Evidence map›Paper›PMID 37582968›Full record

ArticleCommunications biology2023

Sexual dimorphism in the social behaviour of Cntnap2-null mice correlates with disrupted synaptic connectivity and increased microglial activity in the anterior cingulate cortex.

Matt S Dawson, Kevin Gordon-Fleet, Lingxin Yan, Vera Tardos, Huanying He, Kwong Mui, Smriti Nawani, Zeinab Asgarian, Marco Catani, Cathy Fernandes and 1 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
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  4. Drivers of systemic male-female allele frequency divergence in humans.bioRxiv : the preprint server for biology · 2026
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  13. Brain-Resident Immune Cells in Neurodevelopmental Disorders.Advances in experimental medicine and biology · 2025
    Review
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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

11 authors at 1 institution in 1 country.

Matt S DawsonCentre for Developmental Neurobiology, Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King's College London, London, SE1 1UL, UK.
Kevin Gordon-FleetCentre for Developmental Neurobiology, Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King's College London, London, SE1 1UL, UK.
Lingxin YanCentre for Developmental Neurobiology, Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King's College London, London, SE1 1UL, UK.
Vera TardosCentre for Developmental Neurobiology, Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King's College London, London, SE1 1UL, UK.
Huanying HeCentre for Developmental Neurobiology, Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King's College London, London, SE1 1UL, UK.
Kwong MuiCentre for Developmental Neurobiology, Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King's College London, London, SE1 1UL, UK.
Smriti NawaniSocial, Genetic & Developmental Psychiatry Centre, IoPPN, King's College London, London, SE1 1UL, UK.
Zeinab AsgarianCentre for Developmental Neurobiology, Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King's College London, London, SE1 1UL, UK.
Marco CataniNatBrainLab, Departments of Neuroimaging Sciences and Forensic and Neurodevelopmental Sciences, IoPPN, King's College London, London, SE1 1UL, UK.
Cathy FernandesSocial, Genetic & Developmental Psychiatry Centre, IoPPN, King's College London, London, SE1 1UL, UK.ORCID http://orcid.org/0000-0001-7318-3352
Uwe DrescherCentre for Developmental Neurobiology, Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King's College London, London, SE1 1UL, UK. uwe.drescher@kcl.ac.uk.
King's College London · GB

Funding

Biotechnology and Biological Sciences Research Council BB/T013753/1Medical Research Council MR/W006251/1Wellcome Trust 103759/Z/14/Z
6 · The paper itself

Abstract

A biological understanding of the apparent sex bias in autism is lacking. Here we have identified Cntnap2 KO mice as a model system to help better understand this dimorphism. Using this model, we observed social deficits in juvenile male KO mice only. These male-specific social deficits correlated with reduced spine densities of Layer 2/3 and Layer 5 pyramidal neurons in the Anterior Cingulate Cortex, a forebrain region prominently associated with the control of social behaviour. Furthermore, in male KO mice, microglia showed an increased activated morphology and phagocytosis of synaptic structures compared to WT mice, whereas no differences were seen in female KO and WT mice. Our data suggest that sexually dimorphic microglial activity may be involved in the aetiology of ASD, disrupting the development of neural circuits that control social behaviour by overpruning synapses at a developmentally critical period.

Indexed as

MicrogliaSex CharacteristicsAnimalsFemaleGyrus CinguliMaleMiceMice, KnockoutSocial Behavior

Identifiers

PMID37582968
PMCPMC10427688
OpenAlexW4385850744

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.