Evidence map›Paper›PMID 32441222›Full record

ReviewThe Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry2021

Autism Spectrum Disorders: Multiple Routes to, and Multiple Consequences of, Abnormal Synaptic Function and Connectivity.

Liam Carroll, Sven Braeutigam, John M Dawes, Zeljka Krsnik, Ivica Kostovic, Ester Coutinho, Jennifer M Dewing, Christopher A Horton, Diego Gomez-Nicola, David A Menassa

Abstract readReview
In one paragraph

Review in The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
–field-weighted citation impact
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

43 citing papers in PubMed.

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  9. Primate gut microbiota induce evolutionarily salient changes in mouse neurodevelopment.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

10 authors.

Liam CarrollNuffield Department of Clinical Neurosciences, University of Oxford, Oxford, Oxfordshire, UK.
Sven BraeutigamOxford Centre for Human Brain Activity, Wellcome Centre for Integrative Neuroimaging, Department of Psychiatry, University of Oxford, Oxford, Oxfordshire, UK.
John M DawesNuffield Department of Clinical Neurosciences, University of Oxford, Oxford, Oxfordshire, UK.
Zeljka KrsnikCroatian Institute for Brain Research, Centre of Research Excellence for Basic, Clinical and Translational Neuroscience, University of Zagreb School of Medicine, Zagreb, Croatia.
Ivica KostovicCroatian Institute for Brain Research, Centre of Research Excellence for Basic, Clinical and Translational Neuroscience, University of Zagreb School of Medicine, Zagreb, Croatia.
Ester CoutinhoMaurice Wohl Clinical Neuroscience Institute, King's College London, London, UK.
Jennifer M DewingFaculty of Medicine, University of Southampton, Southampton, Hampshire, UK.
Christopher A HortonSir William Dunn School of Pathology, University of Oxford, Oxford, Oxfordshire, UK.
Diego Gomez-NicolaBiological Sciences, Faculty of Environmental and Life Sciences, University of Southampton, Southampton, UK.
David A MenassaNuffield Department of Clinical Neurosciences, University of Oxford, Oxford, Oxfordshire, UK.ORCID 0000-0002-5984-8407

Funding

Medical Research Council MR/M02394X/1Medical Research Council MR/P024572/1Wellcome TrustWellcome Trust 203139/Z/16/Z
6 · The paper itself

Abstract

Autism spectrum disorders (ASDs) are a heterogeneous group of neurodevelopmental disorders of genetic and environmental etiologies. Some ASD cases are syndromic: associated with clinically defined patterns of somatic abnormalities and a neurobehavioral phenotype (e.g., Fragile X syndrome). Many cases, however, are idiopathic or non-syndromic. Such disorders present themselves during the early postnatal period when language, speech, and personality start to develop. ASDs manifest by deficits in social communication and interaction, restricted and repetitive patterns of behavior across multiple contexts, sensory abnormalities across multiple modalities and comorbidities, such as epilepsy among many others. ASDs are disorders of connectivity, as synaptic dysfunction is common to both syndromic and idiopathic forms. While multiple theories have been proposed, particularly in idiopathic ASDs, none address why certain brain areas (e.g., frontotemporal) appear more vulnerable than others or identify factors that may affect phenotypic specificity. In this hypothesis article, we identify possible routes leading to, and the consequences of, altered connectivity and review the evidence of central and peripheral synaptic dysfunction in ASDs. We postulate that phenotypic specificity could arise from aberrant experience-dependent plasticity mechanisms in frontal brain areas and peripheral sensory networks and propose why the vulnerability of these areas could be part of a model to unify preexisting pathophysiological theories.

Indexed as

Autism Spectrum DisorderNerve NetNeuronal PlasticityPeripheral Nervous SystemPrefrontal CortexAnimalsHumansautism spectrum disordersconnectivitymaternal immune activationneurodevelopmentpain sensitivityphenotypic specificitysynaptic dysfunctionsynaptic plasticity

Identifiers

PMID32441222
PMCPMC7804368

What OpenQuestion holds

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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.