Evidence map›Paper›PMID 14569274›Full record

ArticleMolecular psychiatry2004

Linkage of the dopamine receptor D1 gene to attention-deficit/hyperactivity disorder.

V L Misener, P Luca, O Azeke, J Crosbie, I Waldman, R Tannock, W Roberts, M Malone, R Schachar, A Ickowicz and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular psychiatry, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 3 pooled it
3.8field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 3 syntheses or guidelines pooled it, 101 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
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  11. A Dopamine DThe Journal of pharmacology and experimental therapeutics · 2022
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  19. Multivariate analysis of anxiety disorders yields further evidence of linkage to chromosomes 4q21 and 7p in panic disorder families.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2012
    Article
  20. Prenatal exposure to nicotine impairs performance of the 5-choice serial reaction time task in adult rats.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2011
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 2 countries.

V L MisenerCell and Molecular Biology Division, Toronto Western Research Institute, University Health Network, Toronto, Ontario, Canada.
P Luca
O Azeke
J Crosbie
I Waldman
R Tannock
W Roberts
M Malone
R Schachar
A Ickowicz
J L Kennedy
C L Barr
Hospital for Sick Children · CAUniversity Health Network · CACentre for Addiction and Mental Health · CAEmory University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Attention-deficit/hyperactivity disorder (ADHD) has a strong genetic basis, and evidence from human and animal studies suggests the dopamine receptor D1 gene, DRD1, to be a good candidate for involvement. Here, we tested for linkage of DRD1 to ADHD by examining the inheritance of four biallelic DRD1 polymorphisms [D1P.5 (-1251HaeIII), D1P.6 (-800HaeIII), D1.1 (-48DdeI) and D1.7 (+1403Bsp1286I)] in a sample of 156 ADHD families. Owing to linkage disequilibrium between alleles at the four markers, only three haplotypes are common in our sample. Using the transmission/disequilibrium test (TDT), we observed a strong bias for transmission of Haplotype 3 (1.1.1.2) from heterozygous parents to their affected children (P=0.008). Furthermore, using quantitative trait TDT analyses, we found significant and positive relationships between Haplotype 3 transmission and the inattentive symptoms, but not the hyperactive/impulsive symptoms, of ADHD. These findings support the proposed involvement of DRD1 in ADHD, and implicate Haplotype 3, in particular, as containing a potential risk factor for the inattentive symptom dimension of the disorder. Since none of the four marker alleles comprising Haplotype 3 is predicted to alter DRD1 function, we hypothesize that a functional DRD1 variant, conferring susceptibility to ADHD, is on this haplotype. To search for such a variant we screened the DRD1 coding region, by sequencing, focusing on the children who showed preferential transmission of Haplotype 3. DNA from 41 children was analysed, and no sequence variations were identified, indicating that the putative DRD1 risk variant for ADHD resides outside of the coding region of the gene.

Indexed as

AdolescentAllelesAttention Deficit Disorder with HyperactivityChildDNA Mutational AnalysisFemaleGene FrequencyGenotypeHaplotypesHumansImpulsive BehaviorLinkage DisequilibriumMalePolymorphism, GeneticReceptors, Dopamine D1Receptors, Dopamine D1

Identifiers

PMID14569274
OpenAlexW2011907831

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.