4.7 Article

Bridging Anxiety and Depression: A Network Approach in Anxious Adolescents

期刊

JOURNAL OF AFFECTIVE DISORDERS
卷 280, 期 -, 页码 305-314

出版社

ELSEVIER
DOI: 10.1016/j.jad.2020.11.027

关键词

Depression; Adolescent; Generalized anxiety disorder (GAD); Network

资金

  1. National Institute of Mental Health [K23 MH106037]
  2. National Institute of Child Health and Development [R01 HD098757]
  3. National Institute of Environmental Health Sciences [R01 E5027224]

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This study found that in adolescents with GAD, certain symptoms not directly related to anxiety can bridge anxiety and depression, while patients with a heavier burden of depressive symptoms showed alterations in cortical thickness, indicating a unique neurostructural fingerprint. Additionally, youth with high depressive symptoms in GAD had reduced age-cortical thickness correlations, suggesting bidirectional neurobiological relationships between early GAD and cortical development.
Background: The phenomenology and neurobiology of depressive symptoms in anxious youth is poorly understood. Methods: Association networks of anxiety and depressive symptoms were developed in adolescents with generalized anxiety disorder (GAD; N=52, mean age: 15.41.6 years) who had not yet developed major depressive disorder. Community analyses were used to create consensus clusters of depressive and anxiety symptoms and to identify bridge symptoms between the clusters. In a subset of this sample (n=39), correlations between cortical thickness and depressive symptom severity was examined. Results: Ten symptoms clustered into an anxious community, 5 clustered into a depressive community and 5 bridged the two communities: impaired schoolwork, excessive weeping, low self-esteem, disturbed appetite, and physical symptoms of depression. Patients with more depressive cluster burden had altered cortical thickness in prefrontal, inferior and medial parietal (e.g., precuneus, supramarginal) regions and had decreases in cortical thickness-age relationships in prefrontal, temporal and parietal cortices. Limitations: Data are cross-sectional and observational. Limited sample size precluded secondary analysis of comorbidities and demographics. Conclusions: In youth with GAD, a sub-set of symptoms not directly related to anxiety bridge anxiety and depression. Youth with greater depressive cluster burden had altered cortical thickness in cortical structures within the default mode and central executive networks. These alternations in cortical thickness may represent a distinct neurostructural fingerprint in anxious youth with early depressive symptoms. Finally, youth with GAD and high depressive symptoms had reduced age-cortical thickness correlations. The emergence of depressive symptoms in early GAD and cortical development may have bidirectional, neurobiological relationships.

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