Search

Two recent papers associated candidate genes with brooding rumination, a possible cognitive endophenotype for depression, in children ages 8–14 years. Stone et al. reported that BDNF val66met polymorphism predicted brooding in adolescence. Woody et al. reported that children carrying at least one copy of a CRHR1TAThaplotype reported less brooding than their peers in the presence of maternal depression. We attempted to replicate and extend these findings in a sample of twins aged 12–16 years. We analyzed the BDNF val66met (rs6265) polymorphism and two (rs242924 and rs7209436) out of three single nucleotide polymorphisms (SNPs) that Woody et al. used to create a CRHR1 haplotype. We controlled for maternal history of depression and clustering within families. Unlike Stone et al., we found higher brooding among BDNF Met carriers. This main effect was qualified by an interaction with pubertal status, with the effect driven by more physically mature participants. Similar to Woody et al., we found an interaction between CRHR1 SNPs and maternal depression, with the homozygous minor genotype acting as a protective factor against brooding in the presence of maternal depression. Findings provide partial support for the influence of candidate genes in two environmentally sensitive systems on brooding. [ABSTRACT FROM AUTHOR]

This study elucidates genetic influences on reflexive (as opposed to sustained) attention in children (aged 9-16 years; N = 332) who previously participated as infants in visual attention studies using orienting to a moving bar (Dannemiller, 2004). We investigated genetic associations with reflexive attention measures in infancy and childhood in the same group of children. The genetic markers (single nucleotide polymorphisms and variable number tandem repeats on the genes APOE, BDNF, CHRNA4, COMT, DRD4, HTR4, IGF2, MAOA, SLC5A7, SLC6A3, and SNAP25) are related to brain development and/or to the availability of neurotransmitters such as acetylcholine, dopamine, or serotonin. This study shows that typically developing children have differences in reflexive attention associated with their genes, as we found in adults (Lundwall, Guo & Dannemiller, 2012). This effort to extend our previous findings to outcomes in infancy and childhood was necessary because genetic influence may differ over the course of development. Although two of the genes that were tested in our adult study (Lundwall et al., 2012) were significant in either our infant study ( SLC6A3) or child study ( DRD4), the specific markers tested differed. Performance on the infant task was associated with SLC6A3. In addition, several genetic associations with an analogous child task occurred with markers on CHRNA4, COMT, and DRD4. Interestingly, the child version of the task involved an interaction such that which genotype group performed poorer on the child task depended on whether we were examining the higher or lower infant scoring group. These findings are discussed in terms of genetic influences on reflexive attention in infancy and childhood. [ABSTRACT FROM AUTHOR]

We investigated the etiology of attentional control ( AC) and four different anxiety symptom types (generalized, obsessive-compulsive, separation, and social) in an adolescent sample of over 400 twin pairs. Genetic factors contributed to 55% of the variance in AC and between 43 and 58% of the variance in anxiety. Negative phenotypic associations between AC and anxiety indicated that lower attentional ability is related to increased risk for all 4 anxiety categories. Genetic correlations between AC and anxiety phenotypes ranged from −.36 to −.47, with evidence of nonshared environmental covariance between AC and generalized and separation anxiety. Results suggest that AC is a phenotypic and genetic risk factor for anxiety in early adolescence, with somewhat differing levels of risk depending on symptomatology. [ABSTRACT FROM AUTHOR]

This prospective investigation sought to discriminate children who were both aggressive towards and victimized by peers in the first grade, from those who were only aggressive, only victimized, or neither (i.e., socially adjusted), using early child and family risk factors. Two hundred thirty-eight children, their mothers, and teachers participated in a longitudinal study since birth. All three aggressor/victim subgroups showed greater temperamental dysregulation than the socially adjusted children, but only aggressive victims had significantly poorer social perception skills. Aggressive victims were distinguished from aggressors by greater exposure to maternal depression and from victims by lower levels of early inhibition, but they shared the experiences of negative family emotional expressiveness with aggressors and greater mother-child negativity with victims. The identification of early risk factors is crucial to prevention and early intervention efforts that have the potential to attenuate the long term emotional, social, and academic problems associated with aggressive victim status. [ABSTRACT FROM AUTHOR]

ABSTRACT Although evidence suggests that delta-beta coupling may provide a useful index of trait level cortico-subcortical cross talk in baseline contexts, there has been little work done to clarify the role of delta-beta coupling across contexts and in association with other physiological markers of emotion processing. We examined whether individual differences in coupling were visible across both positive and negative emotion-eliciting episodes during infancy (age 6 months). We also tested the convergence between measures of delta-beta coupling and neuroendocrine reactivity, which is also believed to index emotion processing. Patterns of coupling across emotion-eliciting episodes differed based on infants' levels of cortisol reactivity. Low cortisol-reactive infants largely did not show differences in coupling across emotion contexts while high cortisol-reactive infants showed greater coupling in non-fear contexts during baseline and fear episodes. Moreover, high cortisol-reactive infants showed greater coupling than low-reactive infants in non-positive episodes. © 2015 Wiley Periodicals, Inc. Dev Psychobiol 58: 406-418, 2016. [ABSTRACT FROM AUTHOR]

The authors regret that, in this article, there was an error in the analyses comparing infant male and female regional brain volume differences. [ABSTRACT FROM AUTHOR]