Evidence map›Paper›PMID 28408291›Full record

ArticleProgress in neuro-psychopharmacology & biological psychiatry2017

Altered expression of circadian rhythm and extracellular matrix genes in the medial prefrontal cortex of a valproic acid rat model of autism.

Nikkie F M Olde Loohuis, Gerard J M Martens, Hans van Bokhoven, Barry B Kaplan, Judith R Homberg, Armaz Aschrafi

Abstract read
In one paragraph

Article in Progress in neuro-psychopharmacology & biological psychiatry, 2017. 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
1.8field-weighted citation impact, top 14% 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, 21 citations in OpenAlex.

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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

6 authors at 4 institutions in 2 countries.

Nikkie F M Olde LoohuisDepartment of Cognitive Neuroscience, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Centre, Nijmegen, The Netherlands.
Gerard J M MartensDepartment of Molecular Animal Physiology, Donders Institute for Brain, Cognition and Behavior, Radboud Institute for Molecular Life Sciences (RIMLS), Radboud University, Nijmegen, The Netherlands.
Hans van BokhovenDepartment of Cognitive Neuroscience, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Centre, Nijmegen, The Netherlands.
Barry B KaplanLaboratory of Molecular Biology, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892, USA.
Judith R HombergDepartment of Cognitive Neuroscience, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Centre, Nijmegen, The Netherlands.
Armaz AschrafiLaboratory of Molecular Biology, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: armaz.aschrafi@nih.gov.
National Institutes of Health · USRadboud University Nijmegen · NLRadboud Institute for Molecular Life Sciences · NLRadboud University Medical Center · NL

Funding

Subcellular Compartmentilization of Neuronal Gene ExpressionZIAMH002768 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI KAPLAN, BARRY · 2009 to 2018
$11.5M
Subcellular Compartmentilization of Neuronal Gene ExpressionZ01MH002768 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI KAPLAN, BARRY B. · 1998 to 2008
$1.7M
Intramural NIH HHS Z01 MH002768
6 · The paper itself

Abstract

Autism spectrum disorders (ASD) are a highly heterogeneous group of neurodevelopmental disorders caused by complex interplay between various genes and environmental factors during embryonic development. Changes at the molecular, cellular and neuroanatomical levels are especially evident in the medial prefrontal cortex (mPFC) of ASD patients and are particularly contributing to social impairments. In the present study we tested the hypothesis that altered neuronal development and plasticity, as seen in the mPFC of ASD individuals, may result from aberrant expression of functionally connected genes. Towards this end, we combined transcriptome sequencing and computational gene ontology analysis to identify the molecular networks impaired in the mPFC of a valproic acid (VPA) rat model of autism. This investigation identified two subsets of genes differentially expressed in the mPFC of VPA rats: one group of genes being functionally involved in the regulation of the circadian rhythm, while the second group encompasses a set of differentially expressed collagen genes acting within the extracellular matrix. Ultimately, our integrated transcriptome analysis identified a distinct subset of altered gene networks in the mPFC of VPA rats, contributing to our understanding of autism at the molecular level, thus providing novel insight into the genetic alterations associated with this neurodevelopmental disorder.

Indexed as

AnimalsAutism Spectrum DisorderCircadian RhythmDisease Models, AnimalExtracellular MatrixFemaleMalePrefrontal CortexPregnancyPrenatal Exposure Delayed EffectsRatsTranscriptomeValproic AcidValproic AcidAnimal model of autismCollagenGene ontology analysisPeriod circadian clockTranscriptome sequencing

Identifiers

PMID28408291
PMCPMC5502527
OpenAlexW2607324134

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.