Evidence map›Paper›PMID 27138430›Full record

ArticleJournal of neural transmission (Vienna, Austria : 1996)2016

The role of ASTN2 variants in childhood and adult ADHD, comorbid disorders and associated personality traits.

Christine M Freitag, Thomas Lempp, T Trang Nguyen, Christian P Jacob, Lena Weissflog, Marcel Romanos, Tobias J Renner, Susanne Walitza, Andreas Warnke, Dan Rujescu and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of neural transmission (Vienna, Austria : 1996), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

4 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. 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

12 authors at 6 institutions in 2 countries.

Christine M FreitagDepartment of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, University Hospital Frankfurt, Goethe University, Deutschordenstrasse 50, 60528, Frankfurt am Main, Germany. c.freitag@em.uni-frankfurt.de.
Thomas LemppDepartment of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, University Hospital Frankfurt, Goethe University, Deutschordenstrasse 50, 60528, Frankfurt am Main, Germany.
T Trang NguyenInstitute of Medical Biometry and Epidemiology, University of Marburg, Marburg, Germany.
Christian P JacobDepartment of Psychiatry, Psychosomatics and Psychotherapy, University of Würzburg, Würzburg, Germany.
Lena WeissflogDepartment of Psychiatry, Psychosomatics and Psychotherapy, University of Würzburg, Würzburg, Germany.
Marcel RomanosDepartment of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, University of Würzburg, Würzburg, Germany.
Tobias J RennerDepartment of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, University of Würzburg, Würzburg, Germany.
Susanne WalitzaDepartment of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, University of Würzburg, Würzburg, Germany.
Andreas WarnkeDepartment of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, University of Würzburg, Würzburg, Germany.
Dan RujescuDepartment of Psychiatry and Psychotherapy, University of Munich, Munich, Germany.
Klaus-Peter LeschDepartment of Psychiatry, Psychosomatics and Psychotherapy, University Hospital Frankfurt, Goethe University, Frankfurt am Main, Germany.
Andreas ReifDepartment of Psychiatry, Psychosomatics and Psychotherapy, University of Würzburg, Würzburg, Germany.
University of Würzburg · DEUniversity Hospital Frankfurt · DEGoethe University Frankfurt · DEMartin Luther University Halle-Wittenberg · DEPhilipps University of Marburg · DEUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous linkage and genome wide association (GWA) studies in ADHD indicated astrotactin 2 (ASTN2) as a candidate gene for attention-deficit/hyperactivity disorder (ADHD). ASTN2 plays a key role in glial-guided neuronal migration. To investigate whether common variants in ASTN2 contribute to ADHD disorder risk, we tested 63 SNPs spanning ASTN2 for association with ADHD and specific comorbid disorders in two samples: 171 families of children with ADHD and their parents (N = 592), and an adult sample comprising 604 adult ADHD cases and 974 controls. The C-allele of rs12376789 in ASTN2 nominally increased the risk for ADHD in the trio sample (p = 0.025). This was not observed in the adult case-control sample alone, but retained in the combined sample (nominal p = 0.030). Several other SNPs showed nominally significant association with comorbid disorders, especially anxiety disorder, in the childhood and adult ADHD samples. Some ASTN2 variants were nominally associated with personality traits in the adult ADHD sample and overlapped with risk alleles for comorbid disorders in childhood. None of the findings survived correction for multiple testing, thus, results do not support a major role of common variants in ASTN2 in the pathogenesis of ADHD, its comorbid disorders or ADHD associated personality traits.

Indexed as

PersonalityAdolescentAdultAttention Deficit Disorder with HyperactivityCase-Control StudiesChildFemaleGenetic Association StudiesGenetic Predisposition to DiseaseGlycoproteinsHumansMaleNerve Tissue ProteinsParentsPersonality DisordersPolymorphism, Single NucleotideASTN2 protein, humanGlycoproteinsNerve Tissue ProteinsAnxiety disorderAstrotactin 2Attention-deficit/hyperactivity disorderComorbid disordersPersonality traits

Identifiers

PMID27138430
OpenAlexW2344830430

What OpenQuestion holds

Textmetadata
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.