Cited by 97Autism Spectrum Disorder ResearchAttention Deficit Hyperactivity DisorderGenetic Associations and Epidemiology

Shared genetic influences between dimensional ASD and ADHD symptoms during child and adolescent development

Open access
Stergiakouli, Evie, Davey Smith, George, Martin, Joanna, Skuse, David H., Viechtbauer, Wolfgang, Ring, Susan M., Ronald, Angelica, Evans, David E. +3 more·2017·Molecular Autism

Abstract

Shared genetic influences between attention-deficit/hyperactivity disorder (ADHD) symptoms and autism spectrum disorder (ASD) symptoms have been reported. Cross-trait genetic relationships are, however, subject to dynamic changes during development. We investigated the continuity of genetic overlap between ASD and ADHD symptoms in a general population sample during childhood and adolescence. We also studied uni- and cross-dimensional trait-disorder links with respect to genetic ADHD and ASD risk. Social-communication difficulties (N ≤ 5551, Social and Communication Disorders Checklist, SCDC) and combined hyperactive-impulsive/inattentive ADHD symptoms (N ≤ 5678, Strengths and Difficulties Questionnaire, SDQ-ADHD) were repeatedly measured in a UK birth cohort (ALSPAC, age 7 to 17 years). Genome-wide summary statistics on clinical ASD (5305 cases; 5305 pseudo-controls) and ADHD (4163 cases; 12,040 controls/pseudo-controls) were available from the Psychiatric Genomics Consortium. Genetic trait variances and genetic overlap between phenotypes were estimated using genome-wide data. In the general population, genetic influences for SCDC and SDQ-ADHD scores were shared throughout development. Genetic correlations across traits reached a similar strength and magnitude (cross-trait r g ≤ 1, p min = 3 × 10−4) as those between repeated measures of the same trait (within-trait r g ≤ 0.94, p min = 7 × 10−4). Shared genetic influences between traits, especially during later adolescence, may implicate variants in K-RAS signalling upregulated genes (p-meta = 6.4 × 10−4). Uni-dimensionally, each population-based trait mapped to the expected behavioural continuum: risk-increasing alleles for clinical ADHD were persistently associated with SDQ-ADHD scores throughout development (marginal regression R 2 = 0.084%). An age-specific genetic overlap between clinical ASD and social-communication difficulties during childhood was also shown, as per previous reports. Cross-dimensionally, however, neither SCDC nor SDQ-ADHD scores were linked to genetic risk for disorder. In the general population, genetic aetiologies between social-communication difficulties and ADHD symptoms are shared throughout child and adolescent development and may implicate similar biological pathways that co-vary during development. Within both the ASD and the ADHD dimension, population-based traits are also linked to clinical disorder, although much larger clinical discovery samples are required to reliably detect cross-dimensional trait-disorder relationships.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1186/s13229-017-0131-2

Cites

72 of 72 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • There is growing evidence that ASD and ADHD share common genetic variants, similar psychological deficits and neuroimaging differences.

    “There is also growing evidence that ASD and ADHD share common genetic variants, similar psychological deficits and neuroimaging differences [10–12].”

    From Mental, behavioral and neurodevelopmental disorders in the ICD-11: an international perspective on key changes and controversies (2020) · cites this paper as [10]

    The Discussion (page not specified) reports shared influences tagged by common genetic variants between population-based social-communication difficulties and ADHD symptoms. It also says there was little support for genetic overlap between clinical ASD and clinical ADHD. The paper does not establish the claimed shared psychological deficits or neuroimaging differences. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Stergiakouli, E., Davey Smith, G., Martin, J., Skuse, D. H., Viechtbauer, W., Ring, S. M., Ronald, A., Evans, D. E., Fisher, S. E., Thapar, A., & St Pourcain, B.
Affiliations
  • University of Bristol (GB)
  • Broad Institute (US)
  • University College London (GB)
  • Maastricht University (NL)
  • University of London (GB)
  • Radboud University Nijmegen (NL)
  • Cardiff University (GB)
Venue
Molecular Autism
Published
2017-04-04
Volume
8
Issue
1
Pages
18-18
ISSN
2040-2392 (ISSN-L)
OpenAlex
W2605164917
Cited by
97
References
72
Citations by year
2026: 4 · 2025: 8 · 2024: 9 · 2023: 10 · 2022: 11 · 2021: 22 · 2020: 14 · 2019: 11 · 2018: 6 · 2017: 2
FWCI
5.18
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Molecular Autism (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Bristol Research (University of Bristol) (publishedVersion, cc-by)
  • BIROn (Birkbeck, University of London) (acceptedVersion)
  • ORCA Online Research @Cardiff (Cardiff University) (acceptedVersion)
  • Lirias (submittedVersion, cc-by)
  • MPG.PuRe (Max Planck Society) (submittedVersion, cc-by)
  • Research Publications (Maastricht University) (submittedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • UCL Discovery (University College London) (submittedVersion)
  • Radboud Repository (Radboud University) (submittedVersion)
  • Explore Bristol Research (submittedVersion, cc-by)
  • Radboud Repository (Radboud University) (submittedVersion, other-oa)
  • Research Publications (Maastricht University) (submittedVersion, other-oa)
Funders
  • Wellcome Trust (102215/2/13/2)
  • Autism Speaks (7132)
Topics
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
  • Health Sciences › Medicine › Psychiatry and Mental health › Attention Deficit Hyperactivity Disorder
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
Keywords
autism spectrum disorder, attention deficit hyperactivity disorder, genetic overlap, social communication deficits, child and adolescent development, genetic risk, ALSPAC birth cohort, Strengths and Difficulties Questionnaire, psychiatric genetics
MeSH terms
Autism Spectrum Disorder, Adolescent, Attention Deficit Disorder with Hyperactivity, Child, Child Development, Female, United Kingdom, Humans, Male, Phenotype, Surveys and Questionnaires, Risk Factors, Genetic Variation, Quantitative Trait, Heritable, Adolescent Development, Genome-Wide Association Study, Sociological Factors

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review