From Regulatory Problems in Infancy to Attention-Deficit/Hyperactivity Disorder in Childhood: A Moderating Role for the Dopamine D4 Receptor Gene? - 07/03/14
, Dorothea Blomeyer, MA b, Mahha El-Faddagh, MD c, Guenter Esser, PhD d, Martin H. Schmidt, MD, PhD b, Tobias Banaschewski, MD, PhD b, Manfred Laucht, PhD b, d
Reprint requests: Dr Katja Becker, Department of Child and Adolescent Psychiatry and Psychotherapy, Medical Faculty, Philipps University Marburg, Hans-Sachs-Strasse 6, 35039 Marburg, Germany.Abstract |
Objective |
To examine whether the dopamine receptor D4 gene (DRD4) exon III VNTR moderates the risk of infants with regulatory disorders for developing attention-deficit/hyperactivity disorder (ADHD) later in childhood.
Study design |
In a prospective longitudinal study of children at risk for later psychopathology, 300 participants were assessed for regulatory problems in infancy, DRD4 genotype, and ADHD symptoms and diagnoses from childhood to adolescence. To examine a potential moderating effect on ADHD measures, linear and logistic regressions were computed. Models were fit for the main effects of the DRD4 genotype (presence or absence of the 7r allele) and regulatory problems (presence or absence), with the addition of the interaction term. All models were controlled for sex, family adversity, and obstetric risk status.
Results |
In children without the DRD4-7r allele, a history of regulatory problems in infancy was unrelated to later ADHD. But in children with regulatory problems in infancy, the additional presence of the DRD4-7r allele increased the risk for ADHD in childhood.
Conclusions |
The DRD4 genotype seems to moderate the association between regulatory problems in infancy and later ADHD. A replication study is needed before further conclusions can be drawn, however.
Le texte complet de cet article est disponible en PDF.Mots-clés : ADHD, VNTR
Plan
| Supported in part by grants from the Deutsche Forschungsgemeinschaft as part of the Special Research Program SFB 258, “Indicators and Risk Models of the Genesis and Course of Mental Disorders,” at the University of Heidelberg. The study sponsor had no input into the study design, data collection, or writing of the manuscript. K.B. is/has been involved in research/clinical trials with Eli Lilly and Shire, is on the advisory board of Eli Lilly Germany, serves on the speaker bureaus of Eli Lilly and Astra Zeneca, and has received conference attendance support from Shire. T.B. has served in an advisory or consultancy role for Lilly, Medice, Novartis, Pfizer, Shire, and UCB and has received conference attendance support or has been paid for public speaking by Lilly, Janssen McNeil, Medice, Novartis, and UCB. M.E.-F. has been paid for public speaking by Astra Zeneca and has participated in clinical trials with Eli Lilly, Novartis, and Janssen-Cilag. The other authors declare no conflicts of interest. |
Vol 156 - N° 5
P. 798 - mai 2010 Retour au numéro
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