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

Family-based association study of serotonergic candidate genes and attention-deficit/hyperactivity disorder in a German sample.

Journal of neural transmission (Vienna, Austria : 1996) - 1 Jan 2007

Heiser P, Dempfle A, Friedel S, Konrad K, Hinney A, Kiefl H, Walitza S, Bettecken T, Saar K, Linder M, Warnke A, Herpertz-Dahlmann B, Schäfer H, Remschmidt H, Hebebrand J

Abstract excerpt

Alterations in the serotonergic pathway have been implicated in the pathogenesis of attention-deficit/hyperactivity disorder (ADHD). The aim of this study was to investigate seven genetic variants in three genes (serotonin transporter (5-HTT), serotonin receptor 1B (5-HTR1B) and serotonin receptor 2A (5-HTR2A)), which have previously been shown to be associated with ADHD. The polymorphisms under investigation...

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 Germany

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Pedigree

Share to Polymerase Chain Reaction

Share to Receptor, Serotonin, 5-HT1B

Share to Receptor, Serotonin, 5-HT2A

Share to Serotonin

Share to Serotonin Plasma Membrane Transport Proteins

Source

Identifiers

PMID: 17093889
DOI: 10.1007/s00702-006-0584-5

Genes

HTT

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Family-based association study of serotonergic candidate genes and attention-deficit/hyperactivity disorder in a German sample.PMID 17093889Read ↗

Serotonergic system and attention deficit hyperactivity disorder (ADHD): a potential susceptibility locus at the 5-HT(1B) receptor gene in 273 nuclear families from a multi-centre sample.Semantic proximity Read ↗

No association of attention-deficit/hyperactivity disorder with genes of the serotonergic pathway in Han Chinese subjects.Semantic proximity Read ↗

Family-based association study of serotonin transporter gene polymorphisms in attention deficit hyperactivity disorder: no evidence for association in UK and Taiwanese samples.Semantic proximity Read ↗

Genetic Association of HTR1B and HTR2A Gene Polymorphisms with ADHD in Korean Children and Adolescents: A Case Control Study.Semantic proximity Read ↗

Molecular genetics of attention-deficit/hyperactivity disorder: an overview.Semantic proximity Read ↗

Transmission disequilibrium of polymorphic variants in the tryptophan hydroxylase-2 gene in attention-deficit/hyperactivity disorder.Semantic proximity Read ↗

Family-based association study of the serotonin transporter promoter region polymorphism (5-HTTLPR) in attention deficit hyperactivity disorder.Semantic proximity Read ↗

Candidate gene studies of attention-deficit/hyperactivity disorder.Semantic proximity Read ↗

Family-based association study of tryptophan hydroxylase 2 and serotonin 1A receptor genes in attention deficit hyperactivity disorder.Semantic proximity Read ↗

Family-based association study of the serotonin transporter gene polymorphisms in Korean ADHD trios.Semantic proximity Read ↗

ADHD genetics: 2007 update.Semantic proximity Read ↗

A case-control association study of serotonin 1A receptor gene and tryptophan hydroxylase 2 gene in attention deficit hyperactivity disorder.Semantic proximity Read ↗

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