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An association study of sequence variants in the forkhead box P2 (FOXP2) gene and adulthood attention-deficit/hyperactivity disorder in two European samples

Ribasés, Martaa,b,c; Sánchez-Mora, Cristinaa,b,c,d; Ramos-Quiroga, Josep Antonia,c,h; Bosch, Rosaa,c,h; Gómez, Núriaa,c; Nogueira, Marianaa,c; Corrales, Montsea; Palomar, Gloriaa; Jacob, Christian P.i; Gross-Lesch, Silkei; Kreiker, Susannei; Reif, Andreasi; Lesch, Klaus Peteri; Cormand, Brud,f,g; Casas, Miquela,c,h; Bayés, Mónicae

doi: 10.1097/YPG.0b013e328353957e
Original Articles

Objectives: Attention-deficit/hyperactivity disorder (ADHD) is a common psychiatric disorder manifesting as symptoms of inattention, hyperactivity, and/or impulsivity. Learning disabilities co-occur with ADHD in 20–30% of cases and this high co-occurrence raises the possibility of a common etiological background. Forkhead box P2 (FOXP2) encodes a transcription factor involved in speech and language impairment and in the control of the corticobasal ganglia circuits known to be relevant in ADHD, suggesting a possible role of FOXP2 in ADHD. Our aim was to carry out an association study between FOXP2 and adulthood ADHD.

Methods: We carried out a case–control association study in 643 adult ADHD patients and 619 controls from Germany and in 361 adult ADHD patients and 442 controls from Spain with 12 tagging single nucleotide polymorphisms covering the FOXP2 gene.

Results: The single-marker and multiple-marker analyses showed an association between FOXP2 and combined ADHD in the German cohort [rs12533005: P=0.0033; odds ratio=1.30 (1.09–1.56); rs12533005/rs1229761: P=4.1e−04; odds ratio=1.38 (1.15–1.66)]. These positive results, however, were not confirmed in the Spanish sample.

Conclusion: Although these preliminary findings provide a tentative evidence for the contribution of FOXP2 to ADHD and suggest common genetic factors for this psychiatric disorder and learning disabilities, they should be interpreted with caution. Further studies in larger samples are needed to clarify the role of this transcription factor in ADHD.

aDepartment of Psychiatry, Vall d’Hebron Hospital

bPsychiatric Genetics Unit, Vall d’Hebron Research Institute (VHIR)

cBiomedical Network Research Centre on Mental Health (CIBERSAM)

dGenetics Department, Faculty of Biology, University of Barcelona

eNational Center for Genomic Analysis (CNAG), Barcelona Science Park (PCB)

fBiomedical Network Research Centre on Rare Diseases (CIBERER)

gInstitute of Biomedicine of the University of Barcelona (IBUB)

hDepartment of Psychiatry and Legal Medicine, Autonomus University of Barcelona, Barcelona, Spain

iADHD Clinical Research Network, Molecular Psychiatry, Laboratory of Translational Neuroscience, Department of Psychiatry, Psychosomatics and Psychotherapy, University of Wuerzburg, Germany

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Correspondence to Mònica Bayés, PhD, National Center for Genomic Analysis (CNAG), Barcelona Science Park (PCB), Torre I, 2a planta, Campus Diagonal – University of Barcelona, Baldiri Reixac 4, 08028 Barcelona, Spain Tel: +34 93 402 0564; fax: +34 93 403 7279; e-mail: mbayes@pcb.ub.cat

Received April 13, 2011

Accepted October 3, 2011

© 2012 Lippincott Williams & Wilkins, Inc.