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Molecular Genetics of Attention Deficit Hyperactivity Disorder
Open accessAbstract
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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“The MID task has been repeatedly shown to elicit a neural response in the VS to both reward anticipation and receipt (for review see 15,18-20).”
From Increased neural responses to reward in adolescents and young adults with attention-deficit/hyperactivity disorder and their unaffected siblings (2015) · cites this paper as [19]
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RETRACTED: Universal Design for Learning for Children with ADHD
Frolli, A., Cerciello, F., Esposito, C., Ricci, M., Laccone, R., & Bisogni, F. (2023) · Children · doi:10.3390/children10081350 · Cited by 21
RetractedMachine Learning Prediction of ADHD Severity: Association and Linkage to ADGRL3 , DRD4 , and SNAP25
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Praveena, S., Munisvaradass, R., Masiran, R., Rajendran, R., Lin, C.-C., & Kumar, S. (2020) · Environmental science and pollution research international · doi:10.1007/s11356-020-10652-z · Cited by 21
Huang, Y.-H., Xu, H.-Y., Au, W., Xu, C.-T., & Wu, K.-S. (2018) · Psychology Research and Behavior Management · doi:10.2147/prbm.s178080 · Cited by 21
Imaging genetics in neurodevelopmental psychopathology
Klein, M., van Donkelaar, M. M. J., Verhoef, E., & Franke, B. (2017) · American Journal of Medical Genetics Part B Neuropsychiatric Genetics · doi:10.1002/ajmg.b.32542 · Cited by 30
“(Burt, 2009; Faraone et al., 2005).”
BackgroundYu, C.-J., Du, J.-C., Chiou, H.-C., Yang, S.-H., Liao, K.-W., Yang, W., Chung, M., Chien, L.-C., B. Hwang, & Chen, M.-L. (2016) · PLoS ONE · doi:10.1371/journal.pone.0149558 · Cited by 21
“The heritability of ADHD has been estimated to be as high as 76% [28], and various polymorphisms in dopamine-related genes have been found to increase the risk of ADHD [29, 30].”
BackgroundNeighborhood Characteristics and ADHD
Razani, N., Hilton, J. F., Halpern‐Felsher, B. L., Okumura, M. J., Morrell, H. E. R., & Yen, I. H. (2014) · Journal of Attention Disorders · doi:10.1177/1087054714542002 · Cited by 27
“ADHD is a highly heritable condition (Faraone et al., 2005).”
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Bello, N. T. (2015) · Patient Preference and Adherence · doi:10.2147/ppa.s73167 · Cited by 22
“Hereditability, calculated from dizygotic and monozygotic twin studies, has been estimated to be 76%.(12) An examination of parents (n=198) and siblings (n=112) of adoptive (n=25) and biological (n=101) children diagnosed with ADHD revealed that the rate of ADHD was significantly higher in parents (18%) and siblings (…”
Converging evidence does not support GIT1 as an ADHD risk gene
Klein, M., van der Voet, M., Harich, B., van Hulzen, K. J. E., Onnink, A. M. H., Hoogman, M., Guadalupe, T. M., Zwiers, M. P., Groothuismink, J. M., Verberkt, A., et al. (2015) · American Journal of Medical Genetics Part B Neuropsychiatric Genetics · doi:10.1002/ajmg.b.32327 · Cited by 23
“Attention Deficit/Hyperactivity Disorder (ADHD) is a common and highly heritable neuropsychiatric disorder (heritability 70– 80% [Faraone et al., 2005; Burt 2009]), with prevalence rates of 5– 6% in childhood [Polanczyk et al., 2007; American Psychiatric Association 2013].”
BackgroundSelf-citationAssociation of dopamine transporter gene variants with childhood ADHD features in bipolar disorder
Greenwood, T. A., Joo, E., Shekhtman, T., Sadovnick, A. D., Remick, R. A., Keck, P. E., McElroy, S. L., & Kelsoe, J. R. (2012) · American Journal of Medical Genetics Part B Neuropsychiatric Genetics · doi:10.1002/ajmg.b.32108 · Cited by 22
“Both BD and ADHD are familial with strong genetic components, as evidenced by heritability estimates up to 76–80% [Thapar et al., 2000; McGuffin et al., 2003; Faraone et al., 2005].”
BackgroundPediatric pharmacogenetic and pharmacogenomic studies: the current state and future perspectives
Russo, R., Capasso, M., Paolucci, P., Iolascon, A., & Teddy European Network of Excellence (2011) · European Journal of Clinical Pharmacology · doi:10.1007/s00228-010-0931-1 · Cited by 21
“Genes associated with increased risk for ADHD are the dopamine transporter (DAT1) [25], the dopamine receptors (DRD4 and DRD5) [30], serotonin transporter (5-HTT), and synaptosomalassociated protein (SNAP-25) [31–33].”
BackgroundBalanced Dopamine Is Critical for Pattern Completion during Associative Memory Recall
Li, F. R., Wang, L. P., Shen, X., & Tsien, J. Z. (2010) · PLoS ONE · doi:10.1371/journal.pone.0015401 · Cited by 23
“Given the broad evidence that dopamine is essential for attention and working memory [15–18] and that the genetic polymorphism in the DAT gene is thought to be implicated in ADHD [31–33], it is possible that both attention and working memory might play a role in pattern completion of memory retrieval under the partial…”
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“Although its etiology remains unknown, there is mounting evidence for genetic transmission [5,6] and abnormalities in brain structure and function in affected individuals [7–9].”
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“Evidence from family, adoption, twin, and molecular genetic studies highlights the centrality of genetic factors in the development of ADHD (Faraone and Khan, 2006; Faraone et al., 2005; Waldman and Gizer, 2006).”
InfluentialDNA methylation associated with persistent ADHD suggests TARBP1 as novel candidate
Weiß, A. L., Meijer, M., Budeus, B., Pauper, M., Hakobjan, M., Groothuismink, J. M., Shi, Y., Neveling, K., Buitelaar, J. K., Hoogman, M., et al. (2020) · Neuropharmacology · doi:10.1016/j.neuropharm.2020.108370 · Cited by 21
Integrative genomic analysis of methylphenidate response in attention-deficit/hyperactivity disorder
Pagerols, M., Vanesa Richarte, B., Sánchez‐Mora, C., Rovira, P., Artigas, M. S., Iris Garcia-martinez, A., Calvo-Sánchez, E., Montse Corrales, F., da Silva, B. S., Mota, N. R., et al. (2018) · Scientific Reports · doi:10.1038/s41598-018-20194-7 · Cited by 25
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“While research has identified several potential etiological mechanisms, such as gene variants, brain structural abnormalities, and neurotransmitter deficiency and dysregulation [11,12], much more work is needed to fully understand the early life determinants of ADHD and significant sex differences in ADHD risk.”
Forde, N. J., Ronan, L., Zwiers, M. P., Alexander‐Bloch, A. F., Faraone, S. V., Oosterlaan, J., Heslenfeld, D. J., Hartman, C. A., Buitelaar, J. K., & Hoekstra, P. J. (2017) · Frontiers in Neuroscience · doi:10.3389/fnins.2017.00218 · Cited by 22
“ADHD is a highly heritable (∼80%), genetically complex and heterogeneous disorder (Faraone et al., 2005).”
BackgroundSelf-citationTong, J., Cummins, T. D. R., Johnson, B. P., McKinley, L., Pickering, H. E., Fanning, P. A. J., Stefanac, N., Newman, D. P., Hawi, Z., & Bellgrove, M. A. (2015) · American Journal of Medical Genetics Part B Neuropsychiatric Genetics · doi:10.1002/ajmg.b.32283 · Cited by 18
“When examining specific genetic markers for ADHD, the majority of studies have employed either a case-control or a quantitative trait design [Faraone et al., 2005; Frazier-Wood et al., 2012].”
BackgroundSomkuwar, S. S., Kantak, K. M., & Dwoskin, L. P. (2015) · Journal of Neuroscience Methods · doi:10.1016/j.jneumeth.2015.02.002 · Cited by 23
“ADHD etiology, although multigenetic (Faraone et al., 2005; Gizer et al., 2009; Kuntsi and Klein, 2012), has been associated with polymorphisms of the norepinephrine transporter (NET) gene (Barr et al., 2002; Kollins et al., 2008; McEvoy et al., 2002).”
BackgroundA lack of functional NK1 receptors explains most, but not all, abnormal behaviours of NK1R ‐/‐ mice1
Porter, A. J., Pillidge, K., Tsai, Y., Dudley, J., Hunt, S. P., Peirson, S. N., Brown, L. A., & Stanford, S. C. (2015) · Genes Brain & Behavior · doi:10.1111/gbb.12195 · Cited by 29
“that both genetic (Faraone et al. 2005) and environmental factors (including maternal behaviour; Elia et al.”
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Romirowsky, A. M., & Chronis-Tuscano, A. (2014) · Child: Care, Health and Development · doi:10.1111/cch.12092 · Cited by 20
“Because ADHD is highly heritable (Faraone et al., 2005; Thapar, Langley, Owen, & O’Donovan, 2007), we included only biological fathers.”
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“The 10R-6R haplotype formed between the 30UTR-int 8 VNTR and the 10R/10R genotype of the 30UTR was suggested as risk factors for ADHD in children (Brookes et al. 2006; Asherson et al. 2007; Faraone et al. 2005); 10R/10R homozygous children performed poorly on a sustained attention task as compared to others (Loo et al.”
Sazonova, N., Dasbanerjee, T., Middleton, F. A., Gowtham, S., Schuckers, S., & Faraone, S. (2011) · American Journal of Medical Genetics Part B: Neuropsychiatric Genetics · doi:10.1002/ajmg.b.31230 · Cited by 20
“Our review of 20 twin studies indicates that ADHD has an estimated heritability of 0.76, and meta-analyses of linkage and association studies have implicated several candidate genes: DRD4, SLC6A3, DRD5, HTR1B, SNAP25, DBH, and SLC6A4 (Faraone and Mick, 2010).”
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“Neurobiological studies of ADHD point to the role of genetic factors with its high heritability estimates [1-3].”
BackgroundIlott, N., Saudino, K., & Asherson, P. (2010) · BMC Psychiatry · doi:10.1186/1471-244x-10-102 · Cited by 20
“It is well established that ADHD in children is highly heritable with estimates averaging at ~76% [2], with the same being true of ADHD symptoms in pre-school children [3].”
BackgroundAndersen, S., & Pine, D. (2014) · Current topics in behavioral neurosciences · doi:10.1007/978-3-642-54913-7 · Cited by 20
“A number of genes have been identified that convey risk for ADHD (Faraone et al. 2005; Durston 2008), although the effects of each gene marker are too small to be of clinical utility and explain only a small fraction of the overall genetic influence in ADHD.”
BackgroundKamradt, J. M., Nigg, J. T., Friderici, K. H., & Nikolas, M. A. (2017) · Development and Psychopathology · doi:10.1017/s0954579416000195 · Cited by 19
“…of the 48-bp VNTR in exon III, and more specifically the sevenrepeat allele (7R), of DRD4 because this variant mediates a blunted response to dopamine (Asghari et al., 1995; Faraone et al., 1999; Tol et al., 1992) and has been associated with ADHD (Faraone & Mick, 2010; Li, Sham, Owen, & He, 2006).”
BackgroundMastronardi, C. A., Pillai, E., Pineda, D. A., Martinez, A. F., Lopera, F., Velez, J. I., Palacio, J. D., Patel, H., Easteal, S., Acosta, M. T., et al. (2016) · Molecular Psychiatry · doi:10.1038/mp.2015.172 · Cited by 19
“The etiology and pathophysiology of ADHD are still not completely defined, but twin, adoption, and family-based studies indicate a strong genetic component, particularly since first and second-degree relatives of patients with ADHD have markedly higher prevalence of the illness 2 .”
Ephrin-A5 deficiency alters sensorimotor and monoaminergic development
Sheleg, M., Yochum, C. L., Wagner, G. C., Zhou, R., & Richardson, J. R. (2013) · Behavioural Brain Research · doi:10.1016/j.bbr.2012.08.032 · Cited by 19
“Additionally, identified ADHD susceptibility genes are known to be involved in the regulation of monoamine activity [35] and stimulant therapy for ADHD act as broad-spectrum monoaminergic agonists [36, 37].”
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Koevoet, D., Deschamps, P. K. H., & Kenemans, J. L. (2023) · Frontiers in Neuroscience · doi:10.3389/fnins.2022.1078586 · Cited by 28
“It is generally accepted that dysfunction of the DA system plays a vital role in ADHD pathology (Levy and Swanson, 2001; Faraone et al., 2005; Tripp and Wickens, 2009; Faraone and Mick, 2010; Purper-Ouakil et al., 2011; Faraone, 2018).”
BackgroundAttentional Mechanisms in Autism, ADHD, and Autism-ADHD Using a Local–Global Paradigm
Gargaro, B. A., May, T., Tonge, B. J., Sheppard, D. M., Bradshaw, J. L., & Rinehart, N. (2015) · Journal of Attention Disorders · doi:10.1177/1087054715603197 · Cited by 23
“Both ASD and ADHD are highly heritable conditions, with around 70% to 80% of the phenotypic variance for each disorder explained by genetic factors (Faraone et al., 2005; Lichtenstein, Carlström, Råstam, Gillberg, & Anckarsäter, 2010).”
BackgroundBrinksma, D. M., Hoekstra, P., van den Hoofdakker, B. J., de Bildt, A. D., Buitelaar, J., Hartman, C., & Dietrich, A. (2017) · Journal of Psychiatric Research · doi:10.1016/j.jpsychires.2017.02.014 · Cited by 19
Lamanna, A. L., Craig, F., Matera, E., Simone, M., Buttiglione, M., & Margari, L. (2017) · Neuropsychiatric Disease and Treatment · doi:10.2147/ndt.s132214 · Cited by 19
Childhood attention-deficit/hyperactivity disorder
Verkuijl, N., Perkins, M., & Fazel, M. S. (2015) · BMJ · doi:10.1136/bmj.h2168 · Cited by 45
Efectos sobre el contexto familiar de una intervención psicosocial compleja en niños con TDAH
Presentación, M., Pinto, V., Meliá, A., & Miranda, A. (2009) · Escritos de Psicología · doi:10.24310/espsiescpsi.v2i3.13383 · Cited by 19
Xu, X., Brookes, K. J., Sun, B., Ilott, N. E., & Asherson, P. J. (2009) · BMC Research Notes · doi:10.1186/1756-0500-2-71 · Cited by 20
“Polymorphic variants in several genes involved in regulation of the dopamine, and related neurotransmitter pathways are reported to be associated with ADHD [1-3].”
BackgroundChan, S. S. M., Wong, O. W. H., Hussain, S., Tsoi, K. K. F., Ma, K. K. Y., Chau, S. W. H., Ma, S. L., Lai, K. Y. C., Chu, C. W., Lo, H., et al. (2025) · The Lancet Regional Health - Western Pacific · doi:10.1016/j.lanwpc.2025.101533 · Cited by 12
“39,40 Our study showed that children and adolescents with ADHD were more likely to develop anxiety disorder after controlling for other conditions, which was consistent with earlier reports from both clinical and epidemiological samples where up to 50% of individuals had one or more comorbid…”
The role of snare proteins in cortical development
Vadišiūtė, A., Meijer, E. J., Szabó, F., Hoerder‐Suabedissen, A., Kawashita, E., Hayashi, S., & Molnár, Z. (2022) · Developmental Neurobiology · doi:10.1002/dneu.22892 · Cited by 23
“Association of SNAP25 polymorphisms with ADHD in human patients has also been confirmed in a meta-analysis (Faraone et al., 2005).”
BackgroundWaits, A., Chang, C.-H., Yu, C.-J., Du, J.-C., Chiou, H.-C., Hou, J.-W., Yang, W., Chen, H.-C., Chen, Y.-S., B. Hwang, et al. (2021) · Journal of Exposure Science and Environmental Epidemiology · doi:10.1038/s41370-021-00370-0 · Cited by 18
“The genetic contribution was also likely, since ADHD heritability was estimated as high as 76% [49], and the gene-environment interaction was shown in this sample for DMP and HNE-MA [9].”
BackgroundPineau, G., Villemonteix, T., Slama, H., Kavec, M., Balériaux, D. F., Metens, T., Baijot, S., Mary, A., Ramoz, N., Gorwood, P. A. P. M., et al. (2019) · Research in Developmental Disabilities · doi:10.1016/j.ridd.2019.103430 · Cited by 20
“Additionally, ADHD is supposed to be associated with a high number of genes with minor effects interacting with environmental factors (Faraone & Mick, 2010; Hawi et al., 2015): some combinations may have different effects on brain activity, and some genetic variants may also be associated with…”
BackgroundThe Unique Effects of Maternal ADHD Symptoms and Emotion Dysregulation on Parenting Behavior
Woods, K., Mazursky-Horowitz, H., Thomas, S. R., Dougherty, L. R., & Chronis-Tuscano, A. M. (2019) · Journal of Attention Disorders · doi:10.1177/1087054719829820 · Cited by 21
Modelo Teórico del Trastorno por Déficit de Atención con Hiperactividad I: Definición Operativa
Lavigne-Cerván, R., & Romero, J. F. (2017) · Electronic Journal of Research in Educational Psychology · doi:10.25115/ejrep.v8i22.1417 · Cited by 19
“De tal forma que implicaría una alteración en los genes (Barkley, 2006a, 2008; Faraone et al., 2005; Gizer, Ficks y Waldman, 2009) encargados de la recepción y/o transporte de neurotransmisores -como la dopamina y noradrenalina- muy presentes en los circuitos que inervan las zonas frontales del…”
BackgroundADHD, Socioeconomic Status, Medication Use, and Academic Ethic
Simoni, Z. R., & Drentea, P. (2016) · Sociological Focus · doi:10.1080/00380237.2016.1107713 · Cited by 18
“Research involving ADHD has investigated etiological factors of ADHD, including genetics (Faraone et al. 2005) and neurological explanations (Mostofsky et al. 2002), as well as studies on the prevalence of ADHD diagnosis and medication rates (Olfson et al. 2003).”
BackgroundBalkarlı, A., Şengül, C., Tepeli, E., Balkarlı, H., & Çobankara, V. (2014) · BMC Musculoskeletal Disorders · doi:10.1186/1471-2474-15-191 · Cited by 18
“Several studies investigated the relationship between SNAP-25 gene polymorphism and personality disorders, schizophrenia, and attention deficit and hyperactivity disorder; these studies reported that the SNAP-25 gene might influence development of these disorders [12-17].”
BackgroundAssociation of genetic risk severity with ADHD clinical characteristics
Kotte, A., Faraone, S. V., & Biederman, J. (2013) · American Journal of Medical Genetics Part B Neuropsychiatric Genetics · doi:10.1002/ajmg.b.32171 · Cited by 22
“…places ADHD as one of the most heritable of psychiatric disorders with crosssectional and longitudinal family, twin, and adoption studies demonstrating 70–80% heritability estimates, familial aggregation of symptoms, and familial clustering within and across generations [Faraone et al., 2005].”
BackgroundResultSelf-citationAltered gene expression in the prefrontal cortex of young rats induced by the ADHD drug atomoxetine.
Lempp, T., Toennes, S., Wunder, C., Russe, O. Q., Möser, C. V., Kynast, K., Freitag, C., & Niederberger, E. (2013) · Progress in Neuro-psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2012.08.012 · Cited by 18
“Several polymorphisms in the SNAP-25 gene locus in humans could be linked to ADHD by meta-analysis of case-controlled and family-based reports indicating SNAP-25 as a candidate gene in ADHD (Brophy et al., 2002; Choi et al., 2007; Faraone et al., 2005; Feng et al., 2005; Renner et al., 2008).”
Moss, S. B. (2009) · Neuropsychiatric Disease and Treatment · doi:10.2147/ndt.s4101 · Cited by 19
“also be helpful given that ADHD has approximately 70% heritability.(2,26) Diagnostic interviews are available to assist with the interview process, including the Brown ADD Scale, Connor’s Adult ADHD Diagnostic Interview for DSM-IV and the Diagnostic Interview Schedule.”
Kim, B., Koo, M., Jun, J., Park, I., Oh, D., & Cheon, K. (2009) · Psychiatry Investigation · doi:10.4306/pi.2009.6.3.216 · Cited by 18
Mueller, K. L., & Tomblin, J. B. (2012) · Topics in Language Disorders · doi:10.1097/tld.0b013e318261ffdd · Cited by 17
“The mean heritability across studies has been estimated as 76% (Faraone et al., 2005).”
Two neurosubtypes of ADHD different from the clinical phenotypes
Wang, Q., Zhao, C., Qiu, J., & Lu, W. (2023) · Psychiatry Research · doi:10.1016/j.psychres.2023.115453 · Cited by 16
Nikolaus, S., Mamlins, E., Giesel, F. L., Schmitt, D. R., & Müller, H. (2021) · Reviews in the Neurosciences · doi:10.1515/revneuro-2021-0083 · Cited by 19
“5, 40225 Düsseldorf, Germany DAT1 and SLC6A3, the D4 receptor (R) gene DRD4, the D5R geneDRD5, the 5-HT transporter (SERT) gene 5-HTT and the 5-HT1BR gene HTR1B (Faraone and Mick 2010; Franke et al. 2019; Gizer et al. 2009).”
BackgroundEnergy Metabolism Disturbances in Cell Models of PARK2 CNV Carriers with ADHD
Palladino, V. S., Chiocchetti, A., Frank, L., Haslinger, D., McNeill, R., Radtke, F., Till, A., Haupt, S., Brüstle, O., Günther, K., et al. (2020) · Journal of Clinical Medicine · doi:10.3390/jcm9124092 · Cited by 17
Tinkov, A. A., Mazaletskaya, A. L., Ajsuvakova, O. P., Bjørklund, G., Huang, P.-T., Chernova, L. N., Skalny, A. A., & Skalny, A. V. (2019) · Biological Trace Element Research · doi:10.1007/s12011-019-01947-5 · Cited by 21
“ADHD has a complex multifactorial etiology with a strong genetic component [6].”
BackgroundKo, C.-H., Hsieh, T.-J., Wang, P.-W., Lin, W.-C., Chen, C.-S., & Yen, J. (2018) · Journal of Attention Disorders · doi:10.1177/1087054715572609 · Cited by 17
“Genetic factors contribute to the development of ADHD (Faraone et al., 2005) and adult ADHD (Faraone, 2004).”
BackgroundHoppe, N., Bininda-Emonds, O., & Ganslosser, U. (2017) · Veterinary Medicine - Open Journal · doi:10.17140/vmoj-2-122 · Cited by 17
Optimizing outcomes in ADHD treatment: from clinical targets to novel delivery systems
Mattingly, G., & Anderson, R. H. (2016) · CNS Spectrums · doi:10.1017/s1092852916000808 · Cited by 17
Herken, H., Erdal, M. E., Kenar, A. N. İ., Ünal, G. A., Çakaloz, B., Ay, M. E., Yücel, E., Edgünlü, T., & Şengül, C. (2014) · Psychiatry Investigation · doi:10.4306/pi.2014.11.4.476 · Cited by 17
Advances in molecular genetic studies of attention deficit hyperactivity disorder in China.
Gao, Q., Liu, L., Qian, Q., & Wang, Y. (2014) · PubMed Central · doi:10.3969/j.issn.1002-0829.2014.04.003 · Cited by 16
Liu, L., Chen, Y., Li, H., Qian, Q., Yang, L., Glatt, S. J., Faraone, S. V., & Wang, Y. (2013) · Psychiatry Research · doi:10.1016/j.psychres.2013.04.029 · Cited by 17
“In the past two decades, geneticists have focused on several neurotransmitter systems to explore the possible genetic variants leading to the cause of ADHD, including dopamine (DA), norepinephrine (NE), serotonin (5-HT) pathways (Li et al., 2005, 2006, 2007; Faraone and Mick, 2010; Wu et al., 2012) among others.”
InfluentialSelf-citationOhno, Y., Okano, M., Masui, A., Imaki, J., Egawa, M., Yoshihara, C., Tatara, A., Mizuguchi, Y., Sasa, M., & Shimizu, S. (2012) · Neuropharmacology · doi:10.1016/j.neuropharm.2012.04.031 · Cited by 17
“Nonetheless, previous studies have shown that dopamine reuptake activity of DAT is reduced and thereby the basal level of extracellular dopamine in the basal ganglia is elevated in SHR (Carboni et al., 2003; Heal et al., 2008; Leo et al., 2003; McKeon and Hendley, 1988).”
BackgroundInfluentialADHD matures: time for practitioners to do the same?
Bolea-Alamanac, B. M., Adamou, M., Arif, M., Asherson, P. J., Gudjonsson, G. H., Müller, U., Nutt, D., Pitts, M. E., Thome, J., & Young, S. (2011) · Journal of Psychopharmacology · doi:10.1177/0269881111410898 · Cited by 15
Attention deficit hyperactivity disorder pharmacogenetics: the dopamine transporter and D4 receptor.
McGough, J. (2012) · Pharmacogenomics (London) · doi:10.2217/pgs.12.5 · Cited by 17
Vorobyov, V., Schibaev, N., Kaptsov, V., Kovalev, G., & Sengpiel, F. (2011) · Brain Research · doi:10.1016/j.brainres.2011.01.107 · Cited by 17
Liu, L., Cheng, J. R., Li, H., Yang, L., Qian, Q., & Wang, Y. (2014) · Journal of Child Psychology and Psychiatry · doi:10.1111/jcpp.12278 · Cited by 21
“The heritability of attention-deficit/hyperactivity disorder (ADHD) is approximately 0.76 (Faraone & Mick, 2010), which indicates the important role of genetic factors on the predisposition to ADHD.”
InfluentialTrujillo, N., Salazar, D. A. P., & Uribe, L. H. (2012) · Revista de Neurología · doi:10.33588/rn.5405.2011144 · Cited by 11
“Sin embargo, al igual que los estudios previamente descritos, se ha observado baja posibilidad de replicación [84].”
BackgroundAi, Y., Zhao, J., Shi, J., & Zhu, T.-T. (2021) · Psychopharmacology · doi:10.1007/s00213-021-05989-3 · Cited by 16
“Although genetic and biological factors play important roles in ADHD development (Faraone et al. 2005), multiple environmental risk factors have also been identified.”
BackgroundOlsen, D., Wellner, N., Ollendorff, M. K., de Jong, I. E. M., Sotty, F., Didriksen, M., Glerup, S., & Nykjær, A. (2021) · Translational Psychiatry · doi:10.1038/s41398-021-01199-9 · Cited by 21
Zhang‐James, Y., Vaudel, M., Mjaavatten, O., Berven, F. S., Haavik, J., & Faraone, S. V. (2019) · ADHD Attention Deficit and Hyperactivity Disorders · doi:10.1007/s12402-018-0281-x · Cited by 26
Self-citationAfeti, K., & Nyarko, S. (2017) · Annals of General Psychiatry · doi:10.1186/s12991-017-0135-5 · Cited by 16
“The major etiological factor has been identified to be genetic [7].”
BackgroundZayats, T., Johansson, S., & Haavik, J. (2015) · Behavioral and Brain Functions · doi:10.1186/s12993-015-0078-4 · Cited by 18
“This includes attention-deficit hyperactivity disorder (ADHD), which is one of the most common and most heritable childhood-onset mental disorders [2, 3].”
BackgroundAmirabadi, M. R. E., Davari-Ashtiani, R., Khademi, M., Rajeziesfahani, S., Emamalizadeh, B., Movafagh, A., Arabgol, F., Sadr, S., Darvish, H., & Razjouyan, K. (2015) · Iranian Red Crescent Medical Journal · doi:10.5812/ircmj.229961v2 · Cited by 16
Yen, Y.-C., Gassen, N. C., Zellner, A., Rein, T., Landgraf, R., Wotjak, C. T., & Anderzhanova, E. A. (2015) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2015.00067 · Cited by 16
“Attention deficit hyperactivity disorder (ADHD) is a frequent psychiatric disorder with a prevalence of up to 8% in Western populations (Faraone and Mick, 2010).”
BackgroundAre Bottom-Up and Top-Down Traits in Dual-Systems Models of Risky Behavior Genetically Distinct?
Ellingson, J. M., Verges, A. J., Littlefield, A. K., Martin, N. G., & Slutske, W. S. (2013) · Behavior Genetics · doi:10.1007/s10519-013-9615-9 · Cited by 18
“1996) and attention deficit hyperactivity disorder (5-HTR1B; Faraone and Mick 2010).”
Tian, Y.-F., Stamova, B., Ander, B., Jickling, G., Gunther, J. R., Corbett, B., Bos-Veneman, N., Hoekstra, P., Schweitzer, J., & Sharp, F. (2012) · BMC Medical Genomics · doi:10.1186/1755-8794-5-49 · Cited by 16
“551 [21]”
Lampis, V., Maziade, M., & Battaglia, M. (2011) · Pediatric Research · doi:10.1203/pdr.0b013e318212b42e · Cited by 16
Perry, G. M. L., Sagvolden, T., & Faraone, S. V. (2010) · American Journal of Medical Genetics Part B Neuropsychiatric Genetics · doi:10.1002/ajmg.b.31070 · Cited by 18
“The latter seems more likely; the 10-repeat allele at the dopamine transporter (DAT), previously associated with ADHD [Faraone et al., 2005], has also been associated with IIV in specific behavioral [Bellgrove et al., 2005] and neurological [Loo et al., 2003] phenotypes.”
BackgroundInfluentialSelf-citationGenomewide Association Studies: History, Rationale, and Prospects for Psychiatric Disorders
Psychiatric GWAS Consortium Coordinating Committee (2010) · FOCUS The Journal of Lifelong Learning in Psychiatry · doi:10.1176/foc.8.3.foc417 · Cited by 13
Systematic review of mitochondrial genetic variation in attention-deficit/hyperactivity disorder
Giannoulis, S. V., Müller, D., Kennedy, J. L., & Gonçalves, V. (2022) · European Child and Adolescent Psychiatry · doi:10.1007/s00787-022-02030-6 · Cited by 15
Liu, L., Zhang, L., Li, H. M., Wang, Z. R., Xie, X. F., Mei, J., Jin, J., Shi, J., Sun, L., Li, S. C., et al. (2017) · Translational Psychiatry · doi:10.1038/tp.2017.156 · Cited by 17
Cdh13 and AdipoQ gene knockout alter instrumental and Pavlovian drug conditioning
King, C. P., Militello, L., Hart, A., Pierre, C. L. S., Leung, E., Versaggi, C. L., Roberson, N. L., Catlin, J. P., Palmer, A. A., Richards, J. B., et al. (2017) · Genes Brain & Behavior · doi:10.1111/gbb.12382 · Cited by 12
“2012), including attention deficit hyperactivity disorder (ADHD) (Faraone et al. 2005; Hinney et al. 2011; Larsson et al. 2013; Morrison & Stewart 1971; Stergiakouli et al. 2015) and substance use disorders (SUDs) (Bienvenu et al.”
Leung, P. W. L., Chan, J. K.-Y., Chen, L. H., Lee, C. C., Hung, S. F., Ho, T. P., Tang, C. P., Moyzis, R. K., & Swanson, J. M. (2017) · PLoS ONE · doi:10.1371/journal.pone.0173748 · Cited by 16
“Following the first association study between ADHD and DRD4 exon 3 7R allele published in 1996 [24], several subsequent meta-analyses have consistently confirmed an increase of the 7R allele in ADHD probands, based upon both case-control and family studies in European-ancestry population [6,25,26].”
BackgroundMethodInfluentialUnal, D., Unal, M., Alikaşifoğlu, M., & Cetinkaya, A. (2016) · Psychiatry Investigation · doi:10.4306/pi.2016.13.4.427 · Cited by 15
Attention‐deficit/hyperactivity disorder: The past 50 years
Efron, D. (2015) · Journal of Paediatrics and Child Health · doi:10.1111/jpc.12809 · Cited by 18
Karmakar, A., Maitra, S., Verma, D., Chakraborti, B., Goswami, R., Ghosh, P., Sinha, S., Mohanakumar, K. P., Rajamma, U., & Mukhopadhyay, K. (2014) · Neurochemical Research · doi:10.1007/s11064-014-1276-4 · Cited by 17
“Due to high heritability of the disorder, role of different candidate genes in the etiology of ADHD have been reviewed at length [26–28] and it was hypothesized that multiple genes contribute to the total genetic effect in ADHD [8, 29, 30].”
BackgroundDo SNPs of DRD4 gene predict adult persistence of ADHD in a Chinese sample?
Li, Y.-L., Baker-Ericzén, M. J., Ji, N., Chang, W., Guan, L., Qian, Q., Zhang, Y., Faraone, S., & Wang, Y.-F. (2013) · Psychiatry Research · doi:10.1016/j.psychres.2012.08.016 · Cited by 15
“The heritability of ADHD was estimated at approximately 76% in studies involving children (Faraone and Mick, 2010) and approximately 30–40 % in adults (Schultz et al.”
Self-citationChang, S., Zhang, W., Gao, L., & Wang, J. (2012) · Protein & Cell · doi:10.1007/s13238-012-2931-7 · Cited by 13
Steinlechner, S., Bruggemann, N., Sobottka, V., Benthien, A., Behn, B., Klein, C., Schmid, G., & Lencer, R. (2011) · European Archives of Psychiatry and Clinical Neuroscience · doi:10.1007/s00406-010-0140-z · Cited by 15
“Several family studies in ADHD confirmed its strong familial association [5, 6] with a two- to eightfold increased risk for ADHD in parents and siblings of children with ADHD S.”
BackgroundNeurobiology and Genetics of ADHD in Adults
Spencer, T. J. (2008) · CNS Spectrums · doi:10.1017/s1092852900026833 · Cited by 10
Araiza, J. F. R. (2014) · Salud Mental · doi:10.17711/sm.0185-3325.2014.009 · Cited by 15
Liu, L., Wang, Y., Chen, W., Gao, Y., Li, H., Wang, Y., Chan, R. C. K., & Qian, Q. (2022) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2022.974283 · Cited by 18
“Subtypes, gender and age groups have been suggested to be potential confounding factors in ADHD studies, which would increase the sample heterogeneity (36).”
BackgroundGutiérrez-Casares, J. R., Quintero, J., Jorba, G., Junet, V., Martínez, V., Pozo-Rubio, T., Oliva, B., Daura, X., Mas, J. M., & Montoto, C. (2021) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2021.741170 · Cited by 23
“ADHD and its associated comorbid psychiatric disorders present a high genetic and signaling overlap (126, 127), which could act as confounding factors at the clinical and molecular levels.”
BackgroundImpulsive and Omission Errors: Potential Temporal Processing Endophenotypes in ADHD
Acosta-López, J. E., Suárez, I., Pineda, D. A., Cervantes-Henríquez, M. L., Martínez-Banfi, M. L., Lozano-Gutiérrez, S. G., Ahmad, M., Pineda‐Alhucema, W., Noguera-Machacón, L. M., Hoz, M. D. L., et al. (2021) · Brain Sciences · doi:10.3390/brainsci11091218 · Cited by 16
“In particular, first and second degree relatives of patients with ADHD have markedly higher prevalence of symptoms [10].”
BackgroundNaumova, D., Grizenko, N., Sengupta, S. M., & Joober, R. (2019) · World Journal of Biological Psychiatry · doi:10.1080/15622975.2017.1410221 · Cited by 14
“Pharmacological agents, such as methylphenidate (MPH), strongly modulate dopamine signalling in the brain and are known to affect behaviour and improve ADHD symptoms (Faraone and Mick 2010).”
BackgroundFernández‐Jaén, A., Albert, J., Fernández-Mayoralas, D. M., López‐Martín, S., Fernández‐Perrone, A. L., de la Peña, M. J., Calleja‐Pérez, B., Rodríguez, M. R., & Arribas, S. L. (2016) · Journal of Attention Disorders · doi:10.1177/1087054716647483 · Cited by 17
“Notably, meta-analyses of molecular genetic studies indicate an overrepresentation of the 10R allele in children and adolescents with ADHD (Faraone & Mick, 2010; Faraone et al., 2014).”
BackgroundLaugesen, K., Byrjalsen, A., Frøslev, T., Olsen, M., & Sørensen, H. (2017) · BMJ Open · doi:10.1136/bmjopen-2017-016825 · Cited by 14
“An important risk factor for ADHD is heritability.(12) Other proposed risk factors include preterm birth and prenatal exposure to smoking or alcohol.”
Lack of association of polymorphisms in six candidate genes in colombian adhd patients
Fonseca, D. J., Mateus, H., Gálvez, J. M., Forero, D. A., Talero‐Gutiérrez, C., & Vélez-van-Meerbeke, A. (2015) · Annals of Neurosciences · doi:10.5214/ans.0972.7531.220405 · Cited by 16
Trampush, J. W., Jacobs, M. M., Hurd, Y., Newcorn, J., & Halperin, J. (2014) · Developmental Science · doi:10.1111/desc.12131 · Cited by 14
Kiive, E., & Harro, J. (2012) · European Psychiatry · doi:10.1016/j.eurpsy.2012.04.004 · Cited by 12
“ADHD is a highly heritable condition, with the average heritability estimate of 76% [13], which is polygenic in nature [9].”
Background
Metadata
- Authors
- Faraone, S. V., & Mick, E.
- Affiliations
- SUNY Upstate Medical University (US)
- Harvard University (US)
- Corresponding author
- Faraone, Stephen V.
- Venue
- Psychiatric Clinics of North America
- Publisher
- Elsevier BV
- Published
- 2010-03
- Volume
- 33
- Issue
- 1
- Pages
- 159-180
- ISSN
- 0193-953X (ISSN-L)
- 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
- 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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