Dr. M. Romanos and colleagues examined the genetic make-up of several families and found that there are common elements that appear to be associated with ADHD. Although these findings point toward a genetic contribution to ADHD, it is important to note the caveat implied by the final sentence of the abstract: So many factors contribute to ADHD, that these results should not be construed as identifying the precise cause of the disorder. In the full article, the authors are circumspect about this: “The identification [in this study] of several novel linkage regions as well as replication of previously reported loci provides further evidence for the highly heterogeneous genetic etiology of ADHD.”
Genome-wide linkage analysis of ADHD using high-density SNP arrays: Novel loci at 5q13.1 and 14q12
M Romanos, C. Freitag, C. Jacob, D. W Craig, A. Dempfle, T. T. Nguyen, R. Halperin, S. Walitza, T. J Renner, C. Seitz, J. Romanos, H. Palmason, A. Reif, M. Heine, C. Windemuth-Kieselbach, C. Vogler, J. Sigmund, A. Warnke, H. Schäfer, J. Meyer, D. A. Stephan, & K. P. Lesch
Molecular Psychiatry (2008) 13, 522–530; doi:10.1038/mp.2008.12; published online 26 February 2008
Abstract
Previous genome-wide linkage studies applied the affected sib-pair design; one investigated extended pedigrees of a. genetic isolate. Here, results of a. genome-wide high-density linkage scan of attention-deficit/hyperactivity disorder (ADHD) using an array-based genotyping of approx ~50 K. single nucleotide polymorphism (SNPs) markers are presented. We investigated eight extended pedigrees of German origin that were non-related, not part of a. genetic isolate and ascertained on the basis of clinical referral. Two parametric analyses maximizing LOD scores (MOD) and a. non-parametric analysis for both a. broad and a. narrow phenotype approach were conducted. Novel linkage loci across all families were detected at 2q35, 5q13.1, 6q22-23 and 14q12, within individual families at 18q11.2-12.3. Further linkage regions at 7q21.11, 9q22 and 16q24.1 in all families, and at 1q25.1, 1q25.3, 9q31.1-33.1, 9q33, 12p13.33, 15q11.2-13.3 and 16p12.3-12.2 in individual families replicate previous findings. High-resolution linkage mapping points to several novel candidate genes characterized by dense expression in the brain and potential impact on disorder-relevant synaptic transmission. Our study provides further evidence for common gene effects throughout different populations despite the complex multifactorial etiology of ADHD.

Posts from the West
Last week, Liz Ditz teased us with notices about her whereabouts: She was attending an annual conference about brain research and learning. Don’t think I’ve flipped a wig; she wasn’t hearing the pablum that we usually get on this topic. This is a scholarly event, with presentations by eminent authorities (Is that redundant? Nope.) who are invited to discuss their work. I wrote to Liz that I envied her opportunity to attend.
Liz posted these entries: What I Am Doing This Week: Learning and the Brain Conference and Cognitive Neuroscience and Education: A Ways to Go. Go read them and then monitor her site for updates from her conference adventures. I shall do so, and mayhaps she’ll send LD Blog a heads up when there are going to be new entries!