Abnormal resting-state functional connectivity in adolescent depressive episodes

Depression is linked to abnormalities in brain networks. Resting-state functional connectivity (FC), as measured using resting-state fMRI (rs-fMRI), is a crucial tool for exploring the brain network abnormalities associated with depressive symptoms, as it reveals how disruptions in brain region interactions occur. However, research focusing on adolescents with depression is limited and inconsistent, highlighting the need for further studies in this area.

Fifty-five adolescents with Depressive episodes (DE) and 26 healthy controls (HCs) underwent resting-state fMRI. Depressive symptoms were assessed using the 17-item Hamilton Rating Scale for Depression (HAMD-17). Seed regions were defined based on Yeo's seven-network scheme, including the sensorimotor network (SMN), ventral attention network (VAN), dorsal attention network (DAN), visual network (VN), frontoparietal network (FPN), default mode network (DMN), and limbic network (LN). These seed regions were derived from analysis of large-scale FC in healthy individuals, and were selected for their relevance to cognition, emotion, and depression research. Network-based statistical analyses were used to compare the adolescents with DE to the HCs, and correlation analyses were employed to examine the relationships between FC changes and cognitive performance.

The results showed significant differences in FC between the DE and HCs groups, involving 17 nodes and 17 edges across seven networks. Decreased FC was observed within the FPN, as well as between the FPN and VAN, the FPN and DMN, and the SMN and both the DAN and VN. Increased FC was observed between the FPN and VN, between the DAN and other networks (i.e., the DMN and FPN), and between the SMN and multiple networks. Notably, FC between the right superior parietal (SMN) and right precuneus (DMN) showed a negative correlation with HAMD-17 scores.

These results suggest that adolescents with DE experience widespread brain network abnormalities characterized by hypoactivity in external networks such as the SMN and VN, as well as hyperactivity in associative regions, including the DMN, FPN, SMN, and LN. Although these changes in FC are evident, the specific mechanisms linking them to clinical symptoms remain unclear and warrant further investigation.