Evidence map›Paper›PMID 23712748›Full record

ArticleJournal of neural transmission (Vienna, Austria : 1996)2013

Bipolar disorder risk alleles in children with ADHD.

B G Schimmelmann, A Hinney, A Scherag, C Pütter, S Pechlivanis, S Cichon, K-H Jöckel, S Schreiber, H E Wichmann, Ö Albayrak and 12 more

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In one paragraph

Article in Journal of neural transmission (Vienna, Austria : 1996), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 3 pooled it
1.3field-weighted citation impact, top 20% 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

7 citing papers in PubMed, 3 syntheses or guidelines pooled it, 18 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Article
  6. DominantAnnals of clinical and translational neurology · 2019
    Article
  7. Review
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

22 authors at 10 institutions in 3 countries.

B G SchimmelmannUniversity Hospital of Child and Adolescent Psychiatry, University of Bern, Bolligenstr. 111, 3000, Bern 60, Switzerland, bschimme@aol.com.
A Hinney
A Scherag
C Pütter
S Pechlivanis
S Cichon
K-H Jöckel
S Schreiber
H E Wichmann
Ö Albayrak
M Dauvermann
K Konrad
C Wilhelm
B Herpertz-Dahlmann
G Lehmkuhl
J Sinzig
T J Renner
M Romanos
A Warnke
K P Lesch
A Reif
J Hebebrand
Essen University Hospital · DEUniversity of Würzburg · DEFH Aachen · DEUniversity of Cologne · DECenter for Environmental Health · USHeinz Nixdorf Stiftung · DEUniversity Hospital Schleswig-Holstein · DEUniversity of Bern · CHUniversity of Bonn · DEUniversity of Duisburg-Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bipolar disorder (BD) and attention deficit/hyperactivity disorder (ADHD) may share common genetic risk factors as indicated by the high co-morbidity of BD and ADHD, their phenotypic overlap especially in pediatric populations, the high heritability of both disorders, and the co-occurrence in families. We therefore examined whether known polygenic BD risk alleles are associated with ADHD. We chose the eight best SNPs of the recent genome-wide association study (GWAS) of BD patients of German ancestry and the nine SNPs from international GWAS meeting a 'genome-wide significance' level of α = 5 × 10(-8). A GWAS was performed in 495 ADHD children and 1,300 population-based controls using HumanHap550v3 and Human660 W-Quadv1 BeadArrays. We found no significant association of childhood ADHD with single BD risk alleles surviving adjustment for multiple testing. Yet, risk alleles for BD and ADHD were directionally consistent at eight of nine loci with the strongest support for three SNPs in or near NCAN, BRE, and LMAN2L. The polygene analysis for the BP risk alleles at all 14 loci indicated a higher probability of being a BD risk allele carrier in the ADHD cases as compared to the controls. At a moderate power to detect association with ADHD, if true effects were close to estimates from GWAS for BD, our results suggest that the possible contribution of BD risk variants to childhood ADHD risk is considerably lower than for BD. Yet, our findings should encourage researchers to search for common genetic risk factors in BD and childhood ADHD in future studies.

Indexed as

AllelesGenetic Predisposition to DiseasePolymorphism, Single NucleotideAdolescentAttention Deficit Disorder with HyperactivityBipolar DisorderChildFemaleGenome-Wide Association StudyHaplotypesHumansMaleWhite People

Identifiers

PMID23712748
OpenAlexW2082977225

What OpenQuestion holds

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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.