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Support for the MnlI polymorphism of SNAP25; a Korean ADHD case–control study

Molecular Psychiatry volume 12, pages 224–226 (2007)Cite this article

Previously, several studies reported association between the synaptosomal-associated protein 25 kDa (SNAP-25) and attention deficit hyperactivity disorder (ADHD). Initially, Barr et al.1 identified two single-nucleotide polymorphisms (SNPs) (MnlI, DdeI) located four bases apart in the 3′ UTR of SNAP-25 and found significant overtransmission of the TC haplotype (P=0.03). Since then, other researchers attempted to replicate this finding by investigating these two SNPs. Brophy et al.2 found significant association for DdeI polymorphism but not for MnlI polymorphism. Kustanovich et al.3 detected a trend for overtransmission of the TC haplotype (P=0.08). Mill et al.4 reported that the TT haplotype was significantly transmitted to ADHD offspring (P=0.01). Although the specific functionality of these SNPs are not known currently, they are located in a region (3′ UTR) which is an important site for mRNA stability and translational efficiency.5 So it is possible that these SNPs may play a role in gene regulation and thus enhance susceptibility to ADHD. In light of these evidence, we sought to investigate whether these SNAP-25 polymorphisms were also associated with ADHD in the Korean population.

ADHD cases were recruited through Bundang Cha Hospital and Yongdong Severance Hospital in Korea. For this study, all children were assessed through an interview with the mother and for children aged 8 years or older, a direct interview was carried out after interviewing with the mother. All interviews were conducted by four board-certified child psychiatrists (Choi TK, Song DH, Park TW, Yook KW). The diagnosis of ADHD was made in accordance with the criteria from the Diagnostic and Statistical Manual of Mental Disorders – Fourth Edition (DSM-IV).6 We excluded children with IQ score lower than 70 and with medical, neurological, or other co-morbid psychiatric disorders such as conduct disorder, oppositional defiant disorder, tic disorder, anxiety disorder, and mood disorder. In this study, we excluded ADHD children with any psychiatric co-morbidity in order to increase the homogeneity of our samples and also because we wanted to find genetic associations that are relevant to the ADHD phenotype only. A previous multisite study showed that the ‘pure’ ADHD group without any co-morbid psychiatric disorders differ from the ADHD group with co-morbidities in key areas such as baseline characteristics, treatment response, and outcome.7 They further suggested that genetic studies may benefit by the discrimination of different ADHD groups according to co-morbidity profiles. There are also evidence from epidemiological studies of ADHD which suggest that this kind of approach may be useful for genetic association studies of ADHD.8

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Acknowledgements

We thank Dr Dae Hyun Cho for the genotyping and genotype analysis. We also thank Drs Chan Hyung Kim and Se Joo Kim for helpful discussions of the manuscript. This study was supported by NARSAD Young Investigator Award to JWK. JWK is a NARSAD Sidney R Baer, Jr Foundation Investigator.

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Authors and Affiliations

  1. Department of Psychiatry, College of Medicine, Pochon CHA University, Seongnam, Korea

    T K Choi, K W Yook, S H Lee, J I Kim & S Y Suh

  2. Department of Psychiatry, College of Medicine, Yonsei University, Seoul, Korea

    H S Lee & D H Song

  3. Psychiatric & Neurodevelopmental Genetics Unit, Massachusetts General Hospital, Boston, MA, USA

    J W Kim

  4. Department of Psychiatry, College of Medicine, Chonbuk National University, Jeonju, Korea

    T W Park

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  1. T K Choi
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Correspondence to J W Kim.

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Choi, T., Lee, H., Kim, J. et al. Support for the MnlI polymorphism of SNAP25; a Korean ADHD case–control study. Mol Psychiatry 12, 224–226 (2007). https://doi.org/10.1038/sj.mp.4001922

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