Cited by 1,001Attention Deficit Hyperactivity DisorderNeurotransmitter Receptor Influence on BehaviorGenetic Associations and Epidemiology

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Molecular Genetics of Attention Deficit Hyperactivity Disorder

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Faraone, Stephen V., Mick, Eric·2010·Psychiatric Clinics of North America

DOI 10.1016/j.psc.2009.12.004PMC PMC2847260

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Abstract

Although twin studies demonstrate that ADHD is a highly heritable condition, molecular genetic studies suggest that the genetic architecture of ADHD is complex. The handful of genome-wide linkage and association scans that have been conducted thus far show divergent findings and are, therefore, not conclusive. Similarly, many of the candidate genes reviewed here (ie, DBH, MAOA, SLC6A2, TPH-2, SLC6A4, CHRNA4, GRIN2A) are theoretically compelling from neurobiological systems perspective but available data are sparse and inconsistent. However, candidate gene studies of ADHD have produced substantial evidence implicating several genes in the etiology of the disorder, with meta-analyses supportive of a role of the genes coding for DRD4, DRD5, SLC6A3, SNAP-25, and HTR1B in the etiology of ADHD.

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Background
Meta-analysis of the association between the 7-repeat allele of the dopamine D(4) receptor gene and attention deficit hyperactivity disorder.
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Increased neural responses to reward in adolescents and young adults with attention-deficit/hyperactivity disorder and their unaffected siblings
von Rhein, D., Cools, R., Zwiers, M. P., van der Schaaf, M., Franke, B., Luman, M., Oosterlaan, J., Heslenfeld, D. J., Hoekstra, P. J., Hartman, C. A., et al. (2015) · Journal of the American Academy of Child & Adolescent Psychiatry · doi:10.1016/j.jaac.2015.02.012 · Cited by 108
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Genome‐wide association study of response to methylphenidate in 187 children with attention‐deficit/hyperactivity disorder
Mick, E., Neale, B., Middleton, F. A., McGough, J. J., & Faraone, S. V. (2008) · American Journal of Medical Genetics Part B: Neuropsychiatric Genetics · doi:10.1002/ajmg.b.30865 · Cited by 108
“Family, twin and adoption studies show that genes play a substantial, albeit not exclusive, role in the etiology of ADHD [Faraone et al., 2005] and an emerging body of molecular genetic research implicates several genes in the etiology of the disorder [Mick and Faraone, 2008].”
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Examining the comorbidity between attention deficit hyperactivity disorder and bipolar I disorder: a meta-analysis of family genetic studies.
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“…attentional disorders and DRD2/ANKK1-Taq1a (Fossella et al., 2006; Rodriguez-Jimenez et al., 2006) or COMT Val158Met (Giakoumaki, Roussos, & Bitsios, 2008; Blasi et al., 2005), several other studies fail to find such a connection (Bombin et al., 2008; Cheuk & Wong, 2006; Faraone et al., 2005).”
Background
Smoking Behaviour and Mental Health Disorders—Mutual Influences and Implications for Therapy
Minichino, A., Bersani, F. S., Calò, W. K., Spagnoli, F., Francesconi, M., Vicinanza, R., Chiaie, R. D., & Biondi, M. (2013) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph10104790 · Cited by 110
“Both ADHD and smoking are highly heritable; genetic factors account for 60%–80% and 56% of the two phenotypes respectively [50,51].”
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Brain imaging genetics in ADHD and beyond – Mapping pathways from gene to disorder at different levels of complexity
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“Some additional genes (encoding dopamine beta-hydroxylase [DBH], adrenoceptor alpha 2A [ADRA2A], tryptophan hydroxylase 2 [TPH2], and monoamine oxidase A [MAOA]) were found suggestively associated with ADHD in meta-analyses (Gizer et al., 2009; Li et al., 2006a; Faraone et al., 2005).”
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Early identification of ADHD risk via infant temperament and emotion regulation: a pilot study
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“Evidence from twin studies estimate heritability of about 70% (Burt, 2009; Faraone et al., 2005).”
Impact of the ADHD-susceptibility gene CDH13 on development and function of brain networks
Rivero, O., Sich, S., Popp, S., Schmitt, A. G., Franke, B., & Lesch, K. (2012) · European Neuropsychopharmacology · doi:10.1016/j.euroneuro.2012.06.009 · Cited by 97
“Polymorphisms in the DA receptor genes, DRD4 and DRD5 (for review e.g.: Thapar et al., 2007; Faraone et al., 2005) are linked to ADHD whereas the gene encoding DA transporter (DAT/SLC6A3) is one of the most comprehensively assessed candidates for ADHD (Franke et al.”
Does parental expressed emotion moderate genetic effects in ADHD? an exploration using a genome wide association scan
Sonuga-Barke, E., Lasky-Su, J., Neale, B., Oades, R., Chen, W., Franke, B., Buitelaar, J., Banaschewski, T., Ebstein, R., Gill, M., et al. (2008) · American Journal of Medical Genetics Part B: Neuropsychiatric Genetics · doi:10.1002/ajmg.b.30860 · Cited by 104
“significant associations with the ADHD diagnosis [Faraone et al., 2005].”
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Familial aggregation of attention‐deficit/hyperactivity disorder
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“While twin studies have repeatedly reported high heritability estimate of 70%–80% for ADHD (Chang, Lichtenstein, Asherson, & Larsson, 2013; Faraone et al., 2005) and the significance of both additive genetic and nonshared environmental factors to the phenotypic variance in ADHD, the relative importance of shared envir…”
Background
Association of Polygenic Risk for Attention-Deficit/Hyperactivity Disorder With Co-occurring Traits and Disorders
Rietz, E. D., Coleman, J. R. I., Glanville, K. P., Choi, S. W., O’Reilly, P. F., & Kuntsi, J. (2017) · Biological Psychiatry Cognitive Neuroscience and Neuroimaging · doi:10.1016/j.bpsc.2017.11.013 · Cited by 129
“…failed to identify rare and common genetic variants underlying ADHD that explain more than a small fraction of its heritability (5 – 7), despite the high heritability of ADHD estimated at 0.76 from twin studies (8) and estimated at 0.22 to 0.32 based on single nucleotide polymorphisms (SNPs) (1,9).”
BackgroundInfluential
Combined Effects of Prenatal Exposure to Polycyclic Aromatic Hydrocarbons and Material Hardship on Child ADHD Behavior Problems
Perera, F., Wheelock, K., Wang, Y., Tang, D., Margolis, A., Badia, G., Cowell, W., Miller, R. L., Rauh, V., Wang, S., et al. (2017) · Environmental Research · doi:10.1016/j.envres.2017.09.002 · Cited by 102
“Known or suggested risk factors include obstetrical complications, maternal smoking, alcohol use, lead exposure, polycyclic aromatic hydrocarbon (PAH) exposure, low socioeconomic status, and psychosocial adversity (Faraone et al., 2005; Grizenko et al., 2012; Sagiv et al., 2013).”
Polymorphisms in dopamine system genes are associated with individual differences in attention in infancy.
Holmboe, K., Nemoda, Z., Fearon, P. R. M., Csibra, G., Sasvári‐Székely, M., & Johnson, M. H. (2010) · Developmental Psychology · doi:10.1037/a0018180 · Cited by 69
“In contrast to the DRD4 48-bp VNTR, the DRD2 TaqIA polymorphism is not associated with ADHD (Faraone et al., 2005).”
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Genetic Overlap between Evoked Frontocentral Theta-Band Phase Variability, Reaction Time Variability, and Attention-Deficit/Hyperactivity Disorder Symptoms in a Twin Study
McLoughlin, G., Palmer, J. A., Rijsdijk, F., & Makeig, S. (2014) · Biological Psychiatry · doi:10.1016/j.biopsych.2013.07.020 · Cited by 100
“Parameters for ADHD (heritability and unique environmental estimates) are fixed values selected according to meta-analysis (57).”
Sexually dimorphic effects of four genes (COMT, SLC6A2, MAOA, SLC6A4) in genetic associations of ADHD: A preliminary study
Biederman, J., Kim, J. W., Doyle, A. E., Mick, E., Fagerness, J., Smoller, J. W., & Faraone, S. V. (2008) · American Journal of Medical Genetics Part B: Neuropsychiatric Genetics · doi:10.1002/ajmg.b.30874 · Cited by 100
“Given that ADHD is known to have a robust genetic component [Faraone et al., 2005], it is possible that different genetic pathways mediate genetic susceptibility to ADHD and that these different pathways create a differential expression of ADHD symptoms and associated features by gender.”
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Gene × environment interactions in reading disability and attention-deficit/hyperactivity disorder.
Pennington, B. F., McGrath, L. M., Rosenberg, J., Barnard, H. D., Smith, S. D., Willcutt, E. G., Friend, A., DeFries, J. C., & Olson, R. K. (2009) · Developmental Psychology · doi:10.1037/a0014549 · Cited by 130
“Current behavior genetic analyses estimate the heritability of RD to be about 58% (Pennington & Olson, 2005) and the heritability of ADHD to be about 76% (Faraone et al., 2005).”
Male sex bias in early and late onset neurodevelopmental disorders: Shared aspects and differences in Autism Spectrum Disorder, Attention Deficit/hyperactivity Disorder, and Schizophrenia
Santos, S., Ferreira, H., Martins, J., Gonçalves, J., & Castelo-Branco, M. S. (2022) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2022.104577 · Cited by 148
ADHD-associated dopamine transporter, latrophilin and neurofibromin share a dopamine-related locomotor signature in Drosophila
van der Voet, M., Harich, B., Franke, B., & Schenck, A. (2016) · Molecular Psychiatry · doi:10.1038/mp.2015.55 · Cited by 99
Higher Prevalence of Iron Deficiency as Strong Predictor of Attention Deficit Hyperactivity Disorder in Children
Bener, A., Kamal, M., Bener, H., & Bhugra, D. (2014) · Annals of Medical and Health Sciences Research · doi:10.4103/2141-9248.141974 · Cited by 98
“Recognition of ADHD, even if accurate, may be harmful through labeling, stigmatization, scapegoating, and effects on self-perception.”
Background
The effect of phosphatidylserine containing Omega3 fatty-acids on attention-deficit hyperactivity disorder symptoms in children: A double-blind placebo-controlled trial, followed by an open-label extension
Manor, I., Magen, A., Keidar, D., Rosen, S., Tasker, H., Cohen, T., Richter, Y., Zaaroor-Regev, D., Manor, Y., & Weizman, A. (2012) · European psychiatry · doi:10.1016/j.eurpsy.2011.05.004 · Cited by 98
“Behavioral genetic investigations and twin studies have suggested that it is a highly heritable disorder, and several genes have been linked to its occurrence [14,37].”
Background
Genetic Markers of ADHD-Related Variations in Intracranial Volume
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Integrating Impairments in Reaction Time and Executive Function Using a Diffusion Model Framework
Karalunas, S. L., & Huang‐Pollock, C. L. (2013) · Research on Child and Adolescent Psychopathology · doi:10.1007/s10802-013-9715-2 · Cited by 107
“Like ADHD itself (Faraone et al. 2005), RT and RT variability are also highly heritable (Kuntsi et al. 2006; Kuntsi and Stevenson 2001), leading some to suggest that these performance characteristics may be important cognitive mechanisms in the disorder that may elucidate underlying neural…”
Genome‐wide association study in German patients with attention deficit/hyperactivity disorder
Hinney, A., Scherag, A., Jarick, I., Albayrak, Ö., Pütter, C., Pechlivanis, S., Dauvermann, M. R., Beck, S., Weber, H., Scherag, S., et al. (2011) · American Journal of Medical Genetics Part B Neuropsychiatric Genetics · doi:10.1002/ajmg.b.31246 · Cited by 92
“Genetic variants in single, mostly dopaminergic, candidate genes have been implicated in meta-analyses (for review see: [Heiser et al., 2004; Li et al., 2006;Gizer et al., 2009; Banaschewski et al., 2010; Faraone and Mick, 2010; Franke et al., 2010]); however, none of these variants achieved genome-wide significance a…”
BackgroundInfluentialSelf-citation
Linear and non-linear EEG analysis of adolescents with attention-deficit/hyperactivity disorder during a cognitive task.
Sohn, H., Kim, I.-H., Lee, W., Peterson, B., Hong, H., Chae, J., Hong, S.-Y., & Jeong, J. (2010) · Clinical Neurophysiology · doi:10.1016/j.clinph.2010.04.007 · Cited by 97
“Many previous studies of ADHD have revealed that both environmental factors and genetic factors play important roles in the onset of the disease (Faraone et al., 2005).”
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Continuity of aggressive antisocial behavior from childhood to adulthood: The question of phenotype definition
Hofvander, B., Ossowski, D., Lundström, S., & Anckarsäter, H. S. (2009) · International Journal of Law and Psychiatry · doi:10.1016/j.ijlp.2009.04.004 · Cited by 89
“, Farrington, D. P., Stouthamer-Loeber, M., Moffitt, T. E., Caspi, A., & Lynam, D. (2001). Male mental health problems, psychopathy, and personality traits: key findings from the first 14 years of the Pittsburgh Youth Study.”
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Prenatal Exposure to Nicotine Impairs Performance of the 5-Choice Serial Reaction Time Task in Adult Rats
Schneider, T., Ilott, N., Brolese, G., Bizarro, L., Asherson, P. J. E., & Stolerman, I. P. (2011) · Neuropsychopharmacology · doi:10.1038/npp.2010.249 · Cited by 97
Early life exposure to air pollution particulate matter (PM) as risk factor for attention deficit/hyperactivity disorder (ADHD): Need for novel strategies for mechanisms and causalities
Myhre, O., Låg, M., Villanger, G. D., Oftedal, B., Øvrevik, J., Holme, J. A., Aase, H., Paulsen, R. E., Bal‐Price, A., & Dirven, H. A. A. M. (2018) · Toxicology and Applied Pharmacology · doi:10.1016/j.taap.2018.03.015 · Cited by 105
“The incidence of diagnosed ADHD seems to have increased rapidly in developed countries since the 1980s (Biederman and Faraone, 2005; Nigg, 2006; Kieling et al., 2008; Faraone and Mick, 2010).”
Background
ADHD, altered dopamine neurotransmission, and disrupted reinforcement processes: Implications for smoking and nicotine dependence
Kollins, S. H., & Adcock, R. A. (2014) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2014.02.002 · Cited by 95
Assessing the Validity of the Quality of Life Enjoyment and Satisfaction Questionnaire—Short Form in Adults With ADHD
Mick, E., Faraone, S. V., Spencer, T., Zhang, H. F., & Biederman, J. (2008) · Journal of Attention Disorders · doi:10.1177/1087054707308468 · Cited by 95
“2008; 11(4) 504-509) Keywords: ADHD; adult; quality of life; Q-LES-QSF ADHD is a highly heritable condition (Faraone et al.,2005) that is now estimated to affect 3% to 5% of adults in the U.S. population (Faraone & Biederman, 2005; Kessler et al., 2005).”
BackgroundSelf-citation
Cognitive neuroscience of Attention Deficit Hyperactivity Disorder: Current status and working hypotheses
Vaidya, C. J., & Stollstorff, M. (2008) · Developmental Disabilities Research Reviews · doi:10.1002/ddrr.40 · Cited by 95
“Prevalence of ADHD has been associated with genetic polymorphisms for DA receptors (DRD1, DRD4, DRD5) and transporter (DAT1) and NE receptors (DBH, alpha-2-adrenoreceptor) and transporter (NET) (reviewed in [Faraone et al., 2005]), although many studies also failed to find associations.”
Background
Effects of selective dopaminergic compounds on a delay-discounting task
Koffarnus, M. N., Newman, A. H., Grundt, P., Rice, K. C., & Woods, J. H. (2011) · Behavioural Pharmacology · doi:10.1097/fbp.0b013e3283473bcb · Cited by 100
PDD symptoms in ADHD, an independent familial trait?
Nijmeijer, J. S., Hoekstra, P. J., Minderaa, R. B., Buitelaar, J. K., Altink, M. E., Buschgens, C. J. M., Fliers, E. A., Rommelse, N. N. J., Sergeant, J. A., & Hartman, C. A. (2009) · Journal of Abnormal Child Psychology · doi:10.1007/s10802-008-9282-0 · Cited by 93
Rat Models of ADHD
Sagvolden, T., & Johansen, E. B. (2011) · Current topics in behavioral neurosciences · doi:10.1007/7854_2011_126 · Cited by 97
“It is a heterogeneous disorder affecting about 5% of children (Faraone and Mick 2010), and its prevalence is similar in different cultures (Dwivedi and Banhatti 2005; Meyer et al.”
Background
Genome-wide analysis of rare copy number variations reveals PARK2 as a candidate gene for attention-deficit/hyperactivity disorder
Jarick, I., Volckmar, A., Pütter, C., Pechlivanis, S., Nguyen, T. T., Dauvermann, M. R., Beck, S., Albayrak, Ö., Scherag, S., Gilsbach, S., et al. (2012) · Molecular Psychiatry · doi:10.1038/mp.2012.161 · Cited by 111
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The Dopamine Receptor D4 Gene (DRD4) Moderates Family Environmental Effects on ADHD
Martel, M. M., Nikolas, M. A., Jernigan, K. A., Friderici, K. H., Waldman, I. D., & Nigg, J. T. (2010) · Research on Child and Adolescent Psychopathology · doi:10.1007/s10802-010-9439-5 · Cited by 90
“Note that this polymorphism has shown inconsistent associations with ADHD (Faraone et al. 2005; Gizer et al. 2009), suggesting the possibility of G × E.”
Influential
Alterations in Pain Response are Partially Reversed by Methylphenidate (Ritalin) in Adults with Attention Deficit Hyperactivity Disorder ( ADHD )
Treister, R., Eisenberg, E., Demeter, N., & Pud, D. (2015) · Pain Practice · doi:10.1111/papr.12129 · Cited by 92
Epileptiform Activity and Cognitive Deficits in SNAP-25+/− Mice are Normalized by Antiepileptic Drugs
Corradini, I., Donzelli, A., Antonucci, F., Welzl, H., Loos, M., Martucci, R., Astis, S. D., Pattini, L., Inverardi, F., Wolfer, D. P., et al. (2012) · Cerebral Cortex · doi:10.1093/cercor/bhs316 · Cited by 86
“The coloboma mice, largely used as a model for ADHD (Wilson 2000; reviewed in Faraone et al. 2005; Russell 2007), display a hyperactive phenotype, which is reduced by the expression of the SNAP-25 © The Author 2012.”
BackgroundMethodInfluential
Progress and Promise of Attention-Deficit Hyperactivity Disorder Pharmacogenetics
Froehlich, T. E., McGough, J., & Stein, M. (2010) · CNS Drugs · doi:10.2165/11530290-000000000-00000 · Cited by 91
“The search for candidate genes associated with ADHD has been largely driven by the understanding that medications for the disorder have drug targets in the catecholamine system.([9]) Conversely, it is likely”
Influential
Pharmacogenetics predictors of methylphenidate efficacy in childhood ADHD
Myer, N. M., Boland, J. R., & Faraone, S. V. (2018) · Molecular Psychiatry · doi:10.1038/mp.2017.234 · Cited by 91
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Abnormal striatal BOLD responses to reward anticipation and reward delivery in ADHD
Furukawa, E., Bado, P., Tripp, G., Mattos, P., Wickens, J. R., Bramati, I. E., Alsop, B., Ferreira, F. M., Lima, D., Tovar-Moll, F., et al. (2014) · PLoS ONE · doi:10.1371/journal.pone.0089129 · Cited by 90
“Associations have been established with genetic variations in the dopamine D4 receptor [2], [3] and the dopamine transporter (DAT1) [4], the dopamine D5 receptors, serotonin transporters [5] and dopamine beta-hydroxylase (DBH), 5-hydroxytryptamine (serotonin) receptor 1B (HTR1B) and synaptosomal-associated protein, 25…”
Background
New suggestive genetic loci and biological pathways for attention function in adult attention‐deficit/hyperactivity disorder
Alemany, S., Marta Ribasés, A., Vilor‐Tejedor, N., Bustamante, M., Sánchez‐Mora, C., Bosch, R., Vanesa Richarte, B., Cormand, B., Casas, M., Ramos‐Quiroga, J. A., et al. (2015) · American Journal of Medical Genetics Part B Neuropsychiatric Genetics · doi:10.1002/ajmg.b.32341 · Cited by 90
“In this regard, despite the high heritability estimated for childhood ADHD, ranging from 70% to 80% [Faraone et al., 2005; Burt, 2009], no genome-wide significant associations have been documented so far [Neale et al.”
Background
Atypical alpha asymmetry in adults with ADHD
Hale, T., Smalley, S., Hanada, G., Macion, J., McCracken, J., McGough, J., & Loo, S. (2009) · Neuropsychologia · doi:10.1016/j.neuropsychologia.2009.03.021 · Cited by 89
“…may have DHD affected offspring (i.e., de novo mutation, brain injury, or nvironmental factors), family and twin studies support a multiactorial model of inheritance (Faraone et al., 2005) and under this odel it is more likely that such parents would be elevated on putaive ADHD endophenotypes.”
Background
Neural substrates of trait impulsivity, anhedonia, and irritability: Mechanisms of heterotypic comorbidity between externalizing disorders and unipolar depression
Zisner, A. R., & Beauchaine, T. P. (2016) · Development and Psychopathology · doi:10.1017/s0954579416000754 · Cited by 101
“…for heritable influences on psychopathology, including externalizing disorders, unipolar depression, and their comorbidity, yet molecular genetics research explains very little of this heritability by specific alleles (Faraone & Mick, 2010; Sullivan, Neale, & Kendler, 2000; Wray et al., 2012).”
Background
Association between SNAP-25 gene polymorphisms and cognition in autism: functional consequences and potential therapeutic strategies
Braida, D., Guerini, F. R., Ponzoni, L., Corradini, I., Astis, S. D., Pattini, L., Bolognesi, E., Benfante, R., Fornasari, D., Chiappedi, M. A., et al. (2015) · Translational Psychiatry · doi:10.1038/tp.2014.136 · Cited by 87
Low Dopamine Function in Attention Deficit/Hyperactivity Disorder: Should Genotyping Signify Early Diagnosis in Children?
Gold, M. S., Blum, K., Oscar‐Berman, M., & Braverman, E. R. (2014) · Postgraduate Medicine · doi:10.3810/pgm.2014.01.2735 · Cited by 93
A SNAP25 promoter variant is associated with early-onset bipolar disorder and a high expression level in brain
Étain, B., Dumaine, A., Mathieu, F., Chevalier, F., Henry, C., Kahn, J., Deshommes, J., Bellivier, F., Leboyer, M., & Jamain, S. (2010) · Molecular Psychiatry · doi:10.1038/mp.2008.148 · Cited by 88
Separation of genetic influences on attention deficit hyperactivity disorder symptoms and reaction time performance from those on IQ
Wood, A. C., Asherson, P. J., van der Meere, J. J., & Kuntsi, J. (2009) · Psychological Medicine · doi:10.1017/s003329170999119x · Cited by 67
“The high heritability of attention deficit hyperactivity disorder (ADHD), averaging at 76% (Faraone et al. 2005), has led to studies aiming to identify cognitive endophenotypes that underlie the genetic liability for the disorder (Castellanos & Tannock, 2002 ; Kuntsi et al.”
Background
ADHD as a (non) allergic hypersensitivity disorder: A hypothesis
Pelsser, L. M. J., Buitelaar, J. K., & Savelkoul, H. F. J. (2009) · Pediatric Allergy and Immunology · doi:10.1111/j.1399-3038.2008.00749.x · Cited by 87
“Polymorphic variants in several genes involved in regulation of the dopamine, and related neurotransmitter pathways are reported to be associated with ADHD (22).”
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ADHD classification by a texture analysis of anatomical brain MRI data
Chang, C.-W., Ho, C., & Chen, J. (2012) · Frontiers in Systems Neuroscience · doi:10.3389/fnsys.2012.00066 · Cited by 83
“ADHD is a complex disorder with a composite etiology (Faraone and Mick, 2010).”
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Genetics of attention-deficit/hyperactivity disorder: an update
Akutagava‐Martins, G. C., Rohde, L. A., & Hutz, M. H. (2015) · Expert Review of Neurotherapeutics · doi:10.1586/14737175.2016.1130626 · Cited by 97
“eight fold in biological parents and siblings of ADHD children, but adoptive parents of ADHD children present a risk similar to the general population.[21] The”
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Electrophysiological markers of genetic risk for attention deficit hyperactivity disorder
Tye, C., McLoughlin, G., Kuntsi, J., & Asherson, P. J. (2011) · Expert Reviews in Molecular Medicine · doi:10.1017/s1462399411001797 · Cited by 73
Attention Deficit Hyperactivity Disorder comorbid oppositional defiant disorder and its predominately inattentive type: evidence for an association with COMT but not MAOA in a Chinese sample
Qian, Q., Liu, J., Wang, Y.-F., Yang, L., Guan, L., & Faraone, S. (2009) · Behavioral and Brain Functions · doi:10.1186/1744-9081-5-8 · Cited by 86
“76 [7], evidence that the etiology of ADHD is partially due to genes is compelling.”
Self-citation
A high-density SNP linkage scan with 142 combined subtype ADHD sib pairs identifies linkage regions on chromosomes 9 and 16
Asherson, P., Zhou, K., Anney, R., Franke, B., Buitelaar, J., Ebstein, R., Gill, M., Altink, M., Arnold, R., Boer, F., et al. (2008) · Molecular Psychiatry · doi:10.1038/sj.mp.4002140 · Cited by 86
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Epigenetic histone modification regulates developmental lead exposure induced hyperactivity in rats
Luo, M., Xu, Y., Cai, R., Tang, Y., Ge, M.-M., Liu, Z., Xu, L., Hu, F., Ruan, D., & Wang, H.-L. (2013) · Toxicology Letters · doi:10.1016/j.toxlet.2013.11.025 · Cited by 90
“In addition, there was mounting evidence to suggest the pathophysiologically relevant contribution of monoaminergic pathways in the etiology of ADHD (Faraone and Mick, 2010; Peterson et al., 2011; Szczerbak et al., 2007; White et al., 2007; Zuch et al., 1998).”
Background

Authors: Faraone, S. V., & Mick, E.
Affiliations: SUNY Upstate Medical University (US)
Harvard University (US)
Corresponding author: Faraone, Stephen V.
ORCID: Faraone, Stephen V.
Mick, Eric
Venue: Psychiatric Clinics of North America
Publisher: Elsevier BV
Published: 2010-03
Volume: 33
Issue: 1
Pages: 159-180
ISSN: 0193-953X (ISSN-L)
DOI: 10.1016/j.psc.2009.12.004
PMC: PMC2847260
OpenAlex: W2168200222
Cited by: 411
References: 170
Citations by year: 2026: 5 · 2025: 11 · 2024: 12 · 2023: 26 · 2022: 16 · 2021: 20 · 2020: 15 · 2019: 17 · 2018: 24 · 2017: 30 · 2016: 33 · 2015: 32 · 2014: 45 · 2013: 40 · 2012: 39
FWCI: 5.44
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Psychiatric Clinics of North America (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute of Mental Health (R01MH066877, R13MH059126)
Topics: Health Sciences › Medicine › Psychiatry and Mental health › Attention Deficit Hyperactivity Disorder
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
Keywords: attention deficit hyperactivity disorder, genetic etiology, heritability, genome-wide linkage analysis, genome-wide association study, candidate genes, DBH, monoamine oxidase A, norepinephrine transporter, serotonin transporter, CHRNA4, GRIN2A, DRD4, DRD5, dopamine transporter, SNAP-25, 5-HT1B receptor, dopamine, monoamine transporters, neurotransmitter systems
MeSH terms: Attention Deficit Disorder with Hyperactivity, Humans, Molecular Biology, Twins, Gene Expression, Prevalence, Genome-Wide Association Study

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Molecular Genetics of Attention Deficit Hyperactivity Disorder

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