The error‐related negativity (ERN) and the error positivity (Pe) are electrophysiological components associated with error processing that are thought to exhibit distinctive developmental trajectories from childhood to adulthood. To investigate the age and age moderation effects on the ERN and the Pe strength during development, we conducted a preregistered three‐level meta‐analysis synthesizing 120 and 41 effect sizes across 18 group comparison studies and 19 correlational studies, respectively. The meta‐analysis included studies with mean age between 3.6 and 28.7 (min‐max age range: 3.5 and 49.8) years for age‐group comparisons and 6.1 to 18.7 (min‐max age range: 4.0–35.7) years for age correlations. Results showed that age was associated with a more negative ERN (SMD = −.433, r = −.230). No statistically significant association between age and the Pe was found (SMD = .059, r = −.091), except for in a group comparison between younger and older adolescents. The age effects were not significantly moderated by whether a Flanker or a Go/No‐Go task was used, whereas a probabilistic learning task moderated the age effect on the Pe. Moreover, the Fz and Cz electrode sites yielded stronger negative associations between age and the ERN and the Pe, respectively. The results confirm that the ERN and the Pe show differential development courses and suggest that sample and methodological characteristics influence the age effects, and lay the foundation for investigations of developmental patterns of the ERN and the Pe in relation to psychopathology and early genetic and environmental risk factors.

Low-frequency 1q21.1 distal deletion and duplication copy number variant (CNV) carriers are predisposed to multiple neurodevelopmental disorders, including schizophrenia, autism and intellectual disability. Human carriers display a high prevalence of micro- and macrocephaly in deletion and duplication carriers, respectively. The underlying brain structural diversity remains largely unknown. We systematically called CNVs in 38 cohorts from the large-scale ENIGMA-CNV collaboration and the UK Biobank and identified 28 1q21.1 distal deletion and 22 duplication carriers and 37,088 non-carriers (48% male) derived from 15 distinct magnetic resonance imaging scanner sites. With standardized methods, we compared subcortical and cortical brain measures (all) and cognitive performance (UK Biobank only) between carrier groups also testing for mediation of brain structure on cognition. We identified positive dosage effects of copy number on intracranial volume (ICV) and total cortical surface area, with the largest effects in frontal and cingulate cortices, and negative dosage effects on caudate and hippocampal volumes. The carriers displayed distinct cognitive deficit profiles in cognitive tasks from the UK Biobank with intermediate decreases in duplication carriers and somewhat larger in deletion carriers—the latter potentially mediated by ICV or cortical surface area. These results shed light on pathobiological mechanisms of neurodevelopmental disorders, by demonstrating gene dose effect on specific brain structures and effect on cognitive function.

Human cognitive development is manifold, with different functions developing at different speeds at different ages. Attention is an important domain of this cognitive development, and involves distinct developmental trajectories in separate functions, including conflict processing, selection of sensory input and alertness. In children, several studies using the Attention Network Test (ANT) have investigated the development of three attentional networks that carry out the functions of executive control, orienting and alerting. There is, however, a lack of studies on the development of these attentional components across adolescence, limiting our understanding of their protracted development. To fill this knowledge gap, we performed a mixed cross-sectional and longitudinal study using mixed methods to examine the development of the attentional components and their intraindividual variability from late childhood to young adulthood (n = 287, n observations = 408, age range = 8.5–26.7 years, mean follow up interval = 4.4 years). The results indicated that executive control stabilized during late adolescence, while orienting and alerting continued to develop into young adulthood. In addition, a continuous development into young adulthood was observed for the intraindividual variability measures of orienting and alerting. In a subsample with available magnetic resonance imaging (MRI) data (n =169, n observations = 281), higher alerting scores were associated with thicker cortices within a right prefrontal cortical region and greater age-related cortical thinning in left rolandic operculum, while higher orienting scores were associated with greater age-related cortical thinning in frontal and parietal regions. Finally, increased consistency of orienting performance was associated with thinner cortex in prefrontal regions and reduced age-related thinning in frontal regions.

Background: The error-related negativity (ERN) and the error positivity (Pe) are electrophysiological signals linked to error processing, a crucial aspect of self-monitoring and regulation. Previous research suggests different developmental trajectories for the ERN and Pe, with the ERN increasing in strength during the course of childhood and adolescence, while the Pe appears to reach a plateau by late childhood. There are, however, reports that are discrepant with this pattern, and effects of participant, task and methodological characteristics are poorly understood. The main objectives of this systematic review and meta-analysis are to evaluate the effect of age on ERN and Pe magnitude in children and adolescents, and to examine potential moderators of these effects, including age, sex, experimental task, task difficulty, and topography and quantification of the ERN and Pe. Methods/design: Studies that report group differences between age-groups or associations with age for the ERN and/or Pe magnitude in typically developing children and/or adolescents will be identified. The literature search will be conducted through PubMed and Scopus, all abstracts will be screened, and reference lists of relevant articles cross-checked for inclusion. The present protocol will also be disseminated on social media platforms to call for unpublished data. The data will be extracted from the eligible studies and will be included in random-effect meta-analyses in R. The results will include the estimation of age and age-group effect sizes, heterogeneity, risk of publication bias, and effects of moderating variables. Discussion: The study will include a systematic literature search and meta-analyses to better understand age-related differences in the ERN and Pe magnitudes. The results will provide estimates of effect sizes that are relevant for calculating statistical power and sample sizes for future studies. In addition, it will provide benchmark effect sizes for typical development of the ERN and the Pe that could be used for comparison purposes in developmental studies of clinical or at-risk groups.