Evidence map›Paper›PMID 20856918›Full record

ArticleNeuropsychiatric disease and treatment2010

Fitting the pieces together: current research on the genetic basis of attention-deficit/hyperactivity disorder (ADHD).

Evangelia Stergiakouli, Anita Thapar

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Neuropsychiatric disease and treatment, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02323633 (A Single-blind, Randomised, Sham Controlled, Phase IIa Exploratory Clinical Trial, to Examine the Safety and Efficacy of BGX-3006), which is not on this map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
5.8field-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.

NCT02323633 phase2unknown statusnot on this mapstarted 2015, after this paper: background citation

A Single-blind, Randomised, Sham Controlled, Phase IIa Exploratory Clinical Trial, to Examine the Safety and Efficacy of BGX-3006 (tPCS) on Paediatric ADHD Participants.

TypeinterventionalSponsorBraingear Technologies GmbHRan2015 to 2015Enrolled48ConditionsAttention Deficit Disorder With HyperactivityArmsBraingear Brainbuds Pulsed Current stimulation device, Sham
3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 76 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Academic textbooks [corrected] on ADHD genetics: balanced or biased?International journal of qualitative studies on health and well-being · 2017
    Article
  11. Indian journal of clinical biochemistry : IJCB · 2017
    Article
  12. Article
  13. Article
  14. Article
  15. Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2016
    Article
  16. DAT1 and DRD4 genes involved in key dimensions of adult ADHD.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2015
    Article
  17. Article
  18. Review
  19. Article
  20. What have we learnt about the causes of ADHD?Journal of child psychology and psychiatry, and allied disciplines · 2013
    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

2 authors at 1 institution in 1 country.

Evangelia StergiakouliDepartment of Psychological, Medicine and Neurology, MRC Centre, for Neuropsychiatric Genetics and Genomics, School of Medicine, Cardiff, University, United Kingdom.
Anita Thapar
Cardiff University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Attention-deficit/hyperactivity disorder (ADHD) is a highly disruptive childhood-onset disorder that often persists into adolescence and adulthood. Comorbidity with other problems, such as autism, dyslexia and conduct disorder (CD) is very common. Although little is known about the pathophysiology of ADHD, family, twin and adoption studies have shown that it is highly heritable. Whole genome linkage studies suggest there are no common susceptibility genes of moderate effect size. Most published research has been based on functional candidate gene studies. The most consistent evidence for association with ADHD relates to a dopamine D4 receptor (DRD4) gene variable number tandem repeat (VNTR), a dopamine D5 receptor (DRD5) gene microsatellite and a dopamine transporter (DAT1) gene VNTR. In addition, the catechol-O-methyltransferase (COMT) val158/108 met variant has been shown to increase risk for associated antisocial behavior. The first genome-wide association studies (GWAS) of ADHD have been completed and although larger studies are still required to detect common risk variants, novel risk pathways are being suggested for ADHD. Further research on the contribution of rare variants, larger genome-wide association and sequencing studies and ADHD phenotype refinement is now needed.

Indexed as

attention-deficit/hyperactivity disorder (ADHD)gene-environment interplaygeneticsgenome-wide association study (GWAS)molecular genetics

Identifiers

PMID20856918
PMCPMC2938304
OpenAlexW1987620627

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.