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The norepinephrine transporter gene and attention-deficit hyperactivity disorder.

Abstract
The adrenergic system plays a known role in attentional systems and a suspected causal role in attention-deficit hyperactivity disorder (ADHD), based on evidence from pharmacological interventions and animal models. The efficacy of the highly selective noradrenergic reuptake inhibitor, tomoxetine, in treating ADHD symptoms supports the system's role in ADHD and points to the norephinephrine transporter as a candidate gene. This study tested the gene for the norepinephrine transporter (NET1) as a susceptibility factor in ADHD using three polymorphisms located in exon 9, intron 9, and intron 13. We examined the inheritance of these polymorphisms in a sample of 122 families with a total of 155 children with ADHD identified through an ADHD proband. Use of the transmission disequilibrium test failed to show significant evidence for biased transmission of any of the alleles or the haplotypes of these polymorphisms. We further investigated this gene by screening the probands for five known amino acid variants to determine if they contributed to the ADHD phenotype but observed only one (Thr99Ile) in our sample. Since the frequency of this variant (1.8%) was similar to that previously reported in a control sample (2.2%), it is unlikely that this variant is related to the ADHD phenotype. Our results do not support the NET1 gene as a major genetic susceptibility factor in ADHD.
AuthorsCathy L Barr, Jamie Kroft, Yu Feng, Karen Wigg, Wendy Roberts, Molly Malone, Abel Ickowicz, Russell Schachar, Rosemary Tannock, James L Kennedy
JournalAmerican journal of medical genetics (Am J Med Genet) Vol. 114 Issue 3 Pg. 255-9 (Apr 08 2002) ISSN: 0148-7299 [Print] United States
PMID11920844 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright 2002 Wiley-Liss, Inc.
Chemical References
  • Norepinephrine Plasma Membrane Transport Proteins
  • SLC6A2 protein, human
  • Symporters
  • DNA
Topics
  • Alleles
  • Attention Deficit Disorder with Hyperactivity (genetics)
  • DNA (chemistry, genetics)
  • DNA Mutational Analysis
  • Family Health
  • Female
  • Gene Frequency
  • Humans
  • Male
  • Mutation, Missense
  • Norepinephrine Plasma Membrane Transport Proteins
  • Point Mutation
  • Symporters (genetics)

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