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Corrections have been made throughout the article to clarify how daily smoking during the 12- through 16-year assessments was defined in the original report. In this corrigendum, daily smoking during these assessments was defined by participant's responding either (a) once a day or more in response to In the past year, how often did you smoke cigarettes? or (b) responding yes to Are you currently a daily smoker? The authors repeated their analyses and this updated definition of daily smoking did not change findings in terms of statistical significance for Aims 1, 2, or 3 with one exception. In Aim 2, the initiation age (linear) by childhood ADHD status interaction was significant in this correction (p=.025), indicating that progression to daily smoking was faster for LNCG participants who initiated smoking at an older age than ADHD participants. For instance, mean latency was 5.61 years (SD=3.28) for ADHD participants and 5.29 (SD=3.22) for LNCG participants who initiated at 17 year-old or younger, but 2.14 (SD=2.26) for ADHD participants and 1.20 (SD=1.23) for LNCG participants who initiated at 18 years-old and older. This re-analysis did not impact the main findings from this study. This corrigendum includes updated values in the main article and supplemental material based on how we operationalize daily smoking status between 12- through 16-year assessments. The authors also clarify that for the 2- through 10-year assessments, participants were coded as daily smokers if they smoked at least one cigarette per day in response to During the past month, how many cigarettes have you smoked on an average day? The authors also clarify in this correction that weekly smoking in Aim 1 analysis was defined as those who responded once a week or more in response to In the past year, how often did you smoke cigarettes? These two clarifications did not require any re-analysis.

Item does not contain fulltext, Low birth weight is associated with increased risk for Attention-Deficit/Hyperactivity Disorder (ADHD); however, the etiological underpinnings of this relationship remain unclear. This study investigated if genetic variants in angiogenic, dopaminergic, neurotrophic, kynurenine, and cytokine-related biological pathways moderate the relationship between birth weight and ADHD symptom severity. A total of 398 youth from two multi-site, family-based studies of ADHD were included in the analysis. The sample consisted of 360 ADHD probands, 21 affected siblings, and 17 unaffected siblings. A set of 164 SNPs from 31 candidate genes, representing five biological pathways, were included in our analyses. Birth weight and gestational age data were collected from a state birth registry, medical records, and parent report. Generalized Estimating Equations tested for main effects and interactions between individual SNPs and birth weight centile in predicting ADHD symptom severity. SNPs within neurotrophic (NTRK3) and cytokine genes (CNTFR) were associated with ADHD inattentive symptom severity. There was no main effect of birth weight centile on ADHD symptom severity. SNPs within angiogenic (NRP1 & NRP2), neurotrophic (NTRK1 & NTRK3), cytokine (IL16 & S100B), and kynurenine (CCBL1 & CCBL2) genes moderate the association between birth weight centile and ADHD symptom severity. The SNP main effects and SNP x birth weight centile interactions remained significant after adjusting for multiple testing. Genetic variability in angiogenic, neurotrophic, and inflammatory systems may moderate the association between restricted prenatal growth, a proxy for an adverse prenatal environment, and risk to develop ADHD. (c) 2014 Wiley Periodicals, Inc.

Contains fulltext : 96400.pdf (publisher's version ) (Closed access), Intelligence is a highly heritable trait for which it has proven difficult to identify the actual genes. In the past decade, five whole-genome linkage scans have suggested genomic regions important to human intelligence; however, so far none of the responsible genes or variants in those regions have been identified. Apart from these regions, a handful of candidate genes have been identified, although most of these are in need of replication. The recent growth in publicly available data sets that contain both whole genome association data and a wealth of phenotypic data, serves as an excellent resource for fine mapping and candidate gene replication. We used the publicly available data of 947 families participating in the International Multi-Centre ADHD Genetics (IMAGE) study to conduct an in silico fine mapping study of previously associated genomic locations, and to attempt replication of previously reported candidate genes for intelligence. Although this sample was ascertained for attention deficit/hyperactivity disorder (ADHD), intelligence quotient (IQ) scores were distributed normally. We tested 667 single nucleotide polymorphisms (SNPs) within 15 previously reported candidate genes for intelligence and 29451 SNPs in five genomic loci previously identified through whole genome linkage and association analyses. Significant SNPs were tested in four independent samples (4,357 subjects), one ascertained for ADHD, and three population-based samples. Associations between intelligence and SNPs in the ATXN1 and TRIM31 genes and in three genomic locations showed replicated association, but only in the samples ascertained for ADHD, suggesting that these genetic variants become particularly relevant to IQ on the background of a psychiatric disorder.