Evidence map›Paper›PMID 33564104›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2021

Antioxidant treatment ameliorates prefrontal hypomyelination and cognitive deficits in a rat model of schizophrenia.

D A Maas, V D Eijsink, J A van Hulten, R Panic, P De Weerd, J R Homberg, A Vallès, B Nait-Oumesmar, G J M Martens

Open access · hybridAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

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  4. Metabolic implications of axonal demyelination and its consequences for synchronized network activity: AnJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
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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

9 authors at 3 institutions in 2 countries.

D A MaasDept of Molecular Animal Physiology, Donders Centre for Neuroscience, Radboud University, Nijmegen, The Netherlands. d.a.maas@outlook.com.ORCID http://orcid.org/0000-0002-2142-6743
V D EijsinkDept of Molecular Animal Physiology, Donders Centre for Neuroscience, Radboud University, Nijmegen, The Netherlands.
J A van HultenDept of Molecular Animal Physiology, Donders Centre for Neuroscience, Radboud University, Nijmegen, The Netherlands.
R PanicSorbonne Université, Paris Brain Institute-ICM, Inserm U1127, CNRS UMR 7225, Hôpital Pitié-Salpêtrière, Paris, France.
P De WeerdDept of Neurocognition, Faculty of Psychology and Neurosciences, Maastricht University, Maastricht, The Netherlands.
J R HombergDept of Cognitive Neuroscience, Donders Centre for Medical Neuroscience, Radboud University Medical Center, Nijmegen, The Netherlands.
A VallèsDept of Molecular Animal Physiology, Donders Centre for Neuroscience, Radboud University, Nijmegen, The Netherlands.
B Nait-Oumesmar *Sorbonne Université, Paris Brain Institute-ICM, Inserm U1127, CNRS UMR 7225, Hôpital Pitié-Salpêtrière, Paris, France. brahim.nait_oumesmar@upmc.fr.
G J M Martens *Dept of Molecular Animal Physiology, Donders Centre for Neuroscience, Radboud University, Nijmegen, The Netherlands. g.martens@ncmls.ru.nl.
Radboud University Nijmegen · NLCentre National de la Recherche Scientifique · FRMaastricht University Medical Centre · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cognitive dysfunction in schizophrenia (SZ) is thought to arise from neurodevelopmental abnormalities that include interneuron hypomyelination in the prefrontal cortex (PFC). Here we report that RNA-sequencing of the medial (m)PFC of the APO-SUS rat model with SZ-relevant cognitive inflexibility revealed antioxidant metabolism as the most-enriched differentially expressed pathway. Antioxidant-related gene expression was altered throughout postnatal development and preceded hypomyelination. Furthermore, reduced glutathione levels and increased mitochondria numbers were observed in the mPFC. Strikingly, chronic treatment with the glutathione precursor N-acetylcysteine (NAC) from postnatal days 5-90 restored not only antioxidant-related mRNA expression and mitochondria numbers, but also myelin-related mRNA expression and mPFC-dependent cognitive dysfunction, while blood glutathione levels remained unaffected. The promyelinating effect of NAC was at least partly due to a positive effect on oligodendrocyte lineage progression. Together, our findings highlight that oxidative stress may contribute to cognitive symptoms in the APO-SUS rat model of SZ and encourage antioxidant therapy in early phases of SZ.

Indexed as

Cognitive DysfunctionSchizophreniaAnimalsAntioxidantsCognitionPrefrontal CortexRatsAntioxidants

Identifiers

PMID33564104
PMCPMC8115238
OpenAlexW3128791962

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.