Research Project 1: Neuroimmune Mechanisms, Addictive Behaviors, and Cardiometabolic Health among African American Emerging Adults: A Prospective Study

项目总结：研究项目1 佐治亚大学(UGA)转化和预防科学中心(CTAPS；P20 MH068666， P30 DA027827)自2003年以来一直得到资助，以推进下一代基础和预防 对生活在资源贫乏地区的非裔美国年轻人的风险、复原力和药物使用情况的调查 社区。CTAPS P50提案是基于一种假设，即药物预防方面的进展 非裔美国人中的虐待和心脏代谢性疾病需要通过 长期的、多代人的贫困和社会逆境在生物和行为中根深蒂固 系统的方式增加了对成瘾行为的易感性。从概念上讲，该中心的 研究计划以中心科学家撰写的神经免疫网络(NIN)模型为基础 强调大脑和免疫系统之间的双向信号在成瘾的病理生理学中的作用 行为。NIN模型认为，慢性应激源放大外周炎症之间的串扰 以及为情绪产生和调节服务的神经回路。这种串扰导致慢性低级别 炎症一旦进入大脑，就会加剧大脑皮质-杏仁核环路中的威胁处理， 减弱皮质-纹状体环路中的奖赏处理，并抑制前额叶执行控制。nin 假设失调是为了使个人容易滥用物质和高脂肪饮食，部分原因是自我 治疗与神经信号传导中断相关的负面情绪。这些行为会产生 额外的炎症，以及奖赏回路中的神经适应性变化，进一步增加了 滥用药物。在研究项目(RP)1中，我们提出了测试NIN的首批前瞻性研究之一 来自225名非裔美国青年样本的预测。参与者将在18-19岁之间注册学习，a 在非裔美国人中，物质使用和不健康饮食迅速升级的一段时间。在… 时间1(T1)和T2(2.5年后)，参与者将完成抽血以量化低级别 炎症、威胁、奖励和执行控制神经活动的fMRI扫描，以及 压力暴露、成瘾行为和心脏代谢风险。RP1整合多器官研究 系统(即大脑和免疫系统)促进成瘾行为风险和复原力的科学研究 及其对心脏代谢健康的影响，特别是在低收入非裔美国人社区 以及其他暴露在慢性压力下的美国人。

PROJECT SUMMARY: Research Project 1 The University of Georgia’s (UGA) Center for Translational and Prevention Science (CTAPS; P20 MH068666, P30 DA027827) has been funded continuously since 2003 to advance next-generation basic and preventive investigations of risk, resilience, and drug use among African American young people living in resource poor communities. The CTAPS P50 proposal is based on the hypothesis that progress in the prevention of drug abuse and cardiometabolic disease among African Americans requires consideration of the processes through which chronic, multigenerational poverty and social adversity become embedded in biological and behavioral systems in ways that confer heightened vulnerability to addictive behaviors. Conceptually, the Center’s research program is grounded in a neuroimmune network (NIN) model authored by Center scientists that highlights bidirectional signaling between the brain and immune system in the pathophysiology of addictive behaviors. The NIN model proposes that chronic stressors amplify crosstalk between peripheral inflammation and neural circuitries subserving emotion generation and regulation. This crosstalk results in chronic low-grade inflammation, which upon accessing the brain, accentuates threat processing in cortico-amygdala circuity, attenuates reward processing in cortico-striatal circuity, and dampens prefrontal executive control. NIN dysregulation is hypothesized to predispose individuals to substance misuse and high fat diets, in part, to self- medicate the negative emotions associated with disrupted neural signaling. These behaviors generate additional inflammation, as well as neuroadaptive changes in reward circuitry, further elevating risk for substance misuse. In Research Project (RP) 1, we propose one of the first prospective studies to test NIN predictions from a sample of 225 African American youth. Participants will be ages 18-19 at study enrollment, a period of time in which substance use and unhealthy eating rapidly escalate among African Americans. At Time 1 (T1) and T2 (2.5 years later), participants will complete a blood draw to quantify low-grade inflammation, fMRI scanning of threat-, reward-, and executive control neural activity, and assessments of stress exposure, addictive behaviors, and cardiometabolic risk. RP1 integrates research on multiple organ systems (i.e., brain and immune system) to advance the science of risk and resilience for addictive behaviors and their cardiometabolic health consequences, especially among low income African American communities and other US populations exposed to chronic stress.