Evidence map›Paper›PMID 28044064›Full record

ArticleMolecular psychiatry2018

ASD and schizophrenia show distinct developmental profiles in common genetic overlap with population-based social communication difficulties.

B St Pourcain, E B Robinson, V Anttila, B B Sullivan, J Maller, J Golding, D Skuse, S Ring, D M Evans, S Zammit and 14 more

Abstract read
In one paragraph

Article in Molecular psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 4 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

69 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. The Autism-Psychosis Continuum Conundrum: Exploring the Role of the Endocannabinoid System.International journal of environmental research and public health · 2022
    Pooled it
  4. Pooled it
  5. Article
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  7. Polygenic and developmental profiles of autism differ by age at diagnosis.medRxiv : the preprint server for health sciences · 2025
    Article
  8. How pharmacology can aid in the diagnosis of mental disorders.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
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9 more citing papers are in PubMed but not listed here.

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

24 authors.

B St PourcainMRC Integrative Epidemiology Unit, University of Bristol, Bristol, UK.
E B RobinsonAnalytic and Translational Genetics Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
V AnttilaAnalytic and Translational Genetics Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
B B SullivanAnalytic and Translational Genetics Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
J MallerAnalytic and Translational Genetics Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
J GoldingCentre for Child and Adolescent Health, University of Bristol, Bristol, UK.
D SkuseBehavioural and Brain Sciences, Institute of Child Health, University College London, London, UK.
S RingMRC Integrative Epidemiology Unit, University of Bristol, Bristol, UK.
D M EvansMRC Integrative Epidemiology Unit, University of Bristol, Bristol, UK.
S ZammitMRC Integrative Epidemiology Unit, University of Bristol, Bristol, UK.
S E FisherLanguage and Genetics Department, Max Planck Institute for Psycholinguistics, Nijmegen, The Netherlands.
B M NealeAnalytic and Translational Genetics Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
R J L AnneyDepartment of Psychiatry, Harvard Medical School, Boston, MA, USA.
S RipkeAnalytic and Translational Genetics Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
M V HollegaardStatens Serum Institut, Department of Congenital Disorders, Copenhagen, Denmark.
T WergeThe Lundbeck Foundation Initiative for Integrative Psychiatric Research, iPSYCH, Aarhus, Denmark.
iPSYCH-SSI-Broad Autism Group
A RonaldDepartment of Psychological Sciences, Birkbeck, University of London, London, UK.
J GroveThe Lundbeck Foundation Initiative for Integrative Psychiatric Research, iPSYCH, Aarhus, Denmark.
D M HougaardStatens Serum Institut, Department of Congenital Disorders, Copenhagen, Denmark.
A D BørglumThe Lundbeck Foundation Initiative for Integrative Psychiatric Research, iPSYCH, Aarhus, Denmark.
P B MortensenThe Lundbeck Foundation Initiative for Integrative Psychiatric Research, iPSYCH, Aarhus, Denmark.
M J DalyAnalytic and Translational Genetics Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
G Davey SmithMRC Integrative Epidemiology Unit, University of Bristol, Bristol, UK.

Funding

2/4-Psychiatric GWAS Consortium: Genomic Follow-Up Next-Gen Sequencing & GenotypiU01MH094432 · NIMH · MASSACHUSETTS GENERAL HOSPITAL · PI DALY, MARK JOSEPH · 2012 to 2015
$3.0M
The genomic bridge project (GBP)K01MH099286 · NIMH · MASSACHUSETTS GENERAL HOSPITAL · PI ROBINSON, ELISE B · 2013 to 2016
$647k
Medical Research Council G0801418Medical Research Council G9815508Medical Research Council MC_PC_15018Medical Research Council MC_UU_12013/4Medical Research Council MR/L010305/1NIMH NIH HHS K01 MH099286NIMH NIH HHS U01 MH094432Wellcome Trust 102215
6 · The paper itself

Abstract

Difficulties in social communication are part of the phenotypic overlap between autism spectrum disorders (ASD) and schizophrenia. Both conditions follow, however, distinct developmental patterns. Symptoms of ASD typically occur during early childhood, whereas most symptoms characteristic of schizophrenia do not appear before early adulthood. We investigated whether overlap in common genetic influences between these clinical conditions and impairments in social communication depends on the developmental stage of the assessed trait. Social communication difficulties were measured in typically-developing youth (Avon Longitudinal Study of Parents and Children, N⩽5553, longitudinal assessments at 8, 11, 14 and 17 years) using the Social Communication Disorder Checklist. Data on clinical ASD (PGC-ASD: 5305 cases, 5305 pseudo-controls; iPSYCH-ASD: 7783 cases, 11 359 controls) and schizophrenia (PGC-SCZ2: 34 241 cases, 45 604 controls, 1235 trios) were either obtained through the Psychiatric Genomics Consortium (PGC) or the Danish iPSYCH project. Overlap in genetic influences between ASD and social communication difficulties during development decreased with age, both in the PGC-ASD and the iPSYCH-ASD sample. Genetic overlap between schizophrenia and social communication difficulties, by contrast, persisted across age, as observed within two independent PGC-SCZ2 subsamples, and showed an increase in magnitude for traits assessed during later adolescence. ASD- and schizophrenia-related polygenic effects were unrelated to each other and changes in trait-disorder links reflect the heterogeneity of genetic factors influencing social communication difficulties during childhood versus later adolescence. Thus, both clinical ASD and schizophrenia share some genetic influences with impairments in social communication, but reveal distinct developmental profiles in their genetic links, consistent with the onset of clinical symptoms.

Indexed as

AdolescentAttention Deficit Disorder with HyperactivityAutism Spectrum DisorderChildChild Development Disorders, PervasiveCommunicationFemaleGenome-Wide Association StudyHumansLanguageLongitudinal StudiesMaleMultifactorial InheritanceRisk FactorsSchizophreniaSocial Behavior

Identifiers

PMID28044064
PMCPMC5382976

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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.