Evidence map›Paper›PMID 28322275›Full record

ArticleMolecular psychiatry2017

Oxidative stress-driven parvalbumin interneuron impairment as a common mechanism in models of schizophrenia.

P Steullet, J-H Cabungcal, J Coyle, M Didriksen, K Gill, A A Grace, T K Hensch, A-S LaMantia, L Lindemann, T M Maynard and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 217 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
217citing papers in PubMed, 5 pooled it
14.8field-weighted citation impact, top 1% 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

217 citing papers in PubMed, 5 syntheses or guidelines pooled it, 352 citations in OpenAlex.

  1. Pooled it
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  6. Article
  7. Parvalbumin interneurons under stress: converging mechanisms of vulnerability.The international journal of neuropsychopharmacology · 2026
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157 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

16 authors at 9 institutions in 3 countries.

P SteulletCentre for Psychiatric Neuroscience, Department of Psychiatry, Lausanne University Hospital, Prilly-Lausanne, Switzerland.
J-H CabungcalCentre for Psychiatric Neuroscience, Department of Psychiatry, Lausanne University Hospital, Prilly-Lausanne, Switzerland.
J CoyleLaboratory for Psychiatric and Molecular Neuroscience, Harvard Medical School, McLean Hospital, Belmont, MA, USA.ORCID 0000-0002-0702-1395
M DidriksenSynaptic transmission H. Lundbeck A/S, Valby, Denmark.
K GillDepartments of Neuroscience, Psychiatry and Psychology, University of Pittsburgh, Pittsburgh, PA, USA.
A A GraceDepartments of Neuroscience, Psychiatry and Psychology, University of Pittsburgh, Pittsburgh, PA, USA.
T K HenschCenter for Brain Science, Department of Molecular Cellular Biology, Harvard University, Cambridge, MA USA.
A-S LaMantiaGeorge Washington Institute for Neuroscience, The George Washington University, Washington, DC, USA.
L LindemannF. Hoffmann-La Roche, Roche Pharmaceutical and Early Development, Neuroscience, Opthalmology &Rare Disease (NORD) DTA, Discovery Neuroscience, Roche Innovation Center Basel, Basel, Switzerland.
T M MaynardGeorge Washington Institute for Neuroscience, The George Washington University, Washington, DC, USA.
U MeyerInstitute of Pharmacology and Toxicology, University of Zurich-Vetsuisse, Zurich, Switzerland.
H MorishitaCenter for Brain Science, Department of Molecular Cellular Biology, Harvard University, Cambridge, MA USA.ORCID 0000-0002-1045-1337
P O'DonnellNeuroscience and Pain Research Unit, BioTherapeutics Research and Development, Pfizer, Cambridge, MA, USA.
M PuhlLaboratory for Psychiatric and Molecular Neuroscience, Harvard Medical School, McLean Hospital, Belmont, MA, USA.
M CuenodCentre for Psychiatric Neuroscience, Department of Psychiatry, Lausanne University Hospital, Prilly-Lausanne, Switzerland.
K Q DoCentre for Psychiatric Neuroscience, Department of Psychiatry, Lausanne University Hospital, Prilly-Lausanne, Switzerland.
University of Lausanne · CHBoston Children's Hospital · USGeorge Washington University · USHarvard University · USUniversity of Pittsburgh · USLundbeck (Denmark) · DKPfizer (United States) · USRoche (Switzerland) · CHUniversity of Zurich · CH

Funding

Res Support CoreP50MH094271 · NIMH · HARVARD UNIVERSITY · PI HENSCH, TAKAO K · 2011 to 2022
$18.6M
Regulation of 22q11 Genes in Embryonic and Adult ForebrainR01HD042182 · NICHD · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI ANTHONY S LAMANTIA · 2003 to 2026
$8.6M
Regulation of adult visual cortex plasticity by endogenous nicotinic modulatorsR01EY024918 · NEI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI MORISHITA, HIROFUMI · 2015 to 2019
$2.5M
Proteolytic Regulation of Inhibitory Circuits to Gate Cortical PlasticityR01EY026053 · NEI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI MORISHITA, HIROFUMI · 2016 to 2018
$1.4M
Mechanisms regulating developmental critical period for establishing attentionR21MH106919 · NIMH · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI MORISHITA, HIROFUMI · 2016 to 2017
$462k
Structure-Function Relationships of Experience-Dependent Spine PlasticityR21EY026702 · NEI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI ELLIS-DAVIES, GRAHAM, MORISHITA, HIROFUMI · 2017 to 2018
$461k
NIMH NIH HHS P50 MH094271
6 · The paper itself

Abstract

Parvalbumin inhibitory interneurons (PVIs) are crucial for maintaining proper excitatory/inhibitory balance and high-frequency neuronal synchronization. Their activity supports critical developmental trajectories, sensory and cognitive processing, and social behavior. Despite heterogeneity in the etiology across schizophrenia and autism spectrum disorder, PVI circuits are altered in these psychiatric disorders. Identifying mechanism(s) underlying PVI deficits is essential to establish treatments targeting in particular cognition. On the basis of published and new data, we propose oxidative stress as a common pathological mechanism leading to PVI impairment in schizophrenia and some forms of autism. A series of animal models carrying genetic and/or environmental risks relevant to diverse etiological aspects of these disorders show PVI deficits to be all accompanied by oxidative stress in the anterior cingulate cortex. Specifically, oxidative stress is negatively correlated with the integrity of PVIs and the extracellular perineuronal net enwrapping these interneurons. Oxidative stress may result from dysregulation of systems typically affected in schizophrenia, including glutamatergic, dopaminergic, immune and antioxidant signaling. As convergent end point, redox dysregulation has successfully been targeted to protect PVIs with antioxidants/redox regulators across several animal models. This opens up new perspectives for the use of antioxidant treatments to be applied to at-risk individuals, in close temporal proximity to environmental impacts known to induce oxidative stress.

Indexed as

AnimalsAutism Spectrum DisorderDisease Models, AnimalGyrus CinguliHumansInterneuronsMiceOxidation-ReductionOxidative StressParvalbuminsSchizophreniaParvalbumins

Identifiers

PMID28322275
PMCPMC5491690
OpenAlexW2603460853

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.