Evidence map›Paper›PMID 28189530›Full record

ReviewSchizophrenia research2017

Postmortem studies on mitochondria in schizophrenia.

Rosalinda C Roberts

Open access · greenAbstract readReview
In one paragraph

Review in Schizophrenia research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

61 citing papers in PubMed, 93 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Imaging brain energetics to advance metabolic psychiatry.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Mitochondrial Oxidative Phosphorylation System Dysfunction in Schizophrenia.International journal of molecular sciences · 2025
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Enlarged basal ganglia in drug-naïve patients with first-episode psychosis immediately upon symptom onset.Dusunen adam : Bakirkoy Ruh ve Sinir Hastaliklari Hastanesi yayin organi · 2024
    Article
  17. Article
  18. Research progress in mitochondrial quality control in schizophrenia.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024
    Article
  19. Article
  20. Article

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

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

1 author at 1 institution in 1 country.

Rosalinda C RobertsDepartment of Psychiatry and Behavioral Neurobiology, University of Alabama, Birmingham, AL 35294, United States. Electronic address: rosalindaroberts@uabmc.edu.
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
White matter pathology in postmortem schizophrenia brainR21MH108867 · NIMH · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ROBERTS, ROSALINDA C · 2016 to 2017
$404k
NIMH NIH HHS R01 MH066123NIMH NIH HHS R21 MH108867
6 · The paper itself

Abstract

The aim of this paper is to provide a brief review of mitochondrial structure as it relates to function and then present abnormalities in mitochondria in postmortem schizophrenia with a focus on ultrastructure. Function, morphology, fusion, fission, motility, ΔΨmem, ATP production, mitochondrial derived vesicles, and mitochondria-associated ER membranes will be briefly covered. Pathology in mitochondria has long been implicated in schizophrenia, as shown by genetic, proteomic, enzymatic and anatomical abnormalities. The cortex and basal ganglia will be reviewed. In the anterior cingulate cortex, the number of mitochondria per neuronal somata in layers 5/6 in schizophrenia is decreased by 43%. There are also fewer mitochondria in terminals forming axospinous synapses. In the caudate and putamen the number of mitochondria is abnormal in both glial cells and neurons in schizophrenia subjects, the extent of which depends on treatment, response and predominant lifetime symptoms. Treatment-responsive schizophrenia subjects had about a 40% decrease in the number of mitochondria per synapse in the caudate nucleus and putamen, while treatment resistant cases had normal values. A decrease in mitochondrial density in the neuropil distinguishes paranoid from undifferentiated schizophrenia. The appearance, size and density of mitochondria were normal in the nucleus accumbens. In the substantia nigra, COX subunits were affected in rostral regions. Mitochondrial hyperplasia occurs within axon terminals that synapse onto dopamine neurons, but mitochondria in dopamine neuronal somata are similar in size and number. In schizophrenia, mitochondria are differentially affected depending on the brain region, cell type, subcellular location, treatment status, treatment response and symptoms.

Indexed as

AnimalsAntipsychotic AgentsHumansMitochondriaMitochondrial DiseasesSchizophreniaAntipsychotic AgentsCytochrome oxidaseElectron microscopyNeuropathologyPostmortemPsychosis

Identifiers

PMID28189530
PMCPMC5550365
OpenAlexW2587753055

What OpenQuestion holds

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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.