Attention Deficit Hyperactivity Disorder (ADHD) is one of the most prevalent childhood onset syndromes affecting 3-6% of school age children worldwide. Dopamine as well as serotonin systems have been implicated in the aetiology of the disorder. Administration of the serotonin transporter inhibitor, fluoxetine, markedly attenuated the activity of the DAT1 knockout mice, whereas it had no effect on the wild type animals (Gainetdinov et al, 1999). This action was mediated by increased extracellular concentration of serotonin (5-HT) due to blockade of the serotonin transporter. In addition, when mice were treated with 5-hydroxytryptophan or with the dietary 5-HT precursor (L-tryptophan), hyperlocomotion in the DAT1 knock-out mice was profoundly reduced. This work implicates serotonin in the pathogenesis of ADHD. Polymorphisms mapped to serotonin transporter gene(at the regulatory region and the second intron of the gene) were genotyped in ADHD Irish trios (father, mother and affected child). Haplotype based haplotype relative risk analysis revealed no significant differences in the transmission of the alleles of serotonin polymorphisms in ADHD. However, it is important to examine additional polymorphisms across the gene and promotor regions before excluding serotonin transporter gene from playing a role in the predisposition to ADHD.
|Number of pages||1|
|Journal||American Journal of Medical Genetics Part B: Neuropsychiatric Genetics|
|Publication status||Published - 7 Aug 2000|
Hawi, Z., Kirley, A., Mullins, C., Fitzgerald, M. F., & Gill, M. (2000). No association of serotonin transporter gene polymorphisms with Attention Deficit Hyperactivity Disorder. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics, 96(4), 490.