Evidence map›Paper›PMID 34911565›Full record

ArticleMolecular autism2021

Preference for biological motion is reduced in ASD: implications for clinical trials and the search for biomarkers.

L Mason, F Shic, T Falck-Ytter, B Chakrabarti, T Charman, E Loth, J Tillmann, T Banaschewski, S Baron-Cohen, S Bölte and 13 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular autism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 17% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
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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

23 authors at 13 institutions in 8 countries.

L MasonCentre for Brain and Cognitive Development, Birkbeck, University of London, Malet St, London, WC1E 7HX, UK. l.mason@bbk.ac.uk.ORCID 0000-0001-9978-7349
F ShicCenter for Child Health, Behavior and Development, Seattle Children's Research Institute, Seattle, WA, USA.
T Falck-YtterDevelopment and Neurodiversity Lab, Department of Psychology, Uppsala University, Uppsala, Sweden.
B ChakrabartiCentre for Autism, School of Psychology and Clinical Language Sciences, University of Reading, Reading, RG6 6AL, UK.
T CharmanInstitute of Psychiatry, Psychology and Neuroscience, King's College, London, London, UK.
E LothInstitute of Psychiatry, Psychology and Neuroscience, King's College, London, London, UK.
J TillmannInstitute of Psychiatry, Psychology and Neuroscience, King's College, London, London, UK.
T BanaschewskiCentral Institute of Mental Health, University of Heidelberg, Mannheim, Germany.
S Baron-CohenDepartment of Psychology, University of Cambridge, Cambridge, UK.
S BölteCenter of Neurodevelopmental Disorders (KIND), Centre for Psychiatry Research; Department of Women's and Children's Health, Karolinska Institutet and Child and Adolescent Psychiatry, Stockholm Health Care Services, Region Stockholm, Stockholm, Sweden.
J BuitelaarDepartment of Cognitive Neuroscience, Donders Institute for Brain, Cognition and Behaviour, Radboudumc, Nijmegen, The Netherlands.
S DurstonNICHE-Lab, Dept. of Psychiatry, UMC Utrecht Brain Center, Utrecht, The Netherlands.
B OranjeNICHE-Lab, Dept. of Psychiatry, UMC Utrecht Brain Center, Utrecht, The Netherlands.
A M PersicoInterdepartmental Program "Autism 0-90", University of Messina, Messina, Italy.
C BeckmannDepartment of Cognitive Neuroscience, Donders Institute for Brain, Cognition and Behaviour, Radboudumc, Nijmegen, The Netherlands.
T BougeronHuman Genetics and Cognitive Functions, Institut Pasteur, UMR3571 CNRS, Université de Paris, 75015, Paris, France.
F Dell'AcquaInstitute of Psychiatry, Psychology and Neuroscience, King's College, London, London, UK.
C EckerInstitute of Psychiatry, Psychology and Neuroscience, King's College, London, London, UK.
C MoessnangDepartment of Psychiatry and Psychotherapy, Central Institute of Mental Health, University of Heidelberg, Mannheim, Germany.
D MurphyInstitute of Psychiatry, Psychology and Neuroscience, King's College, London, London, UK.
M H JohnsonCentre for Brain and Cognitive Development, Birkbeck, University of London, Malet St, London, WC1E 7HX, UK.
E J H JonesCentre for Brain and Cognitive Development, Birkbeck, University of London, Malet St, London, WC1E 7HX, UK.
LEAP Team*
King's College London · GBBirkbeck, University of London · GBHeidelberg University · DERadboud University Nijmegen · NLUniversity Medical Center Utrecht · NLUniversity of Cambridge · GBAction for Autism · INCentre National de la Recherche Scientifique · FRGoethe University Frankfurt · DEKarolinska Institutet · SESeattle Children's Hospital · USUniversity of Messina · ITUppsala University · SE

Funding

Medical Research Council MR/K021389/1Medical Research Council MR/T003057/1
6 · The paper itself

Abstract

backgroundThe neurocognitive mechanisms underlying autism spectrum disorder (ASD) remain unclear. Progress has been largely hampered by small sample sizes, variable age ranges and resulting inconsistent findings. There is a pressing need for large definitive studies to delineate the nature and extent of key case/control differences to direct research towards fruitful areas for future investigation. Here we focus on perception of biological motion, a promising index of social brain function which may be altered in ASD. In a large sample ranging from childhood to adulthood, we assess whether biological motion preference differs in ASD compared to neurotypical participants (NT), how differences are modulated by age and sex and whether they are associated with dimensional variation in concurrent or later symptomatology.

methodsEye-tracking data were collected from 486 6-to-30-year-old autistic (N = 282) and non-autistic control (N = 204) participants whilst they viewed 28 trials pairing biological (BM) and control (non-biological, CTRL) motion. Preference for the biological motion stimulus was calculated as (1) proportion looking time difference (BM-CTRL) and (2) peak look duration difference (BM-CTRL).

resultsThe ASD group showed a present but weaker preference for biological motion than the NT group. The nature of the control stimulus modulated preference for biological motion in both groups. Biological motion preference did not vary with age, gender, or concurrent or prospective social communicative skill within the ASD group, although a lack of clear preference for either stimulus was associated with higher social-communicative symptoms at baseline. LIMITATIONS: The paired visual preference we used may underestimate preference for a stimulus in younger and lower IQ individuals. Our ASD group had a lower average IQ by approximately seven points. 18% of our sample was not analysed for various technical and behavioural reasons.

conclusionsBiological motion preference elicits small-to-medium-sized case-control effects, but individual differences do not strongly relate to core social autism associated symptomatology. We interpret this as an autistic difference (as opposed to a deficit) likely manifest in social brain regions. The extent to which this is an innate difference present from birth and central to the autistic phenotype, or the consequence of a life lived with ASD, is unclear.

Indexed as

Autism Spectrum DisorderAutistic DisorderAdolescentBiomarkersCase-Control StudiesChildHumansSeverity of Illness IndexYoung AdultBiomarkersAutismBiological motionBiomarkerDevelopmentEye tracking

Identifiers

PMID34911565
PMCPMC8672507
OpenAlexW4200481233

What OpenQuestion holds

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LicenceCC BY
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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.