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Associations of MAOA-VNTR or 5HTT-LPR alleles with attention-deficit hyperactivity disorder symptoms are moderated by platelet monoamine oxidase B activity

Wargelius, Hanna-Linna; Malmberg, Kerstinb; Larsson, Jan-Olovb; Oreland, Larsa

doi: 10.1097/YPG.0b013e328347c1ab
Brief Reports

The monoamine systems have been suggested to play a role in the biological basis of attention-deficit hyperactivity disorder (ADHD) symptoms. Thus, polymorphisms, for example, in the monoamine oxidase A (MAOA) and the serotonin transporter (5HTT) genes have been associated with ADHD-like phenotypes. Furthermore, platelet monoamine oxidase B (MAOB) activity has frequently been linked to impulsiveness-related traits. In this study, we have studied ADHD symptoms with regard to the combination of platelet MAOB activity and MAOA-variable number of tandem repeats (VNTR) or 5HTT-LPR genotype. The study group consisted of 156 adolescent twin pairs, that is, 312 individuals, who participated in a previous study. ADHD symptoms were scored with a structured clinical interview of both the twins and a parent using Kiddie Schedule for Affective Disorders and Schizophrenia for School-Age Children-Present and Lifetime Version. The presence of a short 5HTT-LPR or short MAOA-VNTR allele, in combination with high levels of platelet MAOB enzyme activity was associated with higher scores of ADHD-like problems (P<0.001 and 0.01, respectively). This re-examination of ADHD scores in a nonclinical sample suggests that effects of MAOA-VNTR and 5HTT-LPR are moderated by platelet MAOB activity.

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aDepartment of Neuroscience, Uppsala University, Uppsala

bKarolinska Institutet, Department of Women's and Children's Health, Stockholm, Sweden

Correspondence to Hanna-Linn Wargelius, MSc, Department of Neuroscience, Uppsala University, Husargatan 3 PO box 593, Uppsala 751 24, Sweden Tel: +46 18 471 49 02; fax: +18 51 15 40; e-mail: Hanna-Linn Wargelius and Kerstin Malmberg contributed equally to this study

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Received June 9, 2010

Accepted March 17, 2011

© 2012 Lippincott Williams & Wilkins, Inc.