Evidence map›Paper›PMID 26550561›Full record

ReviewMolecular neuropsychiatry2015

Evidence of Mitochondrial Dysfunction within the Complex Genetic Etiology of Schizophrenia.

Brooke E Hjelm, Brandi Rollins, Firoza Mamdani, Julie C Lauterborn, George Kirov, Gary Lynch, Christine M Gall, Adolfo Sequeira, Marquis P Vawter

Erratum issuedOpen access · bronzeAbstract readReview
In one paragraph

Review in Molecular neuropsychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.

  1. Pooled it
  2. Review
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  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Repurposing medications to prevent psychosis.Npj mental health research · 2025
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
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  17. Article
  18. Effects of antipsychotic drugs on energy metabolism.European archives of psychiatry and clinical neuroscience · 2024
    Article
  19. Review
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 2 countries.

Brooke E HjelmDepartments of Psychiatry & Human Behavior, University of California, Irvine, Calif., USA.
Brandi RollinsDepartments of Psychiatry & Human Behavior, University of California, Irvine, Calif., USA.
Firoza MamdaniDepartments of Psychiatry & Human Behavior, University of California, Irvine, Calif., USA.
Julie C LauterbornDepartments of Anatomy & Neurobiology, University of California, Irvine, Calif., USA.
George KirovMRC Centre for Neuropsychiatric Genetics and Genomics, Institute of Psychological Medicine and Clinical Neurosciences, Cardiff University, Cardiff, UK.
Gary LynchDepartments of Psychiatry & Human Behavior, University of California, Irvine, Calif., USA; Departments of Anatomy & Neurobiology, University of California, Irvine, Calif., USA.
Christine M GallDepartments of Anatomy & Neurobiology, University of California, Irvine, Calif., USA; Departments of Neurobiology & Behavior, University of California, Irvine, Calif., USA.
Adolfo SequeiraDepartments of Psychiatry & Human Behavior, University of California, Irvine, Calif., USA.
Marquis P VawterDepartments of Psychiatry & Human Behavior, University of California, Irvine, Calif., USA.
University of California, Irvine · USCardiff University · GB

Funding

Mitochondrial Dysfunction In SchizophreniaR01MH085801 · NIMH · UNIVERSITY OF CALIFORNIA-IRVINE · PI VAWTER, MARQUIS PHILIP · 2009 to 2020
$5.0M
Mitochondrial Deletions in Mood DisordersR21MH099440 · NIMH · UNIVERSITY OF CALIFORNIA-IRVINE · PI VAWTER, MARQUIS PHILIP · 2013 to 2014
$424k
NIMH NIH HHS R01 MH085801NIMH NIH HHS R21 MH099440
6 · The paper itself

Abstract

Genetic evidence has supported the hypothesis that schizophrenia (SZ) is a polygenic disorder caused by the disruption in function of several or many genes. The most common and reproducible cellular phenotype associated with SZ is a reduction in dendritic spines within the neocortex, suggesting alterations in dendritic architecture may cause aberrant cortical circuitry and SZ symptoms. Here, we review evidence supporting a multifactorial model of mitochondrial dysfunction in SZ etiology and discuss how these multiple paths to mitochondrial dysfunction may contribute to dendritic spine loss and/or underdevelopment in some SZ subjects. The pathophysiological role of mitochondrial dysfunction in SZ is based upon genomic analyses of both the mitochondrial genome and nuclear genes involved in mitochondrial function. Previous studies and preliminary data suggest SZ is associated with specific alleles and haplogroups of the mitochondrial genome, and also correlates with a reduction in mitochondrial copy number and an increase in synonymous and nonsynonymous substitutions of mitochondrial DNA. Mitochondrial dysfunction has also been widely implicated in SZ by genome-wide association, exome sequencing, altered gene expression, proteomics, microscopy analyses, and induced pluripotent stem cell studies. Together, these data support the hypothesis that SZ is a polygenic disorder with an enrichment of mitochondrial targets.

Indexed as

Antipsychotic drugDendritic spinesFluorescence deconvolution tomographyGenomeInduced pluripotent stem cellMitochondriaPolygenic disorderProteomeSchizophreniaTranscriptome

Identifiers

PMID26550561
PMCPMC4635522
OpenAlexW2095790509

What OpenQuestion holds

Textmetadata
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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.