RISK FOR SUBSTANCE ABUSE IN DEPRESSED ADOLESCENTS

这个子项目是利用由NIH/NCRR资助的中心拨款提供的资源的许多研究子项目之一。子项目和调查员(PI)可能从另一个NIH来源获得了主要资金，因此可能会出现在其他CRISE条目中。列出的机构是针对中心的，而不一定是针对调查员的机构。在青少年中，抑郁症和物质使用障碍(SUD)的共病发病率很高。这些疾病的共同发生与显著增加的社会心理和经济负担有关，因此强调需要确定增加并存疾病风险的因素。压力极大地增加了使用药物的风险，尤其是在那些患有抑郁症的人身上。抑郁症患者应激-物质使用的交互作用可能由HPA轴介导。然而，HPA对压力的反应程度以及它调节药物滥用自我给药的能力存在个体间的差异。更好地了解HPA反应的变化可能有助于开发和测试针对这种高度致残的疾病的更具体的干预措施。具体目的：1)研究抑郁症青少年下丘脑-垂体-肾上腺(HPA)系统调节失调与SUD发病风险之间的关系。2)评估心理社会压力是否对抑郁青年的SUD的预测有贡献，以及在有和没有HPA失调的人中，应激的贡献有何不同。3)探讨抑郁症青少年眼眶前额叶皮质及相关脑区的反应性与SUD发病风险的关系。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. There is a high prevalence of comorbidity between depression and substance use disorder (SUD) in adolescents. Co-occurence of these disorders is associated with significant added psychosocial and economic burden, thus emphasizing the need to identify factors that increase the risk for comorbid illness. Stress acutely increases the risk for substance use, specifically in those with depression. Stress-substance use interactions in depressed persons might be mediated by HPA axis. However, there is inter-individual variability in the degree of HPA response to stress, as well as its ability to modulate self-administration of drugs of abuse. A better understanding of the variations in HPA response potentially might be helpful in the development and testing of more specific interventions for this highly disabling illness. Specific aims: 1) To examine the association between dysregulation in hypothalamic-pituitary-adrenal (HPA) system and risk for the development of SUD in depressed adolescents. 2) To assess whether psychosocial stress makes a contribution to the prediction of SUD in depressed youth, and to evaluate how the contribution of stress varies in those with and without HPA dysregulation. 3) To relate responsivity of the orbitofrontal cortex and associated brain regions to risk for development of SUD in depressed adolescents.