Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Effects of dopaminergic genes, prenatal adversities, and their interaction on attention-deficit/hyperactivity disorder and neural correlates of response inhibition.

Journal of psychiatry & neuroscience : JPN - 1 Mar 2017

van der Meer Dennis, Hartman Catharina A, van Rooij Daan, Franke Barbara, Heslenfeld Dirk J, Oosterlaan Jaap, Faraone Stephen V, Buitelaar Jan K, Hoekstra Pieter J

Abstract excerpt

BACKGROUND: Attention-deficit/hyperactivity disorder (ADHD) is often accompanied by impaired response inhibition; both have been associated with aberrant dopamine signalling. Given that prenatal exposure to alcohol or smoking is known to affect dopamine-rich brain regions, we hypothesized that individuals carrying the ADHD risk alleles of the dopamine receptor D4 (DRD4) and dopamine transporter (DAT1) genes may...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Attention Deficit Disorder with Hyperactivity
Share to Dopamine Plasma Membrane Transport Proteins

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Fetal Alcohol Spectrum Disorders

Share to Gene-Environment Interaction

Share to Inhibition, Psychological

Share to Prenatal Exposure Delayed Effects

Share to Receptors, Dopamine D4

Share to Smoking

Source

Open in PubMed Open full text

Identifiers

PMID: 28234207
DOI: 10.1503/jpn.150350
PMCID: PMC5373700

Genes

DRD4

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Effects of dopaminergic genes, prenatal adversities, and their interaction on attention-deficit/hyperactivity disorder and neural correlates of response inhibition.PMID 28234207Read ↗

The dopamine receptor D4 7-repeat allele and prenatal smoking in ADHD-affected children and their unaffected siblings: no gene-environment interaction.Semantic proximity Read ↗

Effects of maternal and paternal smoking on attentional control in children with and without ADHD.Semantic proximity Read ↗

Understanding genes, environment and their interaction in attention-deficit hyperactivity disorder: is there a role for neuroimaging?Semantic proximity Read ↗

Gene-environment interactions in attention-deficit/hyperactivity disorder.Semantic proximity Read ↗

Testing differential susceptibility: Plasticity genes, the social environment, and their interplay in adolescent response inhibition.Semantic proximity Read ↗

Prenatal smoking exposure and dopaminergic genotypes interact to cause a severe ADHD subtype.Semantic proximity Read ↗

Role of dopamine transporter genotype and maternal prenatal smoking in childhood hyperactive-impulsive, inattentive, and oppositional behaviors.Semantic proximity Read ↗

Gene-environment interactions in the development of combined type ADHD: evidence for a synapse-based model.Semantic proximity Read ↗

Neural correlates of inhibitory control and functional genetic variation in the dopamine D4 receptor gene.Semantic proximity Read ↗

Neuropsychological endophenotypes in attention-deficit/hyperactivity disorder: a review of genetic association studies.Semantic proximity Read ↗

Genetics of preparation and response control in ADHD: the role of DRD4 and DAT1.Semantic proximity Read ↗

Candidate genes and neuropsychological phenotypes in children with ADHD: review of association studiesSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.