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The genetics of attention deficit/hyperactivity disorder in adults, a review.

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.

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  • Authors+Show Affiliations

    ,

    Department of Human Genetics, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands. b.franke@antrg.umcn.nl

    , , , , , , , , , , , ,

    Source

    Molecular psychiatry 17:10 2012 Oct pg 960-87

    MeSH

    Adult
    Attention Deficit Disorder with Hyperactivity
    Cadherins
    Family Health
    Genetic Association Studies
    Genetic Linkage
    Genetic Predisposition to Disease
    Genetics
    Humans
    Neuroimaging
    Receptors, G-Protein-Coupled
    Receptors, Peptide

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't
    Review

    Language

    eng

    PubMed ID

    22105624

    Citation

    Franke, B, et al. "The Genetics of Attention Deficit/hyperactivity Disorder in Adults, a Review." Molecular Psychiatry, vol. 17, no. 10, 2012, pp. 960-87.
    Franke B, Faraone SV, Asherson P, et al. The genetics of attention deficit/hyperactivity disorder in adults, a review. Mol Psychiatry. 2012;17(10):960-87.
    Franke, B., Faraone, S. V., Asherson, P., Buitelaar, J., Bau, C. H., Ramos-Quiroga, J. A., ... Reif, A. (2012). The genetics of attention deficit/hyperactivity disorder in adults, a review. Molecular Psychiatry, 17(10), pp. 960-87. doi:10.1038/mp.2011.138.
    Franke B, et al. The Genetics of Attention Deficit/hyperactivity Disorder in Adults, a Review. Mol Psychiatry. 2012;17(10):960-87. PubMed PMID: 22105624.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - The genetics of attention deficit/hyperactivity disorder in adults, a review. AU - Franke,B, AU - Faraone,S V, AU - Asherson,P, AU - Buitelaar,J, AU - Bau,C H D, AU - Ramos-Quiroga,J A, AU - Mick,E, AU - Grevet,E H, AU - Johansson,S, AU - Haavik,J, AU - Lesch,K-P, AU - Cormand,B, AU - Reif,A, AU - ,, Y1 - 2011/11/22/ PY - 2011/11/23/entrez PY - 2011/11/23/pubmed PY - 2013/2/28/medline SP - 960 EP - 87 JF - Molecular psychiatry JO - Mol. Psychiatry VL - 17 IS - 10 N2 - 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. SN - 1476-5578 UR - https://www.unboundmedicine.com/medline/citation/22105624/full_citation L2 - http://dx.doi.org/10.1038/mp.2011.138 DB - PRIME DP - Unbound Medicine ER -