ArticlePsychopharmacology2013
A high density linkage disequilibrium mapping in 14 noradrenergic genes: evidence of association between SLC6A2, ADRA1B and ADHD.
Article in Psychopharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Brain imaging genetics in ADHD and beyond - Mapping pathways from gene to disorder at different levels of complexity.Neuroscience and biobehavioral reviews · 2017Pooled it
- Advances in the etiology and neuroimaging of children with attention deficit hyperactivity disorder.Frontiers in pediatrics · 2024Review
- Influence of Receptor Polymorphisms on the Response to α-Adrenergic Receptor Blockers in Pheochromocytoma Patients.Biomedicines · 2022Article
- Catecholaminergic and cholinergic neuromodulation in autism spectrum disorder: A comparison to attention-deficit hyperactivity disorder.Frontiers in neuroscience · 2022Review
- Association of norepinephrine transporter methylation with in vivo NET expression and hyperactivity-impulsivity symptoms in ADHD measured with PET.Molecular psychiatry · 2021Article
- Genetic analysis for cognitive flexibility in the trail-making test in attention deficit hyperactivity disorder patients from single nucleotide polymorphism, gene to pathway level.The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry · 2019Article
- Association of Monoamine Oxidase A (MAOA) Gene uVNTR and rs6323 Polymorphisms with Attention Deficit and Hyperactivity Disorder in Korean Children.Medicina (Kaunas, Lithuania) · 2018Article
- Common and specific genes and peripheral biomarkers in children and adults with attention-deficit/hyperactivity disorder.The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry · 2018Review
- Pilot study indicate role of preferentially transmitted monoamine oxidase gene variants in behavioral problems of male ADHD probands.BMC medical genetics · 2017Article
- Analysis of shared homozygosity regions in Saudi siblings with attention deficit hyperactivity disorder.Psychiatric genetics · 2017Article
- Rare DNA variants in the brain-derived neurotrophic factor gene increase risk for attention-deficit hyperactivity disorder: a next-generation sequencing study.Molecular psychiatry · 2017Article
- Ethylphenidate as a selective dopaminergic agonist and methylphenidate-ethanol transesterification biomarker.Journal of pharmaceutical sciences · 2014Review
- Advances in molecular genetic studies of attention deficit hyperactivity disorder in China.Shanghai archives of psychiatry · 2014Review
- Association between monoamine oxidase gene polymorphisms and attention deficit hyperactivity disorder in Korean children.Genetic testing and molecular biomarkers · 2014Article
- Potential contribution of monoamine oxidase a gene variants in ADHD and behavioral co-morbidities: scenario in eastern Indian probands.Neurochemical research · 2014Article
- Catecholaminergic gene variants: contribution in ADHD and associated comorbid attributes in the eastern Indian probands.BioMed research international · 2013Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pharmacological evidence suggests the importance of noradrenergic and other monoaminergic neurotransmitters in the aetiology and treatment of attention deficit hyperactivity disorder (ADHD). Until recently, the genes of the noradrenergic pathway were not intensively investigated in ADHD compared to dopaminergic and serotonergic candidates. In this study, 91 SNP markers of 14 noradrenergic genes (an average density of one SNP per 4.5 kbp) were examined in ADHD samples from Ireland and Australia. Although suggestive evidence of association (nominal p ≤ 0.05) with the genes SLC6A2, ADRA1A, ADRA1B and ADRA2B was observed, none remained significant after permutation adjustments. In contrast, haplotype analyses demonstrated a significant association between ADHD and a SLC6A2 haplotype comprising the markers rs36009, rs1800887, rs8049681, rs2242447 and rs9930182 (χ(2) = 9.39, p-corrected = 0.019, OR = 1.51). A rare ADRA1B haplotype made of six SNPs (rs2030373, rs6884105, rs756275, rs6892282, rs6888306 and rs13162302) was also associated (χ(2) = 7.79, p-corrected = 0.042 OR = 2.74) with the disorder. These findings provide evidence of a contribution of the noradrenaline system to the genetic aetiology of ADHD. The observed haplotype association signals may be driven by as yet unidentified functional risk variants in or around the associated regions. Functional genomic analysis is warranted to determine the biological mechanism of the observed association.
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