes in COX subunit expression. These findings suggest that COX subunit expression may be compromised in specific sub-regions of the SN/VTA (i.e. rostral regions), which may lead to a faulty assembly of the enzyme and a greater vulnerability to metabolic insult.

Indexed as

AdultAgedAged, 80 and overAnimalsAntipsychotic AgentsAutopsyElectron Transport Complex IVFemaleHumansMaleMiddle AgedMitochondriaOxidative PhosphorylationRatsSchizophreniaSubstantia NigraAntipsychotic AgentsElectron Transport Complex IV

Identifiers

PMID24941246
PMCPMC4062438
OpenAlexW2064003722

What OpenQuestion holds

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LicenceCC BY
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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.