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.
Sphere: Related Content
More on smoking and neuropsych disorders
New research shows that using nicotine during pregnancy affects genes involved in myelination and, consequently may help explain why the children of mothers who smoke during pregnancy are more likely to develop such psychiatric disorders as attention deficit hyperactivity disorder, depression, autism, and even drug abuse. In a paper presented at Neuroscience 2010, the annual meeting of the Society for Neuroscience, Professor Ming Li, Ph.D., of the University of Virginia (Charlottesville, VA, US) reported that when rats were given nicotine during pregnancy, their offspring manifested changes in myelin genes for the limbic system, especially the prefrontal cortex, a brain region important for decision-making.
“Our research shows that gestational treatment with nicotine significantly modifies myelin gene expression in specific brain regions that are involved in behavioral processes,” according to Professor Li, leader of the study. “Myelin deficits have been observed in adults with various psychiatric disorders. Our findings suggest that abnormal myelination may contribute to the psychiatric disorders associated with maternal smoking.”
Sphere: Related ContentContinue reading ‘More on smoking and neuropsych disorders’