Evidence map›Paper›PMID 30563984›Full record

ArticleTranslational psychiatry2018

A case-control genome-wide association study of ADHD discovers a novel association with the tenascin R (TNR) gene.

Ziarih Hawi, Hannah Yates, Ari Pinar, Aurina Arnatkeviciute, Beth Johnson, Janette Tong, Kealan Pugsley, Callum Dark, Marc Pauper, Marieke Klein and 9 more

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 2 pooled it
6.2field-weighted citation impact, top 3% 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

10 citing papers in PubMed, 2 syntheses or guidelines pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Polygenic Scores for ADHD: A Meta-Analysis.Research on child and adolescent psychopathology · 2021
    Pooled it
  3. Article
  4. Article
  5. Neuroimaging genetic associations betweenJournal of clinical and experimental neuropsychology · 2021
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Loss of TNR causes a nonprogressive neurodevelopmental disorder with spasticity and transient opisthotonus.Genetics in medicine : official journal of the American College of Medical Genetics · 2020
    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

19 authors at 6 institutions in 4 countries.

Ziarih HawiSchool of Psychological Sciences and Monash Institute for Cognitive and Clinical Neurosciences (MICCN), Monash University, Melbourne, Australia. ziarih.hawi@monash.edu.
Hannah YatesSchool of Psychological Sciences and Monash Institute for Cognitive and Clinical Neurosciences (MICCN), Monash University, Melbourne, Australia.
Ari PinarSchool of Psychological Sciences and Monash Institute for Cognitive and Clinical Neurosciences (MICCN), Monash University, Melbourne, Australia.ORCID http://orcid.org/0000-0002-0064-4215
Aurina ArnatkeviciuteSchool of Psychological Sciences and Monash Institute for Cognitive and Clinical Neurosciences (MICCN), Monash University, Melbourne, Australia.
Beth JohnsonSchool of Psychological Sciences and Monash Institute for Cognitive and Clinical Neurosciences (MICCN), Monash University, Melbourne, Australia.
Janette TongSchool of Psychological Sciences and Monash Institute for Cognitive and Clinical Neurosciences (MICCN), Monash University, Melbourne, Australia.ORCID http://orcid.org/0000-0002-3269-1438
Kealan PugsleySchool of Psychological Sciences and Monash Institute for Cognitive and Clinical Neurosciences (MICCN), Monash University, Melbourne, Australia.
Callum DarkSchool of Psychological Sciences and Monash Institute for Cognitive and Clinical Neurosciences (MICCN), Monash University, Melbourne, Australia.
Marc PauperDepartments of Human Genetics, and Psychiatry, Radboud University Medical Center, Nijmegen, The Netherlands.
Marieke KleinDepartments of Human Genetics, and Psychiatry, Radboud University Medical Center, Nijmegen, The Netherlands.ORCID http://orcid.org/0000-0001-8784-5679
Helen S HeusslerMater Research Institute, University of Queensland and Children's Health Queensland, South Brisbane, Australia.
Harriet HiscockPediatrics Royal Children's Hospital, Murdoch Children's Institute, Melbourne, Australia.
Alex FornitoSchool of Psychological Sciences and Monash Institute for Cognitive and Clinical Neurosciences (MICCN), Monash University, Melbourne, Australia.
Jeggan TiegoSchool of Psychological Sciences and Monash Institute for Cognitive and Clinical Neurosciences (MICCN), Monash University, Melbourne, Australia.
Amy FinlaySchool of Psychological Sciences and Monash Institute for Cognitive and Clinical Neurosciences (MICCN), Monash University, Melbourne, Australia.
Alasdair VanceThe Royal Children's Hospital, University of Melbourne, Victoria, Australia.
Michael GillDepartment of Psychiatry, Trinity College, Dublin, Ireland.ORCID http://orcid.org/0000-0003-0206-5337
Lindsey KentSchool of Medicine, University of St Andrews, St. Andrews, Scotland, UK.
Mark A BellgroveSchool of Psychological Sciences and Monash Institute for Cognitive and Clinical Neurosciences (MICCN), Monash University, Melbourne, Australia.
Monash University · AURadboud University Nijmegen · NLRoyal Children's Hospital · AUThe University of Queensland · AUTrinity College Dublin · IEUniversity of St Andrews · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is well-established that there is a strong genetic contribution to the aetiology of attention deficit hyperactivity disorder (ADHD). Here, we employed a hypothesis-free genome-wide association study (GWAS) design in a sample of 480 clinical childhood ADHD cases and 1208 controls to search for novel genetic risk loci for ADHD. DNA was genotyped using Illumina's Human Infinium PsychArray-24v1.2., and the data were subsequently imputed to the 1000 Genomes reference panel. Rigorous quality control and pruning of genotypes at both individual subject and single nucleotide polymorphism (SNP) levels was performed. Polygenic risk score (PGRS) analysis revealed that ADHD case-control status was explained by genetic risk for ADHD, but no other major psychiatric disorders. Logistic regression analysis was performed genome-wide to test the association between SNPs and ADHD case-control status. We observed a genome-wide significant association (p = 3.15E-08) between ADHD and rs6686722, mapped to the Tenascin R (TNR) gene. Members of this gene family are extracellular matrix glycoproteins that play a role in neural cell adhesion and neurite outgrowth. Suggestive evidence of associations with ADHD was observed for an additional 111 SNPs (⩽9.91E-05). Although intriguing, the association between DNA variation in the TNR gene and ADHD should be viewed as preliminary given the small sample size of this discovery dataset.

Indexed as

AdolescentAttention Deficit Disorder with HyperactivityCase-Control StudiesChildChild, PreschoolFemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyGenotypeHumansMaleMultifactorial InheritancePolymorphism, Single NucleotideRisk FactorsTenascinTenascintenascin R

Identifiers

PMID30563984
PMCPMC6298965
OpenAlexW2903760415

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.