Background-Childhood dysregulation, which reflects deficits in the capacity to regulate or control one's thoughts, emotions and behaviours, is associated with psychopathology throughout childhood and into adulthood. Exposures to adversity during the prenatal period, including prenatal depression, can influence the development of dysregulation, and a number of candidate genes have been suggested as moderators of prenatal exposure, including polymorphisms in the promoter region of the serotonin transporter gene (5-HTTLPR). We examined whether prenatal depression and child 5-HTTLPR interact to predict childhood dysregulation.

Prenatal maternal depression and a multilocus genetic profile of two susceptibility genes implicated in the stress response were examined in an interaction model predicting negative emotionality (NE) in the first 3 years. In 179 mother-infant dyads from the Maternal Adversity, Vulnerability and Neurodevelopment cohort, prenatal depression (CES-D) was assessed at 24 to 36 weeks. The multilocus genetic profile score consisted of the number of susceptibility alleles from 5-HTTLPR (No L A (S/S, S/L G or L G /L G ) vs. any L A ) and Dopamine Receptor D4 (6-8R vs. 2-5R). NE was extracted from the IBQ-R at 3 and 6 months and the ECBQ at 18 and 36 months. Mixed and confirmatory regression analyses indicated that prenatal depression and the multilocus genetic profile interacted to predict NE from 3 to 36 months. Results were characterised by a differential susceptibility model at 3 and 6 months and by a diathesis stress model at 36 months. Negative emotionality (NE) is derived from the temperamental dimensions of sadness, distress towards limitations, fear and excessive reactions to minor changes, and reflects a generally stable tendency to show increased emotional reactivity towards negative situations (Gartstein & Rothbart, 2003;Lemery, Goldsmith, Klinnert, & Mrazek, 1999). NE is associated with the development of later problematic behaviour and psychopathology (Eisenberg et al., 2009;Fox, Henderson, Rubin, Calkins, & Schmidt, 2001;Hyde, Mezulis, & Abramson, 2008). For example, fearful temperament is associated with childhood anxiety disorders (Degnan, Alma, & Fox, 2010;Goldsmith & Lemery, 2000), while NE is associated with depression (Phillips, Lonigan, & Driscoll, 2002) and maladjustment (Eisenberg et al., 2009). Understanding early influences of NE on socio-emotional development (Davis, Glynn, Schetter, Hobel, Chicz-demet, & Sandman, 2007;Davis, Snidman, Glynn, Dunkel Schetter, & Sandman, 2004;Hayden et al., 2010;Hayden et al., 2007) could inform efforts at prevention and early intervention. Recent contradictory findings about the role of genetic and prenatal adversity (Braithwaite et al., 2013;, suggest the need for replication (Duncan, 2013) and modeling of genetic risk with multiple genes (Plomin, 2013). Accordingly, we present the findings from a study of the development of NE from 3 to 36 months of age from the interaction of prenatal maternal depression and a multilocus genetic profile. The Role of Prenatal Maternal StressPrenatal maternal stress, measured in diverse ways is associated with NE (Glover, 2011;O'Connor, Heron, & Glover, 2002a). For example, higher prenatal maternal cortisol is associated with fussier behaviour, more negative facial expressions, crying, as well as higher NE at 7 weeks of age (de Weerth, Hees, & Buitelaar, 2003). Symptoms of prenatal maternal anxiety and depression, loosely associated with the stress response predict behavioural reactivity at 4 months of age (Davis et al., 2004) and behavioural/emotional problems at 4 years of age (O'Connor, et al., 2002a). While most studi...

Time estimation of short durations (under 1 sec) was examined in low-functioning individuals with autism spectrum disorder (ASD) and typically developing (TD) children matched on mental age. Temporal bisection and generalization tasks were used to examine basic perceptual timing mechanisms. For both tasks, the participants with ASD demonstrated less sensitivity to variability in short durations than the TD children, adding to a growing body of literature suggesting deficits in timing exist for longer durations. The results highlight the need to examine multiple levels of processing of time-related information from basic perceptual mechanisms to higher level cognitive mechanisms.

Based in classic developmental theory and in more than two centuries of ever increasingly sophisticated medical thinking and science, the developmental approach has transformed the theory, methodology, and interpretation of the study of persons with intellectual disability. The primary contributions include the differentiation among persons with intellectual disability by etiology, the application of developmental principles to the specific etiological groups, the emphasis on mental age (MA) (rather than chronological age; CA), and the consideration of the “whole person” along with his or her family and community. In debunking the monolithic approach to intellectual disability as a single disorder, the developmental approach allows for considerably more precision in the study of this population and the resultant rejection of common myths, albeit as part of a process that highlights the extent to which this field is a nascent one. In highlighting the broadening of the understanding of persons with intellectual disability, we review contributions from the study of social competence, language development, and family relations. We then introduce the potential impact and current limitations of the application of cutting‐edge technology in the study of neuroscience among persons with intellectual disability.

Negative emotionality (NE) was evaluated as a candidate mechanism linking prenatal maternal affective symptoms and offspring internalizing problems during the preschool/early school age period. The participants were 335 mother–infant dyads from the Maternal Adversity, Vulnerability and Neurodevelopment project. A Confirmatory Bifactor Analysis (CFA) based on self-report measures of prenatal depression and pregnancy-specific anxiety generated a general factor representing overlapping symptoms of prenatal maternal psychopathology and four distinct symptom factors representing pregnancy-specific anxiety, negative affect, anhedonia and somatization. NE was rated by the mother at 18 and 36 months. CFA based on measures of father, mother, child-rated measures and a semistructured interview generated a general internalizing factor representing overlapping symptoms of child internalizing psychopathology accounting for the unique contribution of each informant. Path analyses revealed significant relationships among the general maternal affective psychopathology, the pregnancy- specific anxiety, and the child internalizing factors. Child NE mediated only the relationship between pregnancy-specific anxiety and the child internalizing factors. We highlighted the conditions in which prenatal maternal affective symptoms predicts child internalizing problems emerging early in development, including consideration of different mechanistic pathways for different maternal prenatal symptom presentations and child temperament.

Dysregulation is a combination of emotion, behavior, and attention problems associated with lifelong psychiatric comorbidity. There is evidence for the stability of dysregulation from childhood to adulthood, which would be more fully characterized by determining the likely stability from infancy to childhood. Early origins of dysregulation can further be validated and contextualized in association with environmental and biological factors, such as prenatal stress and polygenic risk scores (PRS) for overlapping child psychiatric problems. We aimed to determine trajectories of dysregulation from 3 months to 5 years (N = 582) in association with maternal prenatal depression moderated by multiple child PRS (N = 232 pairs with available PRS data) in a prenatal cohort. Mothers reported depression symptoms at 24-26 weeks' gestation and child dysregulation at 3, 6, 18, 36, 48, and 60 months. The PRS were for major depressive disorder, attention deficit hyperactivity disorder, cross disorder, and childhood psychiatric problems. Covariates were biological sex, maternal education, and postnatal depression. Analyses included latent classes and regression. Two dysregulation trajectories emerged: persistently low dysregulation (94%), and increasingly high dysregulation (6%). Stable dysregulation emerged at 18 months. High dysregulation was associated with maternal prenatal depression, moderated by PRS for child comorbid psychiatric problems. Males were at greater risk of high dysregulation.