Evidence map›Paper›PMID 15520832›Full record

Trial reportMolecular psychiatry2005

Association and linkage of alpha-2A adrenergic receptor gene polymorphisms with childhood ADHD.

L Park, J T Nigg, I D Waldman, K A Nummy, C Huang-Pollock, M Rappley, K H Friderici

Abstract readClinical TrialComparative StudyControlled Clinical Trial
PubMed Publisher
In one paragraph

Trial report in Molecular psychiatry, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 3 pooled it
4.6field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 3 syntheses or guidelines pooled it, 91 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pharmacogenetic predictors of methylphenidate dose-response in attention-deficit/hyperactivity disorder.Journal of the American Academy of Child and Adolescent Psychiatry · 2011
    Trial
  5. Trial
  6. Discovery of a peripherally restricted αCell reports. Medicine · 2026
    Article
  7. The Role of Gene-Gene Interaction BetweenChildren (Basel, Switzerland) · 2025
    Article
  8. Review
  9. Heteromerization between αPharmacological research · 2021
    Article
  10. Genetic influences on ADHD symptom dimensions: Examination of a priori candidates, gene-based tests, genome-wide variation, and SNP heritability.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2017
    Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Sequence analysis of the ADRA2A coding region in children affected by attention deficit hyperactivity disorder.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2013
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

L ParkGenetics Program, Michigan State University, East Lansing, MI 48824, USA.
J T Nigg
I D Waldman
K A Nummy
C Huang-Pollock
M Rappley
K H Friderici
Michigan State University · USEmory University · US

Funding

NEUROPSYCHOLOGICAL AND FAMILIAL MARKERS FOR CHILD ADHDR01MH059105 · NIMH · OREGON HEALTH & SCIENCE UNIVERSITY · PI NIGG, JOEL T · 1999 to 2012
$3.3M
MOLECULAR GENETICS OF CHILDHOOD DISRUPTIVE DISORDERSK01MH001818 · NIMH · EMORY UNIVERSITY · PI WALDMAN, IRWIN D · 2000 to 2004
$679k
NIMH NIH HHS MH-01818NIMH NIH HHS MH59105
6 · The paper itself

Abstract

Attention-deficit hyperactivity disorder (ADHD) is a heritable disorder, prevalent from childhood through adulthood. Although the noradrenergic (NA) system is thought to mediate a portion of the pathophysiology of ADHD, genes in this pathway have not been investigated as frequently as those in the dopaminergic system. Previous association studies of one candidate gene in the NA system, ADRA2A, showed inconsistent results with regard to an MspI polymorphism. In the current study, two nearby single-nucleotide polymorphisms, which define HhaI and DraI restriction fragment length polymorphisms, were also genotyped and were in significant linkage disequilibrium with the MspI RFLP. Transmission disequilibrium tests (TDTs) in a sample of 177 nuclear families showed significant association and linkage of the DraI polymorphism with the ADHD combined subtype (P=0.03), and the quantitative TDT showed association of this polymorphism with the inattentive (P=0.003) and hyperactive-impulsive (P=0.015) symptom dimensions. The haplotype that contained the less common allele of the DraI polymorphism likewise showed a strong relationship with the inattentive (P=0.001) and hyperactive-impulsive (P=0.004) symptom dimensions. This study supports the hypothesis that an allele of the ADRA2A gene is associated and linked with the ADHD combined subtype and suggests that the DraI polymorphism of ADRA2A is linked to a causative polymorphism.

Indexed as

AdolescentAdultAttention Deficit Disorder with HyperactivityChildFemaleGenetic Predisposition to DiseaseHaplotypesHumansLinkage DisequilibriumMalePedigreePolymorphism, Restriction Fragment LengthPolymorphism, Single NucleotideQuantitative Trait, HeritableReceptors, Adrenergic, alpha-2Risk FactorsADRA2A protein, humanReceptors, Adrenergic, alpha-2

Identifiers

PMID15520832
OpenAlexW1981559267

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.