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Novelty-seeking tendencies in adolescents may promote innovation as well as problematic impulsive behaviour, including drug abuse. Previous research has not clarified whether neural hyper- or hypo-responsiveness to anticipated rewards promotes vulnerability in these individuals. Here we use a longitudinal design to track 144 novelty-seeking adolescents at age 14 and 16 to determine whether neural activity in response to anticipated rewards predicts problematic drug use. We find that diminished BOLD activity in mesolimbic (ventral striatal and midbrain) and prefrontal cortical (dorsolateral prefrontal cortex) regions during reward anticipation at age 14 predicts problematic drug use at age 16. Lower psychometric conscientiousness and steeper discounting of future rewards at age 14 also predicts problematic drug use at age 16, but the neural responses independently predict more variance than psychometric measures. Together, these findings suggest that diminished neural responses to anticipated rewards in novelty-seeking adolescents may increase vulnerability to future problematic drug use.

Attention-deficit/hyperactivity disorder (ADHD) often persists into adulthood, albeit with changes in clinical symptoms throughout the life span. Although effect sizes of neuropsychological deficits in ADHD are well established, developmental approaches have rarely been explored and little is yet known about age-dependent changes in cognitive dysfunction from childhood to adulthood. In this cross-sectional study, 20 male children (8-12 years), 20 adolescents (13-16 years), and 20 adults (18-40 years) with ADHD and a matched control group were investigated using six experimental paradigms tapping into different domains of cognitive dysfunction. Subjects with ADHD were more delay-aversive and showed deficits in time discrimination and time reproduction, but they were not impaired in working memory, interference control or time production. Independent of age, the most robust group differences were observed with respect to delay aversion and time reproduction, pointing to persistent dysfunction in the mesolimbic reward circuitry and in the frontal-striatal-cerebellar timing system in subjects with ADHD. Across all tasks, effect sizes were lowest for adolescents with ADHD compared to age-matched controls. Developmental dissociations were found only for simple stimuli comparison, which was particularly impaired in ADHD children. Thus, in line with current multiple-pathway approaches to ADHD, our data suggest that deficits in different cognitive domains are persistent across the lifespan, albeit less pronounced in adolescents with ADHD.

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This study examines the effects of puberty and sex on the intrinsic functional connectivity (iFC) of brain networks, with a focus on the default-mode network (DMN). Consistently implicated in depressive disorders, the DMN’s function may interact with puberty and sex in the development of these disorders, whose onsets peak in adolescence, and which show strong sex disproportionality (females > males). The main question concerns how the DMN evolves with puberty as a function of sex. These effects are expected to involve within- and between-network iFC, particularly, the salience and the central-executive networks, consistent with the Triple-Network Model. Resting-state scans of an adolescent community sample ( n = 304, male/female: 157/147; mean/std age: 14.6/0.41 years), from the IMAGEN database, were analyzed using the AFNI software suite and a data reduction strategy for the effects of puberty and sex. Three midline regions (medial prefrontal, pregenual anterior cingulate, and posterior cingulate), within the DMN and consistently implicated in mood disorders, were selected as seeds. Within- and between-network clusters of the DMN iFC changed with pubertal maturation differently in boys and girls (puberty-X-sex). Specifically, pubertal maturation predicted weaker iFC in girls and stronger iFC in boys. Finally, iFC was stronger in boys than girls independently of puberty. Brain–behavior associations indicated that lower connectivity of the anterior cingulate seed predicted higher internalizing symptoms at 2-year follow-up. In conclusion, weaker iFC of the anterior DMN may signal disconnections among circuits supporting mood regulation, conferring risk for internalizing disorders.