Family-based association study of ADHD and genes increasing the risk for smoking behaviours.
- Authors
- Thakur, Geeta A; Sengupta, Sarojini M; Grizenko, Natalie; Choudhry, Zia; Joober, Ridha
- Year
- 2012
- Journal
- Archives of disease in childhood
- PMID
- 23109089
- DOI
- 10.1136/archdischild-2012-301882
OBJECTIVE: To investigate five top single nucleotide polymorphisms (SNPs) located in different genes and loci (CHRNA3, BDNF, DBH and LOC100188947) that were highly associated with different dimensions of smoking behaviour, in relation to attention-deficit hyperactivity disorder (ADHD). DESIGN: Cohort study consisting of a clinical sample of children with ADHD. SETTING: Douglas Institute ADHD Clinic, Montreal, Canada. PATIENTS: Families of 454 children with ADHD aged 6-12 years old. INTERVENTIONS: Family-based association tests used to study the transmission of risk alleles within these five genetic markers. MAIN OUTCOME MEASURES: Clinical diagnosis of ADHD, and a number of behavioural and neurocognitive phenotypes relevant to the disorder. RESULTS: One SNP (rs1329650) from a non-coding RNA (LOC100188947) was significantly associated with overall ADHD diagnosis with the C* risk allele being over-transmitted from parents to children with ADHD (p=0.02). It was also over-transmitted to children with higher scores on Conners' Parents (p=0.01) and Conners' Teacher (p=0.002) index scores, and Child Behaviour Checklist withdrawn (p=0.001) and aggressive (p=0.007) behaviours. Children with poorer performances on executive and attention tasks were more likely to inherit the risk allele. CONCLUSIONS: The C* allele of rs1329650 may be increasing the risk for ADHD and smoking behaviour through a common mechanism, possibly externalising behaviours and specific cognitive deficits that manifest as ADHD in childhood and are the gateway to smoking behaviour later in life. This exploratory study illustrates the use of comorbid disorders to investigate ADHD genetics. In spite of its relatively large sample size, replication in future studies is warranted.
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|---|---|---|
| Meta-analysis of up to 622,409 individuals identifies 40 novel smoking behaviour associated genetic loci. | 2020 | 30617275 |
External
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|---|---|---|---|---|
| The Potential Future Role of Genetic Markers, Neurophysiological Insights, and AI Innovations in Personalized Attention-Deficit/Hyperactivity Disorder (ADHD) Management. | Satodiya V et al. | β | 2025 | β |
| Hypermethylation at CREBBP Is Associated with Cognitive Impairment in a Mexican American Cohort. | Abraham Daniel A et al. | β | 2023 | β |
| Facing the Methodological Challenge in Dissecting the Genetics of ADHD: A Case for Deep Phenotyping and Heterogeneity Reduction. | Sengupta SM et al. | β | 2020 | β |
| Meta-analysis of up to 622,409 individuals identifies 40 novel smoking behaviour associated genetic loci. | Erzurumluoglu AM et al. | β | 2020 | β |
| Drug Regimen Individualization for Attention-Deficit/Hyperactivity Disorder: Guidance for Methylphenidate and Dexmethylphenidate Formulations. | Patrick KS et al. | β | 2019 | β |
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| Tobacco cessation interventions for young people. | Fanshawe TR et al. | β | 2017 | β |
| Molecular genetic studies of ADHD and its candidate genes: a review. | Li Z et al. | β | 2014 | β |
| Tobacco cessation interventions for young people. | Stanton A et al. | β | 2013 | β |
| Shared biological risks that influence brain and behaviour. | Cooper M et al. | β | 2012 | β |