ArticleJournal of neural transmission (Vienna, Austria : 1996)2007
Family-based association study of serotonergic candidate genes and attention-deficit/hyperactivity disorder in a German sample.
Article in Journal of neural transmission (Vienna, Austria : 1996), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.
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Who cites it
16 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Association of Serotonin Receptors with Attention Deficit Hyperactivity Disorder: A Systematic Review and Meta-analysis.Current medical science · 2018Pooled it
- Candidate gene studies of ADHD: a meta-analytic review.Human genetics · 2009Pooled it
- Article
- Aniracetam restores the excitation-inhibition balance of neurotransmitters in the prefrontal cortex of mice with ADHD.Scientific reports · 2026Article
- Potential contribution of monoamine oxidase a gene variants in ADHD and behavioral co-morbidities: scenario in eastern Indian probands.Neurochemical research · 2014Article
- Candidate gene associations with withdrawn behavior.Journal of child psychology and psychiatry, and allied disciplines · 2013Article
- Two functional serotonin polymorphisms moderate the effect of food reinforcement on BMI.Behavioral neuroscience · 2013Article
- An exploration of the serotonin system in antisocial boys with high levels of callous-unemotional traits.PloS one · 2013Article
- A family based association study of DRD4, DAT1, and 5HTT and continuous traits of attention-deficit hyperactivity disorder.Behavior genetics · 2011Article
- Influence of candidate genes on attention problems in children: a longitudinal study.Behavior genetics · 2011Article
- Molecular genetics of attention deficit hyperactivity disorder.The Psychiatric clinics of North America · 2010Review
- Further evidence for the association between attention deficit/hyperactivity disorder and the serotonin receptor 1B gene.Journal of neural transmission (Vienna, Austria : 1996) · 2009Article
- Development and validation of the high-quality 'rapid method for swab' to genotype the HTTLPR serotonin transporter (SLC6A4) promoter polymorphism.Psychiatric genetics · 2009Article
- The influence of serotonin- and other genes on impulsive behavioral aggression and cognitive impulsivity in children with attention-deficit/hyperactivity disorder (ADHD): Findings from a family-based association test (FBAT) analysis.Behavioral and brain functions : BBF · 2008Article
- ADHD and Disruptive Behavior scores - associations with MAO-A and 5-HTT genes and with platelet MAO-B activity in adolescents.BMC psychiatry · 2008Article
- Genetic aspects in attention-deficit/hyperactivity disorder.Journal of neural transmission (Vienna, Austria : 1996) · 2008Review
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 were the 5-HTTLPR, the VNTR in intron 2 and the 3'UTR SNP in 5-HTT, the 5-HTR1B variations 861G>C and 102T>C, and the 5-HTR2A variations His452Tyr and 1438G>A. We genotyped these variants in a sample of 102 families with 229 children with ADHD according to DSM-IV criteria. Among the affected children, 69% fulfilled criteria for the combined type, 27% for the predominantly inattentive type, and 4% for the predominantly hyperactive-impulsive type. Associations were tested by the pedigree transmission disequilibrium test (PDT). All investigated polymorphisms in serotonergic candidate genes showed no association to ADHD in our sample. Earlier studies of these polymorphisms had also shown inconsistent results, with some studies reporting significant associations and others demonstrating no association. This discordance between studies may reflect variation in patient ascertainment criteria, genetic heterogeneity, too low statistical power for the expected effects or false positive results in the initial reports. We cannot rule out the possibility that other variations in the investigated genes contribute to the etiology of ADHD.
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