Association between the DTNBP1 gene and intelligence: a case-control study in young patients with schizophrenia and related disorders and unaffected siblings

Janneke R Zinkstok¹^,2 , Odette de Wilde¹ , Therese AMJ van Amelsvoort¹ , Michael W Tanck³ , Frank Baas² and Don H Linszen¹

¹Department of Psychiatry, Academic Medical Center of the University of Amsterdam, The Netherlands

²Neurogenetics Laboratory, Academic Medical Center of the University of Amsterdam, The Netherlands

³Department of Clinical Epidemiology, Biostatistics, and Bioinformatics, Academic Medical Center of the University of Amsterdam, The Netherlands

author email corresponding author email

Behavioral and Brain Functions 2007, 3:19doi:10.1186/1744-9081-3-19


Published:	20 April 2007

Abstract

Background

The dystrobrevin-binding protein 1 (DTNBP1) gene is a susceptibility gene for schizophrenia. There is growing evidence that DTNPB1 contributes to intelligence and cognition. In this study, we investigated association between single nucleotide polymorphisms (SNPs) in the DTNBP1 gene and intellectual functioning in patients with a first episode of schizophrenia or related psychotic disorder (first-episode psychosis, FEP), their healthy siblings, and unrelated controls.

Methods

From all subjects IQ measurements were obtained (verbal IQ [VIQ], performance IQ [PIQ], and full scale IQ [FSIQ]). Seven SNPs in the DTNBP1 gene were genotyped using single base primer extension and analyzed by matrix-assisted laser deionization mass spectrometry (MALDI-TOF).

Results

Mean VIQ, PIQ, and FSIQ scores differed significantly (p < 0.001) between patients, siblings, and controls. Using a family-based and a case-control design, several single SNPs were significantly associated with IQ scores in patients, siblings, and controls.

Conclusion

Although preliminary, our results provide evidence for association between the DTNBP1 gene and intelligence in patients with FEP and their unaffected siblings. Genetic variation in the DTNBP1 gene may increase schizophrenia susceptibility by affecting intellectual functioning.