Substrates of Threat and Reward Sensitivity and CVD Risk

项目1的主要目标是确定心理社会和生活方式相关的风险因素是否对 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，人体的高反应性 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-- 抑郁症状、焦虑和敌对倾向的特定指标；自主神经， 神经内分泌和血流动力学指标与心血管风险的潜在相关性； 临床前血管疾病和累积危险因素暴露。它还被假设为提高了 腹侧纹状体对奖赏相关刺激的反应性将与Low的心理测量指数一致 尽责、冲动和跨期选择；有危害健康的行为(例如，吸烟， 体力活动不足)；代谢综合征和组成部分危险因素，以及颈动脉粥样硬化。一个 另一个目的是确定个体这两个神经维度的遗传和环境相关性 不同之处。我们建议招募530名男性和女性的社区样本，年龄在30-55岁之间 无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 神经成像方案，以评估杏仁核和腹侧纹状体对行为刺激的反应，数据将是 在上述每个心血管疾病的行为和生物风险领域收集的数据。这个 后者将包括一系列诊断和评估访谈和问卷、动态 颈动脉的生理和行为监测、生物风险评估和超声评估 动脉疾病。此外，将从所有研究参与者那里获得用于DNA分析的血液。项目1将 首次对心血管疾病行为风险个体差异这一假设进行了系统测试 疾病可能源于神经结构反应性的功能变异，从而导致负面情绪 (威胁敏感度)和冲动决策“奖励敏感度”)。对这一假设的支持将进一步 我们对行为对心脏病影响的起源的理解，并为可能的 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.