The findings suggest that reduced striatal activation operates as a mechanism across the risk spectrum for depression. It is associated with anhedonia in healthy adolescents and is a behavioral indicator of positive valence systems, consistent with predictions based on the Research Domain Criteria.

Childhood AN is a serious disorder with an unfavorable course in many patients and high rates of chronicity and psychiatric comorbidity in young adulthood. Early detection and intervention are urgently needed.

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.

No abstract

BACKGROUND Neuroimaging studies of attention-deficit/hyperactivity disorder (ADHD) have most commonly reported volumetric abnormalities in the basal ganglia, cerebellum, and prefrontal cortices. Few studies have examined the relationship between ADHD symptomatology and brain structure in population-based samples. Herein, we investigate the relationship between dimensional measures of ADHD symptomatology, brain structure, and reaction time variability—an index of lapses in attention. We also test for associations between brain structural correlates of ADHD symptomatology and maps of dopaminergic gene expression. METHODS Psychopathology and imaging data were available for 1,538 youths. Parent ratings of ADHD symptoms were obtained using the Development and Well-Being Assessment (DAWBA) and the Strengths and Difficulties Questionnaire (SDQ). Self-reports of ADHD symptomatology were assessed using the youth version of the SDQ. Reaction time variability was available in a subset of participants. For each measure, whole brain voxel-wise regressions with gray matter volume (GMV) were calculated. RESULTS Parent ratings of ADHD symptoms (DAWBA and SDQ), adolescent self-reports of ADHD symptoms on the SDQ, and reaction time variability were each negatively associated with GMV in an overlapping region of the ventromedial prefrontal cortex (vmPFC). Maps of DRD1 and DRD2 gene expression were associated with brain structural correlates of ADHD symptomatology. CONCLUSIONS This is the first study to reveal relations between vmPFC structure and multi-informant measures of ADHD symptomatology in a large population-based sample of adolescents. Our results indicate that vmPFC structure is a biomarker for ADHD symptomatology. These findings extend previous research implicating the default mode network and dopaminergic dysfunction in ADHD.