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  Exploring the genetic link between RLS and ADHD

Schimmelmann, B. G., Friedel, S., Nguyen, T. T., Sauer, S., Ganz Vogel, C. I., Konrad, K., et al. (2009). Exploring the genetic link between RLS and ADHD. Journal of Psychiatric Research, 43(10), 941-945. doi:10.1016/j.jpsychires.2009.01.003.

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Genre: Journal Article
Alternative Title : J Psychiatr Res

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 Creators:
Schimmelmann, B. G., Author
Friedel, S., Author
Nguyen, T. T., Author
Sauer, S.1, Author           
Ganz Vogel, C. I., Author
Konrad, K., Author
Wilhelm, C., Author
Sinzig, J., Author
Renner, T. J., Author
Romanos, M., Author
Palmason, H., Author
Dempfle, A., Author
Walitza, S., Author
Freitag, C., Author
Meyer, J., Author
Linder, M., Author
Schäfer, H., Author
Warnke, A., Author
Lesch, K. P., Author
Herpertz-Dahlman, B., Author
Hinney, A., AuthorHebebrand, J., Author more..
Affiliations:
1Nutrigenomics and Gene Regulation (Sascha Sauer), Independent Junior Research Groups (OWL), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1479662              

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Free keywords: Attention deficit/hyperactivity disorder; RLS; Genome-wide association study
 Abstract: Attention deficit/hyperactivity disorder (ADHD) is a highly heritable neurodevelopmental disorder of childhood onset. Clinical and biological evidence points to shared common central nervous system (CNS) pathology of ADHD and restless legs syndrome (RLS). It was hypothesized that variants previously found to be associated with RLS in two large genome-wide association studies (GWA), will also be associated with ADHD. SNPs located in MEIS1 (rs2300478), BTBD9 (rs9296249, rs3923809, rs6923737), and MAP2K5 (rs12593813, rs4489954) as well as three SNPs tagging the identified haplotype in MEIS1 (rs6710341, rs12469063, rs4544423) were genotyped in a well characterized German sample of 224 families comprising one or more affected sibs (386 children) and both parents. We found no evidence for preferential transmission of the hypothesized variants to ADHD. Subsequent analyses elicited nominal significant association with haplotypes consisting of the three SNPs in BTBD9 (χ2 = 14.8, df = 7, nominal p = 0.039). According to exploratory post hoc analyses, the major contribution to this finding came from the A–A–A-haplotype with a haplotype-wise nominal p-value of 0.009. However, this result did not withstand correction for multiple testing. In view of our results, RLS risk alleles may have a lower effect on ADHD than on RLS or may not be involved in ADHD. The negative findings may additionally result from genetic heterogeneity of ADHD, i.e. risk alleles for RLS may only be relevant for certain subtypes of ADHD. Genes relevant to RLS remain interesting candidates for ADHD; particularly BTBD9 needs further study, as it has been related to iron storage, a potential pathophysiological link between RLS and certain subtypes of ADHD.

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Language(s): eng - English
 Dates: 2009-07
 Publication Status: Issued
 Pages: -
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Title: Journal of Psychiatric Research
  Alternative Title : J Psychiatr Res
Source Genre: Journal
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Affiliations:
Publ. Info: -
Pages: - Volume / Issue: 43 (10) Sequence Number: - Start / End Page: 941 - 945 Identifier: ISSN: 0022-3956