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Early life stress (ELS) may accelerate frontoamygdala development related to socioemotional processing, serving as a potential source of resilience. Whether this circuit is associated with other proposed measures of accelerated development is unknown. In a sample of young adolescents, we examined the relations among ELS, frontoamygdala circuitry during viewing of emotional faces, cellular aging as measured by telomere shortening, and pubertal tempo. We found that greater cumulative severity of ELS was associated with stronger negative coupling between bilateral centromedial amygdala and the ventromedial prefrontal cortex, a pattern that may reflect more mature connectivity. More negative frontoamygdala coupling (for distinct amygdala subdivisions) was associated with slower telomere shortening and pubertal tempo over 2 years. These potentially protective associations of negative frontoamygdala connectivity were most pronounced in adolescents who had been exposed to higher ELS. Our findings provide support for the formulation that ELS accelerates maturation of frontoamygdala connectivity and provide novel evidence that this neural circuitry confers protection against accelerated biological aging, particularly for adolescents who have experienced higher ELS. Although negative frontoamygdala connectivity may be an adaptation to ELS, frontoamygdala connectivity, cellular aging, and pubertal tempo do not appear to be measures of the same developmental process.

Additive genetic, common environment and unique environment effects as well as age by heritability interactions are estimated using structural equation modeling on measures of brain volumes from the magnetic resonance imaging brain scans acquired on a pediatric sample of monozygotic and dyzygotic twin pairs, and unrelated singletons. Results suggest additive genetic effects accounted for a substantial portion of variability in all brain regions with notable exception of the cerebellum.

Abstract: Adolescence is a period characterized by continued improvements in inhibitory control, and this persisting immaturity is believed to interact with affective/motivational behavior to generate the impulsive and risk‐taking behavior evidenced at this time. Puberty is a central event of adolescence that has been shown to influence affective/motivational behavior. However, despite plausible mechanisms by which puberty might influence inhibitory control, researchers have yet to test this possibility rigorously. Thus, we designed a study to examine the unique role of pubertal maturation, independent of age, in the development of inhibitory control. In order to minimize age‐related variability while maximizing pubertal status variability, we recruited 78 participants (34 F) whose ages narrowly spanned the mean age of gonadarche for each sex (F: ages 11–13, M: ages 12–14). Two complementary measures were used to assess pubertal status: (1) circulating blood serum testosterone and estradiol levels reflecting internal manifestations of pubertal maturation, and (2) Tanner staging by a trained nurse reflecting pubertal maturation's external manifestations. Inhibitory control was assessed using the antisaccade task, and findings were adjusted for the potential effect of age. Results revealed no association between testosterone levels and error rates or response latencies in either sex. In girls, estradiol levels were not associated with error rates, but were associated with faster response latencies. There was similarly no association between Tanner status and error rates, although girls in more advanced pubertal stages showed faster response latencies. Power analyses indicate that findings of a lack of association did not reflect limited statistical power. Thus, in a study designed to isolate the effects of pubertal maturation independent of age, both external and internal indices of pubertal maturation converged to indicate that age‐related improvements in cold antisaccade performance are independent of pubertal maturation. [ABSTRACT FROM AUTHOR]

Neuroimaging studies suggest that developmental improvements in inhibitory control are primarily supported by changes in prefrontal executive function. However, studies are contradictory with respect to how activation in prefrontal regions changes with age, and they have yet to analyze longitudinal data using growth curve modeling, which allows characterization of dynamic processes of developmental change, individual differences in growth trajectories, and variables that predict any interindividual variability in trajectories. In this study, we present growth curves modeled from longitudinal fMRI data collected over 302 visits (across ages 9 to 26 years) from 123 human participants. Brain regions within circuits known to support motor response control, executive control, and error processing (i.e., aspects of inhibitory control) were investigated. Findings revealed distinct developmental trajectories for regions within each circuit and indicated that a hierarchical pattern of maturation of brain activation supports the gradual emergence of adult-like inhibitory control. Mean growth curves of activation in motor response control regions revealed no changes with age, although interindividual variability decreased with development, indicating equifinality with maturity. Activation in certain executive control regions decreased with age until adolescence, and variability was stable across development. Error-processing activation in the dorsal anterior cingulate cortex showed continued increases into adulthood and no significant interindividual variability across development, and was uniquely associated with task performance. These findings provide evidence that continued maturation of error-processing abilities supports the protracted development of inhibitory control over adolescence, while motor response control regions provide early-maturing foundational capacities and suggest that some executive control regions may buttress immature networks as error processing continues to mature. [ABSTRACT FROM AUTHOR]

Exposure to stress has been causally linked to changes in hippocampal volume (HV). Given that the hippocampus undergoes rapid changes in the first years of life, stressful experiences during this period may be particularly important in understanding individual differences in the development of the hippocampus. One hundred seventy‐eight early adolescents (ages 9–13 years; 43% male) were interviewed regarding exposure to and age of onset of experiences of stress; the severity of each stressful event was rated by an objective panel. All participants underwent structural magnetic resonance imaging, from which HVs were automatically segmented. Without considering the age of onset for stressful experiences, there was a small but statistically significant negative association of stress severity with bilateral HV. When considering the age of onset, there was a moderate and significant negative association between stress severity during early childhood (through 5 years of age) and HV; there was no association between stress severity during later childhood (age 6 years and older) and HV. We provide evidence of a sensitive period through 5 years of age for the effects of life stress on HV in adolescence. It will be important in future research to elucidate how reduced HV stemming from early life stress may contribute to stress‐related health outcomes. [ABSTRACT FROM AUTHOR]