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We Hawi et al. 2005; Am J Hum Genet 77:958–965 reported paternal overtransmission of risk alleles in some ADHDassociated genes. This was particularly clear in the case of the DAT1 3′UTR VNTR. In the current investigation, we analyzed three new sample comprising of 1,248 ADHD nuclear families to examine the allelic overtransmission of DAT1 in ADHD. The IMAGE sample, the largest of the threereplication samples, provides strong support for a parent of origin effect for allele 6 and the 10 repeat allele intron 8 and 3′UTR VNTR, respectively of DAT1. In addition, a similar pattern of overtransmission of paternal risk haplotypes constructed from the above alleles was also observed. Some support is also derived from the two smaller samples although neither is independently significant. Although the mechanism driving the paternal overtransmission of the DAT risk alleles is not known, these finding provide further support for this phenomenon. © 2009 WileyLiss, Inc.

Multiple studies have reported an association between attention deficit hyperactivity disorder ADHD and the 10repeat allele of a variable number tandem repeat VNTR polymorphism in the 3′untranslated region 3′UTR of the dopamine transporter gene DAT1. Yet, recent metaanalyses of available data find little or no evidence for this association; although there is strong evidence for heterogeneity between datasets. This pattern of findings could arise for several reasons including the presence of relatively rare risk alleles on common haplotype backgrounds or the functional interaction of two or more loci within the gene. We previously described the importance of a specific haplotype at the 3′ end of DAT1, as well as the identification of associated single nucleotide polymorphisms SNPs within or close to 5′ regulatory sequences. In this study we replicate the association of SNPs at the 5′ end of the gene and identify a specific risk haplotype spanning the 5′ and 3′ markers. These findings indicate the presence of at least two loci associated with ADHD within the DAT1gene and suggest that either additive or interaction effects of these two loci on the risk for ADHD. Overall these data provide further evidence that genetic variants of the dopamine transporter gene confer an increased risk for ADHD. © 2008 WileyLiss, Inc.

Replication is a key to resolving whether a reported genetic association represents a false positive finding or an actual genetic risk factor. In a previous study screening 51 candidate genes for association with ADHD in a multicentre European sample the IMAGE project, two single nucleotide polymorphisms SNPs within the norepinephrine transporter SLC6A2 gene were found to be associated with attention deficit hyperactivity disorder ADHD. The same SNP alleles were also reported to be associated with ADHD in a separate study from the Massachusetts General Hospital in the US. Using two independent samples of ADHD DSMIV combined subtype trios we attempted to replicate the reported associations with SNPs rs11568324 and rs3785143 in SLC6A2. Significant association of the two markers was not observed in the two independent replication samples. However, across all four datasets the overall evidence of association with ADHD was significant for SNP rs11568324 P  0.0001; average odds ratio  0.33; for SNP rs3785143 P  0.008; average odds ratio  1.3. The data were consistent for rs11568324, suggesting the existence of a rare allele conferring protection for ADHD within the SLC6A2gene. Further investigations should focus on identifying the mechanisms underlying the protective effect. © 2008 WileyLiss, Inc.

Several independent studies have reported association between serotonin transporter gene SLC6A4 polymorphisms and attention deficit hyperactivity disorder ADHD. Five studies found evidence for association between the longallele of a 44bp insertiondeletion polymorphism 5HTTLPR and ADHD. Another two studies corroborated this finding while a further six studies did not find such an association. For a second polymorphism within the gene, a variable number tandem repeat VNTR within intron 2, one study demonstrated that the 1212 genotype was significantly less frequent in ADHD cases compared to controls, while a second study found that the 12allele was preferentially transmitted to offspring affected with ADHD. To provide further clarification of the reported associations, we investigated the association of these two markers with ADHD in a sample of 1,020 families with 1,166 combined type ADHD cases for the International MultiCentre ADHD Genetics project, using the Transmission Disequilibrium Test. Given the large body of work supporting the association of the promoter polymorphism and mood disorders, we further analyzed the group of subjects with ADHD plus mood disorder separately. No association was found between either of the two markers and ADHD in our large multisite study or with depression within the sample of ADHD cases. © 2008 WileyLiss, Inc.

Season of birth (SOB) has been associated with attention deficit hyperactivity disorder (ADHD) in two existing studies. One further study reported an interaction between SOB and genotypes of the dopamine D4 receptor (DRD4) gene. It is important that these findings are further investigated to confirm or refute the findings. In this study, we investigated the SOB association with ADHD in four independent samples collected for molecular genetic studies of ADHD and found a small but significant increase in summer births compared to a large population control dataset. We also observed a significant association with the 7‐repeat allele of the DRD4 gene variable number tandem repeat polymorphism in exon three with probands born in the winter season, with no significant differential transmission of this allele between summer and winter seasons. Preferential transmission of the 2‐repeat allele to ADHD probands occurred in those who were born during the summer season, but did not surpass significance for association, even though the difference in transmission between the two seasons was nominally significant. However, following adjustment for multiple testing of alleles none of the SOB effects remained significant. We conclude that the DRD4 7‐repeat allele is associated with ADHD but there is no association or interaction with SOB for increased risk for ADHD. Our findings suggest that we can refute a possible effect of SOB for ADHD. © 2007 Wiley‐Liss, Inc.

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The article to which this erratum refers was published in Am J Med Genet Part B 2008 147B: 1306–1309. © 2008 WileyLiss, Inc.