Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
, 17 (10), 960-87

The Genetics of Attention Deficit/Hyperactivity Disorder in Adults, a Review

Affiliations
Review

The Genetics of Attention Deficit/Hyperactivity Disorder in Adults, a Review

B Franke et al. Mol Psychiatry.

Abstract

The adult form of attention deficit/hyperactivity disorder (aADHD) has a prevalence of up to 5% and is the most severe long-term outcome of this common neurodevelopmental disorder. Family studies in clinical samples suggest an increased familial liability for aADHD compared with childhood ADHD (cADHD), whereas twin studies based on self-rated symptoms in adult population samples show moderate heritability estimates of 30-40%. However, using multiple sources of information, the heritability of clinically diagnosed aADHD and cADHD is very similar. Results of candidate gene as well as genome-wide molecular genetic studies in aADHD samples implicate some of the same genes involved in ADHD in children, although in some cases different alleles and different genes may be responsible for adult versus childhood ADHD. Linkage studies have been successful in identifying loci for aADHD and led to the identification of LPHN3 and CDH13 as novel genes associated with ADHD across the lifespan. In addition, studies of rare genetic variants have identified probable causative mutations for aADHD. Use of endophenotypes based on neuropsychology and neuroimaging, as well as next-generation genome analysis and improved statistical and bioinformatic analysis methods hold the promise of identifying additional genetic variants involved in disease etiology. Large, international collaborations have paved the way for well-powered studies. Progress in identifying aADHD risk genes may provide us with tools for the prediction of disease progression in the clinic and better treatment, and ultimately may help to prevent persistence of ADHD into adulthood.

Figures

Figure 1
Figure 1
Plotted is the sample size (cases+controls) analyzed in the first meta-analyses of the Psychiatric Genome-Wide Association Study (GWAS) Consortium on schizophrenia, bipolar disorder, major depressive disorder, autistic spectrum disorders and attention deficit/hyperactivity disorder (ADHD) against the −log of the minimal association P-value observed in the GWAS. The P-value indicating genome-wide significance of findings is indicated. The data show the strong (r=0.91) and significant (P=0.03) correlation between the two parameters. Drawing a line through the points suggests that at least 12 000 samples (cases+controls) will be needed before genome-wide significant findings for ADHD will be observed.

Similar articles

See all similar articles

Cited by 86 PubMed Central articles

See all "Cited by" articles

References

    1. American Psychiatric Association Diagnostic and Statistical Manual of Mental Disorders4th edn, revised. American Psychiatric Press: Washington, DC; 2000
    1. Faraone SV, Biederman J, Mick E. The age-dependent decline of attention deficit hyperactivity disorder: a meta-analysis of follow-up studies. Psychol Med. 2006;36:159–165. - PubMed
    1. Simon V, Czobor P, Balint S, Meszaros A, Bitter I. Prevalence and correlates of adult attention-deficit hyperactivity disorder: meta-analysis. Br J Psychiatry. 2009;194:204–211. - PubMed
    1. Barkley RA, Murphy KR, Fischer M. ADHD in Adults: What the Science Says. Guilford Press: New York, NY; 2008.
    1. Haavik J, Halmoy A, Lundervold AJ, Fasmer OB. Clinical assessment and diagnosis of adults with attention-deficit/hyperactivity disorder. Expert Rev Neurother. 2010;10:1569–1580. - PubMed

Publication types

Feedback