Evidence map›Paper›PMID 33221354›Full record

ArticleMitochondrion2021

Mitochondrial dysfunction in schizophrenia: With a focus on postmortem studies.

Rosalinda C Roberts

Open access · greenAbstract read
In one paragraph

Article in Mitochondrion, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 8% 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

64 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Context-Dependent modulation of astrocytic CaJournal of computational neuroscience · 2026
    Article
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  15. DifferentialScience advances · 2026
    Article
  16. Imaging brain energetics to advance metabolic psychiatry.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  17. Article
  18. Article
  19. Article
  20. Review

4 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
PATHOLOGY IN POSTMORTEM SCHIZOPHRENIC BASAL GANGLIAR01MH060744 · NIMH · UNIVERSITY OF MARYLAND BALTIMORE · PI ROBERTS, ROSALINDA C · 2000 to 2010
$2.9M
Dopamine levels in postmortem human nucleus accumbens in schizophreniaF31MH098566 · NIMH · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MCCOLLUM, LESLEY A · 2013 to 2014
$55k
Minority Predoctoral Fellowship ProgramF31MH073461 · NIMH · UNIVERSITY OF MARYLAND BALTIMORE · PI SOMERVILLE, SHAHZA M · 2004 to 2006
$34k
NIMH NIH HHS F31 MH073461NIMH NIH HHS F31 MH098566NIMH NIH HHS R01 MH060744NIMH NIH HHS R01 MH066123
6 · The paper itself

Abstract

Among the many brain abnormalities in schizophrenia are those related to mitochondrial functions such as oxidative stress, energy metabolism and synaptic efficacy. The aim of this paper is to provide a brief review of mitochondrial structure and function and then to present abnormalities in mitochondria in postmortem brain in schizophrenia with a focus on anatomy. Deficits in expression of various mitochondrial genes have been found in multiple schizophrenia cohorts. Decreased activity of complexes I and IV are prominent as well as abnormal levels of individual subunits that comprise the complexes of the electron transport chain. Ultrastructural studies have shown layer, input and cell specific decreases in mitochondria. In cortex, there are fewer mitochondria in axon terminals, neuronal somata of pyramidal neurons and oligodendrocytes in both grey and white matter. In the caudate and putamen mitochondrial number is linked with symptoms and symptom severity. While there is a decrease in the number of mitochondria in astrocytes, mitochondria are smaller in oligodendrocytes. In the nucleus accumbens and substantia nigra, mitochondria are similar in density, size and structural integrity in schizophrenia compared to controls. Mitochondrial production of ATP and calcium buffering are essential in maintaining synaptic strength and abnormalities in these processes could lead to decreased metabolism and defective synaptic activity. Abnormalities in mitochondria in oligodendrocytes might contribute to myelin pathology and underlie dysconnectivity in the brain. In schizophrenia, mitochondria are affected differentially depending on the brain region, cell type in which they reside, subcellular location, treatment status, treatment response and predominant symptoms.

Indexed as

AutopsyBrainEnergy MetabolismGene Expression RegulationHumansMitochondriaMitochondrial ProteinsOxidative StressSchizophreniaMitochondrial ProteinsCytochrome oxidaseElectron microscopyNeuropathologyPsychosis

Identifiers

PMID33221354
PMCPMC7810242
OpenAlexW3106837219

What OpenQuestion holds

Textmetadata
LicenceTDM
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.