Evidence map›Paper›PMID 37794485›Full record

ArticleMolecular autism2023

The neuroanatomical substrates of autism and ADHD and their link to putative genomic underpinnings.

Lisa M Berg, Caroline Gurr, Johanna Leyhausen, Hanna Seelemeyer, Anke Bletsch, Tim Schaefer, Charlotte M Pretzsch, Bethany Oakley, Eva Loth, Dorothea L Floris and 11 more

Open access · goldAbstract readMulticenter Study
In one paragraph

Article in Molecular autism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 6% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
  2. Autism and Cortical Thickness Deviation From Neurotypical Controls: Evidence for a Spatial Association With Serotonin Receptors.Autism research : official journal of the International Society for Autism Research · 2026
    Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Connectome-based symptom mapping andmedRxiv : the preprint server for health sciences · 2024
    Article
  10. Expression of CLDN1 and EGFR in PTC.Discover oncology · 2024
    Article
  11. Article
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

21 authors at 15 institutions in 10 countries.

Lisa M BergDepartment of Child and Adolescent Psychiatry, University Hospital, Goethe University, Deutschordenstrasse 50, 60528, Frankfurt am Main, Germany. lisamarie.berg@kgu.de.
Caroline GurrDepartment of Child and Adolescent Psychiatry, University Hospital, Goethe University, Deutschordenstrasse 50, 60528, Frankfurt am Main, Germany.
Johanna LeyhausenDepartment of Child and Adolescent Psychiatry, University Hospital, Goethe University, Deutschordenstrasse 50, 60528, Frankfurt am Main, Germany.
Hanna SeelemeyerDepartment of Child and Adolescent Psychiatry, University Hospital, Goethe University, Deutschordenstrasse 50, 60528, Frankfurt am Main, Germany.
Anke BletschDepartment of Child and Adolescent Psychiatry, University Hospital, Goethe University, Deutschordenstrasse 50, 60528, Frankfurt am Main, Germany.
Tim SchaeferFries Lab, Ernst Strüngmann Institute (ESI) for Neuroscience in Cooperation with Max Planck Society, 60528, Frankfurt, Germany.
Charlotte M PretzschDepartment of Forensic and Neurodevelopmental Sciences, Institute of Psychiatry, Psychology and Neuroscience, King's College, London, SE5 8AF, UK.
Bethany OakleyDepartment of Forensic and Neurodevelopmental Sciences, Institute of Psychiatry, Psychology and Neuroscience, King's College, London, SE5 8AF, UK.
Eva LothDepartment of Forensic and Neurodevelopmental Sciences, Institute of Psychiatry, Psychology and Neuroscience, King's College, London, SE5 8AF, UK.
Dorothea L FlorisDepartment of Cognitive Neuroscience, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands.
Jan K BuitelaarDepartment of Cognitive Neuroscience, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands.
Christian F BeckmannDepartment of Cognitive Neuroscience, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands.
Tobias BanaschewskiChild and Adolescent Psychiatry, Medical Faculty Mannheim, Central Institute of Mental Health, University of Heidelberg, Mannheim, Germany.
Tony CharmanDepartment of Psychology, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, SE5 8AF, UK.
Emily J H JonesCentre for Brain and Cognitive Development, Birkbeck, University of London, Malet Street, London, WC1E 7JL, UK.
Julian TillmannF. Hoffmann-La Roche, Innovation Center Basel, Basel, Switzerland.
Chris H ChathamF. Hoffmann-La Roche, Innovation Center Basel, Basel, Switzerland.
Thomas BourgeronHuman Genetics and Cognitive Functions Unit, Institut Pasteur, Paris, France.
EU-AIMS LEAP Group
Declan G MurphyDepartment of Forensic and Neurodevelopmental Sciences, Institute of Psychiatry, Psychology and Neuroscience, King's College, London, SE5 8AF, UK.
Christine EckerDepartment of Child and Adolescent Psychiatry, University Hospital, Goethe University, Deutschordenstrasse 50, 60528, Frankfurt am Main, Germany.
King's College London · GBRadboud University Nijmegen · NLRoche (Switzerland) · CHGoethe University Frankfurt · DEHeidelberg University · DEInstitut Pasteur · FRUniversità Cattolica del Sacro Cuore · ITBirkbeck, University of London · GBUniversity of Cambridge · GBUniversity of Modena and Reggio Emilia · ITCentre for Addiction and Mental Health · CAErnst Strüngmann Institute for Neuroscience · DEItalian Institute of Technology · ITJanssen (United States) · USUtrecht University · NL

Funding

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

Abstract

backgroundAutism spectrum disorders (ASD) are neurodevelopmental conditions accompanied by differences in brain development. Neuroanatomical differences in autism are variable across individuals and likely underpin distinct clinical phenotypes. To parse heterogeneity, it is essential to establish how the neurobiology of ASD is modulated by differences associated with co-occurring conditions, such as attention-deficit/hyperactivity disorder (ADHD). This study aimed to (1) investigate between-group differences in autistic individuals with and without co-occurring ADHD, and to (2) link these variances to putative genomic underpinnings.

methodsWe examined differences in cortical thickness (CT) and surface area (SA) and their genomic associations in a sample of 533 individuals from the Longitudinal European Autism Project. Using a general linear model including main effects of autism and ADHD, and an ASD-by-ADHD interaction, we examined to which degree ADHD modulates the autism-related neuroanatomy. Further, leveraging the spatial gene expression data of the Allen Human Brain Atlas, we identified genes whose spatial expression patterns resemble our neuroimaging findings.

resultsIn addition to significant main effects for ASD and ADHD in fronto-temporal, limbic, and occipital regions, we observed a significant ASD-by-ADHD interaction in the left precentral gyrus and the right frontal gyrus for measures of CT and SA, respectively. Moreover, individuals with ASD + ADHD differed in CT to those without. Both main effects and the interaction were enriched for ASD-but not for ADHD-related genes. LIMITATIONS: Although we employed a multicenter design to overcome single-site recruitment limitations, our sample size of N = 25 individuals in the ADHD only group is relatively small compared to the other subgroups, which limits the generalizability of the results. Also, we assigned subjects into ADHD positive groupings according to the DSM-5 rating scale. While this is sufficient for obtaining a research diagnosis of ADHD, our approach did not take into account for how long the symptoms have been present, which is typically considered when assessing ADHD in the clinical setting.

conclusionThus, our findings suggest that the neuroanatomy of ASD is significantly modulated by ADHD, and that autistic individuals with co-occurring ADHD may have specific neuroanatomical underpinnings potentially mediated by atypical gene expression.

Indexed as

Attention Deficit Disorder with HyperactivityAutism Spectrum DisorderAutistic DisorderBrainGenomicsHumansNeuroanatomyADHDASDComorbidityImaging-geneticsNeurodevelopmental disordersStructural MRI

Identifiers

PMID37794485
PMCPMC10552404
OpenAlexW4387344491

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.