Evidence map›Paper›PMID 29100628›Full record

ArticleBiological psychiatry2018

Developmental Changes Within the Genetic Architecture of Social Communication Behavior: A Multivariate Study of Genetic Variance in Unrelated Individuals.

Beate St Pourcain, Lindon J Eaves, Susan M Ring, Simon E Fisher, Sarah Medland, David M Evans, George Davey Smith

Abstract read
In one paragraph

Article in Biological psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
–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

23 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. The Autism-Psychosis Continuum Conundrum: Exploring the Role of the Endocannabinoid System.International journal of environmental research and public health · 2022
    Pooled it
  2. Article
  3. Developmental Trajectories of Autistic Social Traits in Youth Born Extremely Preterm.Journal of the American Academy of Child and Adolescent Psychiatry · 2026
    Article
  4. Review
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  8. Polygenic and developmental profiles of autism differ by age at diagnosis.medRxiv : the preprint server for health sciences · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Beate St PourcainLanguage and Genetics Department, Max Planck Institute for Psycholinguistics, The Netherlands; Donders Institute for Brain, Cognition and Behaviour, Radboud University, Nijmegen, The Netherlands; Medical Research Council Integrative Epidemiology Unit, University of Bristol, Bristol, United Kingdom. Electronic address: Beate.StPourcain@mpi.nl.
Lindon J EavesDepartment of Human and Molecular Genetics, Institute for Psychiatric and Behavioral Genetics, Commonwealth University School of Medicine, Richmond, Virginia.
Susan M RingMedical Research Council Integrative Epidemiology Unit, University of Bristol, Bristol, United Kingdom; School of Social and Community Medicine, University of Bristol, Bristol, United Kingdom.
Simon E FisherLanguage and Genetics Department, Max Planck Institute for Psycholinguistics, The Netherlands; Donders Institute for Brain, Cognition and Behaviour, Radboud University, Nijmegen, The Netherlands.
Sarah MedlandPsychiatric Genetics, QIMR Berghofer Medical Research Institute, Queensland, Australia.
David M EvansMedical Research Council Integrative Epidemiology Unit, University of Bristol, Bristol, United Kingdom; University of Queensland Diamantina Institute, Translational Research Institute, University of Queensland, Brisbane, Queensland, Australia.
George Davey SmithMedical Research Council Integrative Epidemiology Unit, University of Bristol, Bristol, United Kingdom; School of Social and Community Medicine, University of Bristol, Bristol, United Kingdom.

Funding

Medical Research Council G9815508Medical Research Council MC_PC_15018Medical Research Council MC_UU_12013/1Medical Research Council MC_UU_12013/4Wellcome TrustWellcome Trust 102215/2/13/2
6 · The paper itself

Abstract

backgroundRecent analyses of trait-disorder overlap suggest that psychiatric dimensions may relate to distinct sets of genes that exert maximum influence during different periods of development. This includes analyses of social communication difficulties that share, depending on their developmental stage, stronger genetic links with either autism spectrum disorder or schizophrenia. We developed a multivariate analysis framework in unrelated individuals to model directly the developmental profile of genetic influences contributing to complex traits, such as social communication difficulties, during an approximately 10-year period spanning childhood and adolescence.

methodsLongitudinally assessed quantitative social communication problems (N ≤ 5551) were studied in participants from a United Kingdom birth cohort (Avon Longitudinal Study of Parents and Children; age range, 8-17 years). Using standardized measures, genetic architectures were investigated with novel multivariate genetic-relationship-matrix structural equation models incorporating whole-genome genotyping information. Analogous to twin research, genetic-relationship-matrix structural equation models included Cholesky decomposition, common pathway, and independent pathway models.

resultsA two-factor Cholesky decomposition model described the data best. One genetic factor was common to Social Communication Disorder Checklist measures across development; the other accounted for independent variation at 11 years and later, consistent with distinct developmental profiles in trait-disorder overlap. Importantly, genetic factors operating at 8 years explained only approximately 50% of genetic variation at 17 years.

conclusionsUsing latent factor models, we identified developmental changes in the genetic architecture of social communication difficulties that enhance the understanding of autism spectrum disorder- and schizophrenia-related dimensions. More generally, genetic-relationship-matrix structural equation models present a framework for modeling shared genetic etiologies between phenotypes and can provide prior information with respect to patterns and continuity of trait-disorder overlap.

Indexed as

Genetic VariationGenome-Wide Association StudyModels, StatisticalAdolescentAdolescent DevelopmentChildChild DevelopmentFemaleHumansLongitudinal StudiesMaleMultivariate AnalysisSocial Communication DisorderUnited KingdomALSPACGenetic relationship matrixGenetic-relationship matrix structural equation modelingGenetic variance decompositionLongitudinal analysisStructural equation modeling

Identifiers

PMID29100628
PMCPMC5855319

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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.