Follow-up of genetic linkage findings on chromosome 16p13: evidence of association of N-methyl-D Aspartate Glutamate receptor 2A gene polymorphism with ADHD

D Turic, K Langley, S Mills, M Stephens, D Lawson, C Govan, N Williams, M van den Bree, N Craddock, Lindsey Kent, M Owen, M O'Donovan, A Thapar

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Abstract

Attention deficit hyperactivity disorder (ADHD) is a childhood onset disorder, for which there is good evidence that genetic factors contribute to the aetiology. Recently reported linkage findings suggested evidence of a susceptibility locus on chromosome 16p13 ( maximum LOD score of 4.2, P = 5 x 10(-6)). The GRIN2A (glutamate receptor, ionotropic, N-methyl D-aspartate 2A) gene that encodes the N-methyl D-aspartate receptor subunit 2A ( NMDA2A) maps to this region of linkage. As this is also a good functional candidate gene for ADHD, we undertook family-based association analysis in a sample of 238 families. We found significant evidence of association with a GRIN2A exon 5 polymorphism (chi(2) = 5.7, P = 0.01). Our data suggest that genetic variation in GRIN2A may confer increased risk for ADHD and that this, at least in part, might be responsible for the linkage result on 16p reported by Smalley et al. We conclude that replication is required and that further work examining for association of GRIN2A polymorphisms with ADHD is warranted.

Original languageEnglish
Pages (from-to)169-173
Number of pages5
JournalMolecular Psychiatry
Volume9
Issue number2
DOIs
Publication statusPublished - Feb 2004

Keywords

  • NMDA2A
  • attention deficit hyperactivity disorder
  • genetics
  • DEFICIT HYPERACTIVITY DISORDER
  • ATTENTION-DEFICIT/HYPERACTIVITY DISORDER
  • DOPAMINE TRANSPORTER
  • MICE LACKING
  • SCHIZOPHRENIA
  • SUBUNIT
  • AUTISM

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