Adolescence is the peak period for the incidence of anxiety disorders. Recent findings have revealed the immaturity of neural networks underlying emotional regulation in this population. Brain vulnerability to anxiety in adolescence is related to the unsynchronised development of anxiety-relevant brain functional systems. However, our current knowledge on brain deficits in adolescent anxiety is mainly borrowed from studies on adults. Understanding adolescent-specific brain deficits is essential for developing biomarkers and brain-based therapies targeting adolescent anxiety. This article reviews and compares recent neuroimaging literature on anxiety-related brain structural and functional deficits between adolescent and adult populations, and proposes a model highlighting the differences between adolescence and adulthood in anxiety-related brain networks. This model emphasises that in adolescence the emotional control system tends to be hypoactivated, the fear conditioning system is immature, and the reward and stress response systems are hypersensitive. Furthermore, the striatum’s functional links to the amygdala and the prefrontal cortex are strengthened, while the link between the prefrontal cortex and the amygdala is weakened in adolescence. This model helps to explain why adolescents are vulnerable to anxiety disorders and provides insights into potential brain-based approaches to intervene in adolescent anxiety disorders.

No abstract

Subcortical brain regions play essential roles in the onset of social anxiety disorder (SAD). While adolescence is the peak period of SAD, the relationships between abnormal development of the subcortical regions during this period and SAD are still unclear. This study investigated the agedependent alterations in structural co-variance among subcortical regions and between subcortical and cortical regions, aiming to re ect aberrant coordination during development in adolescents with SAD.High-resolution T1-weighted images were obtained from 76 adolescents with SAD and 67 healthy controls (HC), ranging from 11.0 to 17.9 years. We found that the SAD group exhibited signi cantly enhanced structural co-variance among key striatum regions (putamen and caudate). While the covariance decreased with age in healthy adolescents, the co-variance in SAD adolescents stayed high, leading to more apparent abnormalities in middle adolescence. Moreover, the striatum's mean structural co-variance with cortical regions decreased with age in HC but increased with age in SAD. The agedependence of the abnormal coordination indicates atypical developmental trajectories of the striatum and its balance with the cortical regions in adolescents with SAD.