Evidence map›Paper›PMID 28934193›Full record

ReviewTranslational psychiatry2017

Oxidative stress, prefrontal cortex hypomyelination and cognitive symptoms in schizophrenia.

D A Maas, A Vallès, G J M Martens

Open access · goldAbstract readReview
In one paragraph

Review in Translational psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed, 3 pooled it
5.4field-weighted citation impact, top 3% 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

99 citing papers in PubMed, 3 syntheses or guidelines pooled it, 174 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Vitamin D and schizophrenia: 20 years on.Molecular psychiatry · 2021
    Pooled it
  4. Trial
  5. Change in prefrontal activity and executive functions after action-based cognitive remediation in bipolar disorder: a randomized controlled trial.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
    Trial
  6. Review
  7. Catechol-Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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39 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

3 authors at 1 institution in 1 country.

D A MaasDepartment of Molecular Animal Physiology, Faculty of Science, Donders Centre for Neuroscience, Radboud University Nijmegen, Nijmegen, The Netherlands.
A VallèsDepartment of Molecular Animal Physiology, Faculty of Science, Donders Centre for Neuroscience, Radboud University Nijmegen, Nijmegen, The Netherlands.
G J M MartensDepartment of Molecular Animal Physiology, Faculty of Science, Donders Centre for Neuroscience, Radboud University Nijmegen, Nijmegen, The Netherlands.
Radboud University Nijmegen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Schizophrenia (SZ) is a neurodevelopmental disorder with a broad symptomatology, including cognitive symptoms that are thought to arise from the prefrontal cortex (PFC). The neurobiological aetiology of these symptoms remains elusive, yet both impaired redox control and PFC dysconnectivity have been recently implicated. PFC dysconnectivity has been linked to white matter, oligodendrocyte (OL) and myelin abnormalities in SZ patients. Myelin is produced by mature OLs, and OL precursor cells (OPCs) are exceptionally susceptible to oxidative stress. Here we propose a hypothesis for the aetiology of cognitive symptomatology in SZ: the redox-induced prefrontal OPC-dysfunctioning hypothesis. We pose that the combination of genetic and environmental factors causes oxidative stress marked by a build-up of reactive oxygen species that, during late adolescence, impair OPC signal transduction processes that are necessary for OPC proliferation and differentiation, and involve AMP-activated protein kinase, Akt-mTOR-P70S6K and peroxisome proliferator receptor alpha signalling. OPC dysfunctioning coincides with the relatively late onset of PFC myelination, causing hypomyelination and disruption of connectivity in this brain area. The resulting cognitive deficits arise in parallel with SZ onset. Hence, our hypothesis provides a novel neurobiological framework for the aetiology of SZ cognitive symptoms. Future research addressing our hypothesis could have important implications for the development of new (combined) antioxidant- and promyelination-based strategies to treat the cognitive symptoms in SZ.

Indexed as

Oxidative StressSchizophrenic PsychologyAnimalsHumansMyelin SheathOligodendrocyte Precursor CellsOxidation-ReductionPrefrontal CortexSchizophreniaSignal Transduction

Identifiers

PMID28934193
PMCPMC5538118
OpenAlexW2737227438

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.