Executive functioning (EF) is associated with various aspects of school achievement and cognitive development in children and adolescents. There has been substantial research investigating associations between EF and other factors in young children, such as support processes and parenting, but less research has been conducted about external factors relating to EF in older children and adolescents. Therefore, the present study investigates one possible factor that could correlate with EF in school-age children and adolescents: parenting behavior. The cross-sectional study design gathered data from 169 children in primary schools, middle-schools, and Gymnasien, and their corresponding parents. All children underwent a standardized task to measure EF, the computer-based Erikson Flanker task, which evaluates EF as a function of error rates and response time. A self-report questionnaire was used to assess parenting behavior. Multilevel analysis was implemented to test the effects of parenting behavior on EF in school-age children. The results show significant associations between various parenting behaviors and children's EF: High scores on parental involvement or parental responsibility are associated with low error rates on the Erikson Flanker task, whereas high parental scores on inconsistent discipline are associated with high error rates. These correlations between parenting behavior and EF remained significant despite controlling for child age, maternal education, family income, and baseline performance (i.e., congruent trials on the Erikson Flanker task). No associations were found between parental behavior and reaction time on the Erikson Flanker task. These results indicate the important association between parenting behaviors and EF skills in school-age children, and foster the necessity to inform parents about ways in which they can optimally support their children's cognitive development.

IntroductionIn the past 2 decades, functional and structural neuroimaging techniques have been developing rapidly, yielding a large body of research addressing neural correlates of major depressive disorder (MDD). Neuroimaging has substantially shaped our understanding of depressive etiopathology, indicating its potential to become an objective tool of diagnostic, therapeutic and prognostic value.1 In MDD, first neuroimaging studies examined cerebral metabolism by means of positron emission tomography (PET). Predominantly left-sided decreased regional cerebral blood flow (rCBF) in the dorsolateral prefrontal cortex (DLPFC), medial prefrontal cortex (MPFC) and anterior cingulate cortex (ACC) were found.2,3 Comparing periods of acute illness with periods of recovery, remission of depressive symptoms was associated with a significant increase in rCBF in the left DLPFC cortical midline regions, such as the MPFC and ACC, suggesting state-relatedness of metabolic alterations. 4 Pretreatment metabolism in the rostral (pregenual) part of the ACC was reported to predict positive treatment response, 5-7 whereas hypermetabolism in the subcallosal part of the ACC was related to treatment resistance.8-11 Different treatment modalities have been shown to target distinct regions of the brain in patients with MDD. For instance, cognitive behavioural therapy was found to be associated with increased metabolism in the hippocampus and dorsal ACC together with metabolic decreases in prefrontal areas. In contrast, pharmacotherapy with paroxetine was related to prefrontal metabolism increases and subcortical decreases.12 Based on a rapidly growing body of neuroimaging evidence, specific neurobiological Background: Abnormal regional cerebral blood flow (rCBF) and grey matter volume have been frequently reported in patients with major depressive disorder (MDD). However, it is unclear to what extent structural and functional change co-occurs in patients with MDD and whether markers of neural activity, such as rCBF, can be predicted by structural change. Methods: Using MRI, we investigated resting-state rCBF and brain structure in patients with MDD and healthy controls between July 2008 and January 2013. We acquired perfusion images obtained with continuous arterial spin labelling, used voxel-based morphometry to assess grey matter volume and integrated biological parametric mapping analyses to investigate the impact of brain atrophy on rCBF. Results: We included 43 patients and 29 controls in our study. Frontotemporal grey matter volume was reduced in patients compared with controls. In patients, rCBF was reduced in the anterior cingulate and bilateral parahippocampal areas and increased in frontoparietal and striatal regions. These abnormalities were confirmed by analyses with brain volume as a covariate. In patients with MDD there were significant negative correlations between the extent of depressive symptoms and bilateral parahippocampal rCBF. We found a positive correlation between depressive symptoms and rCBF for right middle fron...

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Repeated learning improves memory. Temporally distributed (“spaced”) learning can be twice as efficient than massed learning. Importantly, learning success is a non-monotonic maximum function of the spacing interval between learning units. Further optimal spacing intervals seem to exist at different time scales from seconds to days. We briefly review the current state of knowledge about this “spacing effect” and then discuss very similar but so far little noticed spacing patterns during a form of synaptic plasticity at the cellular level, called long term potentiation (LTP). The optimization of learning is highly relevant for all of us. It may be realized easily with appropriate spacing. In our view, the generality of the spacing effect points to basic mechanisms worth for coordinated research on the different levels of complexity.

Hypoactivation of the left inferior frontal cortex during error signaling might represent a neurofunctional marker of a crucial prerequisite for error processing in adults with ADHD. This possibly indicates a dysfunction of the neural system that operates task-set related representations and monitoring of erroneous performances in service of ensuing posterror processing.