Genetic factors and socioeconomic status (SES) inequalities play a large role in educational attainment, and both have been associated with variations in brain structure and cognition. However, genetics and SES are correlated, and no prior study has assessed their neural associations independently. Here we used a polygenic score for educational attainment (EduYears-PGS), as well as SES, in a longitudinal study of 551 adolescents to tease apart genetic and environmental associations with brain development and cognition. Subjects received a structural MRI scan at ages 14 and 19. At both time points, they performed three working memory (WM) tasks. SES and EduYears-PGS were correlated (r= 0.27) and had both common and independent associations with brain structure and cognition. Specifically, lower SES was related to less total cortical surface area and lower WM. EduYears-PGS was also related to total cortical surface area, but in addition had a regional association with surface area in the right parietal lobe, a region related to nonverbal cognitive functions, including mathematics, spatial cognition, and WM. SES, but not EduYears-PGS, was related to a change in total cortical surface area from age 14 to 19. This study demonstrates a regional association of EduYears-PGS and the independent prediction of SES with cognitive function and brain development. It suggests that the SES inequalities, in particular parental education, are related to global aspects of cortical development, and exert a persistent influence on brain development during adolescence.

Most psychopathological disorders develop in adolescence. The biological basis for this development is poorly understood. To enhance diagnostic characterisation, and develop improved targeted interventions, it is critical to identify behavioural symptom groups that share neural substrates. We ran analyses to find relations between behavioral symptoms, and neuroimaging measures of brain structure and function in adolescence. We found two symptom groups, consisting of anxiety/depression and executive dysfunction symptoms respectively, which correlated with distinct sets of brain regions and interregional connections, measured by structural and functional neuroimaging modalities. We found that the neural correlates of these symptom groups were present before behavioural symptoms had developed. These neural correlates showed case-control differences in corresponding psychiatric disorders, depression and ADHD, in independent clinical samples. By characterising behavioral symptom groups based on shared neural mechanisms, our results provide a framework for developing a classification system for psychiatric illness, which is based on quantitative neurobehavioural measures.

The aim of the current paper is to evaluate clinical characteristics of 30 children with early onset anorexia nervosa (EO-AN; age = 12.2 ± 1.6 years) compared with 30 patients with adolescent onset AN (AO-AN; age = 15.9 ± 0.7 years) and 60 age-matched healthy controls. Statistical analyses included one-way analyses of variance with three planned comparisons and chi-square tests. Compared with AO-AN, EO-AN patients displayed more restrictive eating behaviour (p = 0.038), received more tube-feeding (p = 0.024), and had less problems with self-esteem (p < 0.001) and perfectionism (p = 0.001). EO-AN patients have similar eating disorder pathology (p = 0.183), body-image distortion (p = 0.060), and number of hospitalizations (p = 0.358) as AO-AN. Only a third of EO-AN patients suffer from low self-esteem. Overall, core AN pathology seems similar in EO-AN and AO-AN. However, EO-AN patients show differences in their pathological eating behaviour and the need for tube-feeding.