Evidence map›Paper›PMID 38413609›Full record

ArticleNature communications2024

Structural models of genome-wide covariance identify multiple common dimensions in autism.

Lucía de Hoyos, Maria T Barendse, Fenja Schlag, Marjolein M J van Donkelaar, Ellen Verhoef, Chin Yang Shapland, Alexander Klassmann, Jan Buitelaar, Brad Verhulst, Simon E Fisher and 2 more

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

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  9. Research Review: A review of the past decade of family and genomic studies on adolescent mental health.Journal of child psychology and psychiatry, and allied disciplines · 2025
    Review
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

12 authors.

Lucía de HoyosLanguage and Genetics Department, Max Planck Institute for Psycholinguistics, Nijmegen, The Netherlands.ORCID 0000-0001-7252-1591
Maria T BarendseLanguage and Genetics Department, Max Planck Institute for Psycholinguistics, Nijmegen, The Netherlands.ORCID 0000-0002-1632-0303
Fenja SchlagLanguage and Genetics Department, Max Planck Institute for Psycholinguistics, Nijmegen, The Netherlands.
Marjolein M J van DonkelaarLanguage and Genetics Department, Max Planck Institute for Psycholinguistics, Nijmegen, The Netherlands.
Ellen VerhoefLanguage and Genetics Department, Max Planck Institute for Psycholinguistics, Nijmegen, The Netherlands.ORCID 0000-0002-8315-1095
Chin Yang ShaplandMRC Integrative Epidemiology Unit, University of Bristol, Bristol, UK.ORCID 0000-0002-5797-1241
Alexander KlassmannInstitute for Genetics, University of Cologne, Cologne, Germany.ORCID 0000-0002-0175-1397
Jan BuitelaarDonders Institute for Brain, Cognition and Behaviour, Radboud University, Nijmegen, The Netherlands.ORCID 0000-0001-8288-7757
Brad VerhulstTexas A&M University, College Station, TX, USA.ORCID 0000-0001-5369-9757
Simon E FisherLanguage and Genetics Department, Max Planck Institute for Psycholinguistics, Nijmegen, The Netherlands.ORCID 0000-0002-3132-1996
Dheeraj RaiPopulation Health Sciences, University of Bristol, Bristol, UK.
Beate St PourcainLanguage and Genetics Department, Max Planck Institute for Psycholinguistics, Nijmegen, The Netherlands. Beate.StPourcain@mpi.nl.ORCID 0000-0002-4680-3517

Funding

Medical Research Council MC_UU_00011/3Simons Foundation 514787
6 · The paper itself

Abstract

Common genetic variation has been associated with multiple phenotypic features in Autism Spectrum Disorder (ASD). However, our knowledge of shared genetic factor structures contributing to this highly heterogeneous phenotypic spectrum is limited. Here, we developed and implemented a structural equation modelling framework to directly model genomic covariance across core and non-core ASD phenotypes, studying autistic individuals of European descent with a case-only design. We identified three independent genetic factors most strongly linked to language performance, behaviour and developmental motor delay, respectively, studying an autism community sample (N = 5331). The three-factorial structure was largely confirmed in independent ASD-simplex families (N = 1946), although we uncovered, in addition, simplex-specific genetic overlap between behaviour and language phenotypes. Multivariate models across cohorts revealed novel associations, including links between language and early mastering of self-feeding. Thus, the common genetic architecture in ASD is multi-dimensional with overarching genetic factors contributing, in combination with ascertainment-specific patterns, to phenotypic heterogeneity.

Indexed as

Autism Spectrum DisorderAutistic DisorderHumansLanguageLatent Class AnalysisPhenotype

Identifiers

PMID38413609
PMCPMC10899248

What OpenQuestion holds

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Registered trials

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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.