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Self-directed speech is considered an important developmental achievement as a self-regulatory mediator of thinking and behavior. Atypical self-directed speech is often implicated in the self-regulatory challenges characteristic of children with neurodevelopmental disorders. A growing body of evidence provides snapshots across age-levels and diagnoses, often presenting conflicting results. This systematic review is undertaken to impose clarity on the nature, extent, and self-regulatory implications of self-directed speech interruption in children with developmental language disorder (DLD), autism spectrum disorder (ASD), and attention deficit hyperactivity disorder (ADHD). A rigorous search process of relevant databases (i.e., PsychInfo, PubMed, CINAHL, ERIC) uncovered 19 relevant peer-reviewed articles that investigate self-directed speech in children with neurodevelopmental disorders. Consistent across the research, children with DLD, ASD, and ADHD present with differential development and use of self-directed speech. In its synthesis of findings, this systematic review clearly explicates the differential ontogenesis of self-directed speech in neurodevelopmental disorders and interprets the self-regulatory implications for children with DLD, ASD, and ADHD. Furthermore, the review spotlights important future research directions to better understand the mechanistic relationship between self-directed speech and self-regulation. [ABSTRACT FROM AUTHOR]

Pharmacological evidence suggests the importance of noradrenergic and other monoaminergic neurotransmitters in the aetiology and treatment of attention deficit hyperactivity disorder (ADHD). Until recently, the genes of the noradrenergic pathway were not intensively investigated in ADHD compared to dopaminergic and serotonergic candidates. In this study, 91 SNP markers of 14 noradrenergic genes (an average density of one SNP per 4.5 kbp) were examined in ADHD samples from Ireland and Australia. Although suggestive evidence of association (nominal p ≤ 0.05) with the genes SLC6A2, ADRA1A, ADRA1B and ADRA2B was observed, none remained significant after permutation adjustments. In contrast, haplotype analyses demonstrated a significant association between ADHD and a SLC6A2 haplotype comprising the markers rs36009, rs1800887, rs8049681, rs2242447 and rs9930182 (χ = 9.39, p-corrected = 0.019, OR = 1.51). A rare ADRA1B haplotype made of six SNPs (rs2030373, rs6884105, rs756275, rs6892282, rs6888306 and rs13162302) was also associated (χ = 7.79, p-corrected = 0.042 OR = 2.74) with the disorder. These findings provide evidence of a contribution of the noradrenaline system to the genetic aetiology of ADHD. The observed haplotype association signals may be driven by as yet unidentified functional risk variants in or around the associated regions. Functional genomic analysis is warranted to determine the biological mechanism of the observed association. [ABSTRACT FROM AUTHOR]