Meta-Analysis of Genome-Wide Association Studies of Attention-Deficit/Hyperactivity Disorder

doi:10.1016/j.jaac.2010.06.008

Journal of the American Academy of Child & Adolescent Psychiatry

Volume 49, Issue 9, September 2010, Pages 884-897

, , , , , , , , , , , , , , , , , , , …

https://doi.org/10.1016/j.jaac.2010.06.008 Get rights and content

Objective

Although twin and family studies have shown attention-deficit/hyperactivity disorder (ADHD) to be highly heritable, genetic variants influencing the trait at a genome-wide significant level have yet to be identified. As prior genome-wide association studies (GWAS) have not yielded significant results, we conducted a meta-analysis of existing studies to boost statistical power.

Method

We used data from four projects: a) the Children's Hospital of Philadelphia (CHOP); b) phase I of the International Multicenter ADHD Genetics project (IMAGE); c) phase II of IMAGE (IMAGE II); and d) the Pfizer-funded study from the University of California, Los Angeles, Washington University, and Massachusetts General Hospital (PUWMa). The final sample size consisted of 2,064 trios, 896 cases, and 2,455 controls. For each study, we imputed HapMap single nucleotide polymorphisms, computed association test statistics and transformed them to z-scores, and then combined weighted z-scores in a meta-analysis.

Results

No genome-wide significant associations were found, although an analysis of candidate genes suggests that they may be involved in the disorder.

Conclusions

Given that ADHD is a highly heritable disorder, our negative results suggest that the effects of common ADHD risk variants must, individually, be very small or that other types of variants, e.g., rare ones, account for much of the disorder's heritability.

Section snippets

Samples

Our total data set comprises four projects: a) the Children's Hospital of Philadelphia (CHOP); b) phase I of the International Multisite ADHD Genetics Project (IMAGE); c) phase II of IMAGE (IMAGE II); and d) the Pfizer-funded study from the University of California, Los Angeles, Washington University, and Massachusetts General Hospital (PUWMa). Each of these datasets has been described elsewhere.10, 12, 13, 15 For this meta-analysis, we attempted to include the same individual-level data as

Genome-Wide Results

The full distribution of results can be seen in the QQ plot in Figure 1. Under the null hypothesis of no association, these points should fall along the diagonal line. The dotted line plots the 95% confidence interval. The QQ plot and the lambda statistic (1.025) show no appreciable inflation of the test statistic. The lambdas for each individual study are 1.085 for IMAGE II, 1.012 for IMAGE, 0.970 for PUWMa, and 1.047 for CHOP, which yields an expected lambda of 1.028 based on the average

Discussion

We have presented the first meta-analysis of genome-wide association datasets for childhood ADHD, including a total of 2,064 trios, 896 cases, and 2,455 controls. Genome-wide significant effects still elude detection for this disorder, suggesting that the effect sizes for the common variants influencing risk for ADHD are likely to be very small. However, these results include a number of promising regions, for which replication is an essential next step. Moreover, our analysis of candidate

References (39)

S.V. Faraone et al.
Molecular genetics of attention-deficit/hyperactivity disorder
Biol Psychiatry
(2005)
S.V. Faraone et al.
Molecular genetics of attention deficit hyperactivity disorder
Psychiatr Clin North Am
(2010)
S.C. Bakker et al.
A whole-genome scan in 164 Dutch sib pairs with attention-deficit/hyperactivity disorder: Suggestive evidence for linkage on chromosomes 7p and 15q
Am J Hum Genet
(2003)
B.L. Browning et al.
A unified approach to genotype imputation and haplotype-phase inference for large data sets of trios and unrelated individuals
Am J Hum Genet
(2009)
S.R. Browning et al.
Rapid and accurate haplotype phasing and missing-data inference for whole-genome association studies by use of localized haplotype clustering
Am J Hum Genet
(2007)
S.V. Faraone et al.
The worldwide prevalence of ADHD: Is it an American Condition?
World Psychiatry
(2003)
G. Polanczyk et al.
The worldwide prevalence of ADHD: A systematic review and metaregression analysis
Am J Psychiatry
(2007)
R.C. Kessler et al.
The prevalence and correlates of adult ADHD in the United States: Results from the National Comorbidity Survey Replication
Am J Psychiatry
(2006)
S.V. Faraone et al.
What is the prevalence of adult ADHD?Results of a population screen of 966 adults
J Attention Disord
(2005)
C.M. Freitag et al.
Phenotypic and measurement influences on heritability estimates in childhood ADHD
Eur Child Adolesc Psychiatry
(2010)

G. McLoughlin et al.

Genetic support for the dual nature of attention deficit hyperactivity disorder: Substantial genetic overlap between the inattentive and hyperactive-impulsive components

J Abnorm Child Psychol

(2007)

D. Li et al.

Meta-analysis shows significant association between dopamine system genes and attention deficit hyperactivity disorder (ADHD)

Hum Mol Genet

(2006)

B.M. Neale et al.

Genome-wide association scan of attention deficit hyperactivity disorder

Am J Med Genet B Neuropsychiatr Genet

(2008)

J. Lasky-Su et al.

Genome-wide association scan of the time to onset of attention deficit hyperactivity disorder

Am J Med Genet B Neuropsychiatr Genet

(2008)

E. Mick et al.

Family-based genome-wide association scan of attention-deficit/hyperactivity disorder

J Am Acad Child Adolesc Psychiatry

(2010)

I.I. Consortium

Case control genome-wide association of attention deficit/hyperactivity disorder

J Am Acad Child Adolesc Psychiatry

(2010)

K.P. Lesch et al.

Molecular genetics of adult ADHD: Converging evidence from genome-wide association and extended pedigree linkage studies

J Neural Transm

(2008)

J. Elia et al.

Rare structural variants found in attention-deficit hyperactivity disorder are preferentially associated with neurodevelopmental genes

Mol Psychiatry

(2010)

B.M. Neale et al.

Genome-wide association scan of attention deficit hyperactivity disorder

Am J Med Genet B Neuropsychiatr Genet

(2008)

Cited by (363)

Novel pharmacological targets for GABAergic dysfunction in ADHD
2024, Neuropharmacology
Attention deficit/hyperactivity disorder (ADHD) is a neurodevelopment disorder that affects approximately 5% of the population. The disorder is characterized by impulsivity, hyperactivity, and deficits in attention and cognition, although symptoms vary across patients due to the heterogenous and polygenic nature of the disorder. Stimulant medications are the standard of care treatment for ADHD patients, and their effectiveness has led to the dopaminergic hypothesis of ADHD in which deficits in dopaminergic signaling, especially in cortical brain regions, mechanistically underly ADHD pathophysiology. Despite their effectiveness in many individuals, almost one-third of patients do not respond to stimulant treatments and the long-term negative side effects of these medications remain unclear. Emerging clinical evidence is beginning to highlight an important role of dysregulated excitatory/inhibitory (E/I) balance in ADHD. These deficits in E/I balance are related to functional abnormalities in glutamate and Gamma-Aminobutyric Acid (GABA) signaling in the brain, with increasing emphasis placed on GABAergic interneurons driving specific aspects of ADHD pathophysiology. Recent genome-wide association studies (GWAS) have also highlighted how genes associated with GABA function are mutated in human populations with ADHD, resulting in the generation of several new genetic mouse models of ADHD. This review will discuss how GABAergic dysfunction underlies ADHD pathophysiology, and how specific receptors/proteins related to GABAergic interneuron dysfunction may be pharmacologically targeted to treat ADHD in subpopulations with specific comorbidities and symptom domains.
This article is part of the Special Issue on “PFC circuit function in psychiatric disease and relevant models”.
Sleep regulation and host genetics
2024, Advances in Genetics
Due to the multifactorial and complex nature of rest, we focus on phenotypes related to sleep. Sleep regulation is a multifactorial process. In this chapter, we focus on those phenotypes inherent to sleep that are highly prevalent in the population, and that can be modulated by lifestyle, such as sleep quality and duration, insomnia, restless leg syndrome and daytime sleepiness. We, therefore, leave in the background those phenotypes that constitute infrequent pathologies or for which the current level of scientific evidence does not favour the implementation of practical approaches of this type. Similarly, the regulation of sleep quality is intimately linked to the regulation of the circadian rhythm. Although this relationship is discussed in the sections that require it, the in-depth study of circadian rhythm regulation at the molecular level deserves a separate chapter, and this is how it is dealt with in this volume.
DNA methylation epi-signature and biological age in attention deficit hyperactivity disorder patients
2023, Clinical Neurology and Neurosurgery
Attention Deficit/Hyperactivity Disorder (ADHD) is a common behavioral syndrome that begins in childhood and affects 3.4% of children worldwide. Due to its etiological complexity, there are no consistent biomarkers for ADHD, however the high heritability presented by the disorder indicates a genetic/epigenetic influence. The main epigenetic mechanism is DNA methylation, a process with an important role in gene expression and in many psychiatric disorders. Thus, our study sought to identify epi-signatures biomarkers in 29 children clinically diagnosed with ADHD.
After DNA extraction and bisulfite conversion, we performed methylation array experiment for differential methylation, ontological and biological age analysis.
The biological response in ADHD patients was not sufficient to determine a conclusive epi-signature in our study. However, our results highlighted the interaction of energy metabolism and oxidative stress pathways in ADHD patients detected by differential methylation patterns. Furthermore, we were able to identify a marginal association between the DNAmAge and ADHD.
Our study present new methylation biomarkers findings associated with energy metabolism and oxidative stress pathways, in addition to DNAmAge in ADHD patients. However, we propose that further multiethnic studies, with larger cohorts and including maternal conditions, are necessary to demonstrate a definitive association between ADHD and these methylation biomarkers.
Enrichment analyses identify shared associations for 25 quantitative traits in over 600,000 individuals from seven diverse ancestries
2022, American Journal of Human Genetics
Since 2005, genome-wide association (GWA) datasets have been largely biased toward sampling European ancestry individuals, and recent studies have shown that GWA results estimated from self-identified European individuals are not transferable to non-European individuals because of various confounding challenges. Here, we demonstrate that enrichment analyses that aggregate SNP-level association statistics at multiple genomic scales—from genes to genomic regions and pathways—have been underutilized in the GWA era and can generate biologically interpretable hypotheses regarding the genetic basis of complex trait architecture. We illustrate examples of the robust associations generated by enrichment analyses while studying 25 continuous traits assayed in 566,786 individuals from seven diverse self-identified human ancestries in the UK Biobank and the Biobank Japan as well as 44,348 admixed individuals from the PAGE consortium including cohorts of African American, Hispanic and Latin American, Native Hawaiian, and American Indian/Alaska Native individuals. We identify 1,000 gene-level associations that are genome-wide significant in at least two ancestry cohorts across these 25 traits as well as highly conserved pathway associations with triglyceride levels in European, East Asian, and Native Hawaiian cohorts.
Association between plasma proteome and childhood neurodevelopmental disorders: A two-sample Mendelian randomization analysis
2022, eBioMedicine
Citation Excerpt :
Patients with such disorders frequently have learning difficulties, as well as attainment, work, and interpersonal problems; the symptoms persist in adulthood for a substantial proportion of the population.3–7 Recent technological advances, particularly genome-wide association studies (GWASs), have successfully identified a number of novel biomarkers for these disorders.8–12 However, further evidence regarding their pathogenesis and the development of drug targets is required.
Childhood neurodevelopmental disorders, including autism spectrum disorder (ASD), attention-deficit hyperactivity disorder (ADHD), and Tourette syndrome (TS), comprise a major cause of health-related disabilities in children. However, biomarkers towards pathogenesis or novel drug targets are still limited. Our study aims to provide a comprehensive investigation of the causal effects of the plasma proteome on ASD, ADHD, and TS using the two-sample Mendelian Randomization (MR) approach.
Genetic associations with 2994 plasma proteins were selected as exposures and genome-wide association data of ASD, ADHD, TS were utilized as outcomes. MR analyses were carried out using the inverse-variance weighted method, and the MR-Egger and weighted median methods were used for sensitivity analysis.
Using single-nucleotide polymorphisms as instruments, the study suggested increased levels of MAPKAPK3 (OR: 1.09; 95% CI: 1.05–1.13; P = 1.43 × 10⁻⁶) and MRPL33 (OR: 1.07; 95% CI: 1.04–1.11; P = 5.37 × 10⁻⁶) were causally associated with a higher risk of ASD, and increased MANBA level was associated with a lower risk of ADHD (OR: 0.91; 95% CI: 0.88–0.95; P = 8.97 × 10⁻⁶). The causal associations were robust in sensitivity analysis, leave-one-out analysis and Multivariable MR, and no pleiotropy was observed. No significant risk protein was identified for TS.
The study findings support the idea that the MAPK/ERK signaling pathway and mitochondrial dysfunction are involved in the pathogenesis of ASD, while a deficiency in beta-mannosidase might play a role in the development of ADHD.
Natural Science Basic Research Program of Shaanxi (2021JQ-390).
Attention-deficit/hyperactivity disorder
2022, Neurobiology of Brain Disorders: Biological Basis of Neurological and Psychiatric Disorders, Second Edition
This chapter reviews attention deficit/hyperactivity disorder (ADHD), a persistent neurodevelopmental disorder that can affect both children and adults. In most cases, ADHD arises from several genetic and environmental risk factors that each have a small individual effect and act together to increase susceptibility. ADHD is a multifactorial disorder, and this is consistent with its heterogeneity, which is shown by an extensive psychiatric comorbidity, multiple impaired neurocognitive domains, and the wide range of structural and functional brain alterations associated with ADHD. This chapter highlights structural and functional magnetic resonance imaging studies that have contributed to a better understanding of the neurobiology of ADHD. Cumulative evidence implicates frontoparietal, striatal, thalamic, and cerebellar involvement in ADHD, in addition to interactions among the visual and sensorimotor cortex and the default mode network and top-down regulatory networks, which are increasingly implicated. The latter are two fundamental cortical systems, and the default mode network mediates introspection and self-referential processes, whereas the top-down regulatory network initiates and maintains task-level control, selects appropriate sensorimotor mapping, and suppresses irrelevant distracting information. This variety of neural systems and brain phenotypes is unlikely to be equally involved in all patients with ADHD, and future studies are needed to better dissect the most relevant neurobiological markers. The inclusion of joint information among brain imaging modalities along with genetic studies, bioinformatic analyses, and functional analyses in cell and animal models will allow a more comprehensive understanding of the neurobiological mechanisms in ADHD. Ultimately, the ongoing clinical and neurobiological research will also advance diagnostic and therapeutic approaches to ADHD.

View all citing articles on Scopus

: This article is discussed in an editorial by Drs. James J. Hudziak and Stephen V. Faraone on page 729 of the August 2010 issue.

: This article was reviewed under and accepted by Ad Hoc Editor Robert Althoff, M.D., Ph.D.

: This project was supported by the following grants: US National of Institute of Health GrantsR13MH059126, R01MH62873, U01MH085518 and R01MH081803 to S.V. Faraone, U01MH085515 to M. Daly K23MH066275-01 to J. Elia; and R01MH58277 to S. Smalley; Institutional Development Award to the Center for Applied Genomics from the Children's Hospital of Philadelphia to H. Hakonarson. Affymetrix Power Award, 2007 to B. Franke; NHMRC (Australia) and Sidney Sax Public Health Fellowship (443036) to S.E. Medland; Wellcome Trust, UK for sample collection to L Kent. UMC Utrecht Genvlag Grant and Internal Grant of Radboud University, Nijmegen Medical Centre to J. Buitelaar, the Deutsche Forschungsgemeinschaft (KFO 125, SFB 581, GRK 1156 to K.P. Lesch, ME 1923/5-1, ME 1923/5-3, GRK 1389 to C. Freitag and J. Meyer, SCHA 542/10-3 to H. Schäfer) and the Bundesministerium für Bildung und Forschung (BMBF 01GV0605 to K.P. Lesch). Additional analytical support was from Foundation for the NIH and R01MH080403 (PI Sullivan). All computational work was conducted on the Genetic Cluster Computer (the Netherlands) which is funded by an NWO Medium Investment grant (480-05-003, PI Posthuma), the Faculty of Psychology and Education of VU University (Amsterdam), and by the Dutch Brain Foundation (PI Ophoff) and is hosted by the Dutch National Computing and Networking Services.

: This is one of several articles published in the August and September issues of the Journal of the American Academy of Child and Adolescent Psychiatry that explores the intersection of genetics and mental health disorders in children and adolescents. The editors invite the reader to investigate the additional articles on this burgeoning area of developmental psychopathology.

: The Psychiatric GWAS Consortium: ADHD Subgroup consists of: Writing team: Benjamin M. Neale, Ph.D. (team leader), Sarah E. Medland, Ph.D., Stephan Ripke, M.D., Philip Asherson, M.R.C.Psych., Ph.D., Barbara Franke, Ph.D., Klaus-Peter Lesch, M.D., Stephen V. Faraone, Ph.D.; Data Analysis team: Sarah E. Medland, Ph.D. (team leader), Stephan Ripke, M.D., Thuy Trang Nguyen, Dipl. Math. oec, Helmut Schäfer, Ph.D., Peter Holmans, Ph.D., Mark Daly, Ph.D., Benjamin M. Neale, Ph.D. (chair); Data Collection Team: Hans-Christoph Steinhausen, M.D., Ph.D., D.M.Sc., Klaus-Peter Lesch, M.D., Christine Freitag, M.D., M.A.; Andreas Reif, M.D., Tobias J. Renner, M.D., Marcel Romanos, M.D., Jasmin Romanos, M.D., Susanne Walitza, M.D., Andreas Warnke, M.D., Ph.D., Thuy Trang Nguyen, Dipl. Math. oec, Helmut Schäfer, Ph.D., Jobst Meyer, Ph.D., Haukur Palmason, Ph.D., Jan Buitelaar, M.D., Barbara Franke, Ph.D., Alejandro Arias Vasquez, Ph.D., Nanda Lambregts-Rommelse, Ph.D., Michael Gill, Mb B.Ch. B.A.O., M.D., M.R.C.Psych., F.T.C.D., Richard J.L. Anney, Ph.D., Kate Langely, Ph.D., Michael O'Donovan, F.R.C.Psych., Ph.D., Nigel Williams, Ph.D., Peter Holmans, Ph.D., Michael Owen, Ph.D., F.R.C.Psych., Anita Thapar, M.D., Lindsey Kent, M.D., Ph.D., Joseph Sergeant, Ph.D., Herbert Roeyers, M.D., Ph.D., Philip Asherson, M.R.C.Psych., Ph.D., Eric Mick, Sc.D, Joseph Biederman, M.D., Alysa Doyle, Ph.D., Susan Smalley, Ph.D., Sandra Loo, Ph.D., Hakon Hakonarson, M.D., Ph.D., Josephine Elia, M.D., Alexandre Todorov, Ph.D., Ana Miranda, M.D., Fernando Mulas, M.D., Ph.D., Richard P. Ebstein, Ph.D., Aribert Rothenberger, M.D., Ph.D., Tobias Banaschewski, M.D., Ph.D., Robert D. Oades, Ph.D., Edmund Sonuga-Barke, Ph.D., James McGough, M.D., Laura Nisenbaum, Ph.D., Stephen V. Faraone, Ph.D. (Chair); Molecular Genetics team: Frank Middleton, Ph.D., Xiaolan Hu, Ph.D., Stan Nelson, M.D.; Project Management team: Anita Thapar, M.D., James McGough, M.D., Eric Mick, Sc.D, Benjamin M. Neale, Ph.D., Stephen V. Faraone, Ph.D. (Chair); Statistical experts: Benjamin M. Neale, Ph.D. Mark Daly, Ph.D.

: Disclosure: Dr. Buitelaar has, in the past 3 years, served as a consultant to, member of the advisory board, and/or served on the speakers' bureau for Janssen Cilag BV, Eli Lilly and Co., Bristol-Myers Squibb, Organon/Shering Plough, UCB, Shire, Medice, and Servier. Dr. Faraone has, in the past year, received consulting fees and has served on advisory boards for Eli Lilly and Co., Ortho-McNeil, and Shire Development, and has received research support from Eli Lilly and Co., Pfizer, Shire, and the National Institutes of Health. In previous years, Dr. Faraone has received consulting fees, served on advisory boards, or been a speaker for Shire, McNeil, Janssen, Novartis, Pfizer, and Eli Lilly and Co. In previous years he has received research support from Eli Lilly and Co., Shire, Pfizer, and the National Institutes of Health. Dr. Banaschewski has served on the Advisory Board or as a consultant for Desitin, Eli Lilly and Co., Medice, Novartis, Pfizer, Shire, UCB, and Viforpharma. He received conference attendance support or served on the speakers' bureau for Eli Lilly and Co., Janssen McNeil, Medice, Novartis, and UCB. He is or has been involved in clinical trials conducted by Eli Lilly and Co., Shire, and Novartis. The present work is unrelated to the above grants and relationships. Dr. M. Romanos, in the past three years, has served on the speakers' bureau for Janssen-Cilag. In previous years he has served on the speakers' bureau for Medice. Dr. Freitag, in the past 3 years, has served on the speakers' bureau for Eli-Lilly and Co., Shire, Novartis, and Janssen-Cilag. Dr. Mick receives research support from Ortho-McNeil Janssen Scientific Affairs, Pfizer, and Shire Pharmaceuticals, and has been an advisory board member for Shire Pharmaceuticals. Dr. Biederman receives research support from Alza, AstraZeneca, Bristol Myers Squibb, Eli Lilly and Co., Janssen Pharmaceuticals Inc., McNeil, Merck, Organon, Otsuka, Shire, the National Institute of Mental Health, and the National Institute of Child Health and Human Development. In 2009, Dr. Biederman served on the speakers' bureau for Fundacion Areces, Medice Pharmaceuticals, and the Spanish Child Psychiatry Association. In previous years, Dr. Biederman has received research support, consultation fees, or speaker's fees for/from Abbott, AstraZeneca, Celltech, Cephalon, Eli Lilly and Co., Esai, Forest, Glaxo, Gliatech, Janssen, McNeil, the National Alliance for Research on Schizophrenia and Depression, the National Institute on Drug Abuse, New River, Novartis, Noven, Neurosearch, Pfizer, Pharmacia, the Prechter Foundation, Shire, the Stanley Foundation, UCB Pharma, Inc., and Wyeth. Dr. Sergeant has served on the advisory boards for Eli Lilly and Co. and Shire. He has received research grant support from Eli Lilly and Co. and served on the speakers' bureau for Shire, Eli Lilly and Co., Janssen-Cilag, and Novartis. Dr. Oades has received research support from UCB GmbH, Janssen-Cilag, and Shire. Dr. Schäfer has served as a consultant for Daiichi Sankyo, served on the speakers' bureau for the European School of Oncology, and receives research grants from the German Federal Government and the German Research Foundation. Drs. Neale, Medland, Ripke, Asherson, Franke, Lesch, Nguyen, Holmans, Daly, Steinhausen, Reif, Renner, J. Romanos, Walitza, Warnke, Meyer, Palmason, Vasquez, Lambregts-Rommelse, Gill, Anney, Langely, O'Donovan, Williams, Owen, Thapar, Kent, Roeyers, Doyle, Smalley, Loo, Hakonarson, Elia, Todorov, Miranda, Mulas, Ebstein, Rothenberger, Sonuga-Barke, McGough, Nisenbaum, Middleton, Hu, and Nelson report no biomedical financial interests or potential conflicts of interest.

View full text

New researchMeta-Analysis of Genome-Wide Association Studies of Attention-Deficit/Hyperactivity Disorder

Objective

Method

Results

Conclusions

Section snippets

Samples

Genome-Wide Results

Discussion

Biol Psychiatry

Psychiatr Clin North Am

Am J Hum Genet

Am J Hum Genet

Am J Hum Genet

The worldwide prevalence of ADHD: Is it an American Condition?

World Psychiatry

The worldwide prevalence of ADHD: A systematic review and metaregression analysis

Am J Psychiatry

The prevalence and correlates of adult ADHD in the United States: Results from the National Comorbidity Survey Replication

Am J Psychiatry

What is the prevalence of adult ADHD?Results of a population screen of 966 adults

J Attention Disord

Phenotypic and measurement influences on heritability estimates in childhood ADHD

Eur Child Adolesc Psychiatry

Genetic support for the dual nature of attention deficit hyperactivity disorder: Substantial genetic overlap between the inattentive and hyperactive-impulsive components

J Abnorm Child Psychol

Meta-analysis shows significant association between dopamine system genes and attention deficit hyperactivity disorder (ADHD)

Hum Mol Genet

Genome-wide association scan of attention deficit hyperactivity disorder

Am J Med Genet B Neuropsychiatr Genet

Genome-wide association scan of the time to onset of attention deficit hyperactivity disorder

Am J Med Genet B Neuropsychiatr Genet

Family-based genome-wide association scan of attention-deficit/hyperactivity disorder

J Am Acad Child Adolesc Psychiatry

Case control genome-wide association of attention deficit/hyperactivity disorder

J Am Acad Child Adolesc Psychiatry

Molecular genetics of adult ADHD: Converging evidence from genome-wide association and extended pedigree linkage studies

J Neural Transm

Rare structural variants found in attention-deficit hyperactivity disorder are preferentially associated with neurodevelopmental genes

Mol Psychiatry

Genome-wide association scan of attention deficit hyperactivity disorder

Am J Med Genet B Neuropsychiatr Genet

New research
Meta-Analysis of Genome-Wide Association Studies of Attention-Deficit/Hyperactivity Disorder