Substrates of Threat and Reward Sensitivity and CVD Risk

项目1的主要目标是确定是否有心理社会和生活方式相关的风险因素， 心血管疾病与关键神经结构反应性的个体差异有关 潜在的情绪处理和食欲动机。据推测，高反应性的 杏仁核对情绪相关刺激的反应将与神经质（或消极情感和情感）的特征共同变化， 抑郁症的具体指标包括神经病学、焦虑和对抗性倾向;自主神经， 与心血管风险潜在相关的神经内分泌和血液动力学指标;以及 临床前血管疾病和累积危险因素暴露。也有人假设， 腹侧纹状体对奖励相关刺激的反应性将与低水平的心理测量指标协变。 冲动性，冲动性和跨期选择;与健康风险行为（例如，吸烟， 缺乏运动）;代谢综合征及其危险因素，以及颈动脉粥样硬化。一个 另一个目的是确定个体的这两个神经维度的遗传和环境相关性， 差异我们建议招募530名男性和女性，年龄在30-55岁之间， 没有动脉粥样硬化性心血管疾病的临床病史。受试者将参加功能磁共振成像 神经影像学协议，以评估杏仁核和腹侧纹状体反应的行为刺激，数据将 在上述心血管疾病的行为和生物风险领域中收集。的 后者将包括一系列诊断和评估访谈和问卷调查， 生理和行为监测、生物风险评估以及颈动脉超声评估 动脉疾病此外，将从所有研究受试者中采集用于DNA分析的血液。项目1将 提供了第一个系统的假设，即心血管疾病行为风险的个体差异， 疾病可能源于神经结构的反应性的功能变异， （威胁敏感性）和冲动决策“奖励敏感性”）。对这一假设的支持将进一步 我们对行为影响心脏病的起源的理解，并提供线索， 病原学和致病性的共性。

The principal objective of Project 1 is to establish whether psychosocial and lifestyle-related risk factors for cardiovascular disease are associated with individual differences in the reactivity of key neural structures underlying emotional processing and appetitive motivation. It is hypothesized that heightened reactivity of the amygdala to emotionally-relevant stimuli will covary with traits of neuroticism (or negative affectivity and affect- specific indicators of depression symptomatology, anxiety, and antagonistic disposition; autonomic, neuroendocrine and hemodynamic indices of potential relevance to cardiovascular risk; and to biomarkers of preclinical vascular disease and cumulative risk factor exposure. It is also hypothesized that heightened reactivity of the ventral striatum to reward-related stimuli will covary with psychometric indices of low conscientiousness, impulsivity, and intertemporal choice; with health risk behaviors (e.g., cigarette smoking, physical inactivity); metabolic syndrome and component risk factors, and carotid artery atherosclerosis. An additional aim is to identify genetic and environmental correlates of these two neural dimensions of individual differences. We propose to recruit a community sample of 530 men and women, 30-55 years of age and without clinical history of atherosclerotic cardiovascular disease. Subjects will participate in an fMRI neuroimaging protocol to assess amygdala and ventral striatal reactivities to behavioral stimuli, and data will be collected in each of the foregoing domains of behavioral and biological risk for cardiovascular disease. The latter will include a battery of diagnostic and assessment interviews and questionnaires, ambulatory physiological and behavioral monitoring, biological risk assessments, and ultrasound evaluations of carotid artery disease. In addition, blood for DNA analysis will be obtained from all study participants. Project 1 will provide the first systematic test of the hypothesis that individual differences in behavioral risk for cardiovascular disease may stem from functional variation in the reactivity of neural structures contributing to negative affect (threat sensitivity) and impulsive decision-making "reward sensitivity"). Support for this hypothesis will further our understanding of the origins of behavioral influences on heart disease and provide clues to possible commonalities of etiology and pathogenicity.