Neurobiological pathways linking stress and emotion to atherosclerosis
将压力和情绪与动脉粥样硬化联系起来的神经生物学途径
基本信息
- 批准号:8804949
- 负责人:
- 金额:$ 50.34万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2008
- 资助国家:美国
- 起止时间:2008-04-01 至 2016-02-29
- 项目状态:已结题
- 来源:
- 关键词:AccountingAcuteAddressAdultAffectAmygdaloid structureAnteriorAreaAtherosclerosisBehavioralBiologicalBlood PressureBrainCaliberCardiovascular DiseasesCardiovascular systemCarotid ArteriesCarotid Atherosclerotic DiseaseCessation of lifeChronicClinicalColorCommunitiesCoronary heart diseaseCouplingCross-Sectional StudiesData CollectionDiseaseEmotionalEmotionsEventFunctional Magnetic Resonance ImagingFutureGrantHumanImageIndividual DifferencesInsula of ReilLifeLinkLongevityMeasuresMediatingMorbidity - disease rateMyocardial InfarctionNeurobiologyParticipantPathway interactionsPeripheralPersonsPhysiologic MonitoringPreclinical TestingProcessProtocols documentationPsychological StressPublic HealthReactionRegulationRiskRisk FactorsSamplingSeveritiesSignal TransductionSite-Directed MutagenesisSourceStressSymptomsSystemTestingTimeTo specifyUltrasonographyVariantWomanWorkagedcardiovascular risk factorcingulate cortexclinical predictorscognitive reappraisaldisabilityemotion regulationemotional experienceemotional stimulusfollow-upheart disease riskin vivointimal medial thickeningmenpre-clinicalprematureprospectivepsychologicpsychological stressorpsychosocialrelating to nervous systemstress reactivitystressortrait
项目摘要
DESCRIPTION (provided by applicant): A person's tendency to show exaggerated blood pressure reactions to acute psychological stressors is associated with an increased risk for preclinical atherosclerosis in the carotid arteries, a known predictor of premature disability and death by coronary heart disease (CHD). Prior work supported by this R01 (HL089850) has characterized a network of brain systems that regulate stressor-evoked blood pressure reactions, encompassing subdivisions of the cingulate cortex, insula, and amygdala. Additional cross-sectional work showed that stressor-evoked functional activity in these brain systems is associated with preclinical carotid atherosclerosis. This continuation project extends HL089850 by testing the organizing hypothesis that stressor-evoked functional activity in the cingulate cortex, insula, and amygdala predicts the 3-year longitudinal progression of preclinical atherosclerosis. It also extends HL089850 by testing the new hypothesis that individual differences in cingulate cortex, insula, and amygdala activity during the regulation of negative emotional experiences also accounts for cross-sectional and longitudinal variation in preclinical atherosclerosis. To test specific predictions derived from these hypothesis, three specific aims will be pursued in a community sample of men and women (aged 30-50 years) who are asymptomatic for clinical cardiovascular disease and who are well characterized for known demographic, anthropometric, biological, and psychosocial cardiovascular risk factors. Participants will complete a battery of psychological stress reactivity and emotion regulation tasks in a functional magnetic resonance imaging (fMRI) session with concurrent peripheral physiological monitoring. They will also complete a non-invasive carotid artery ultrasound protocol to assess preclinical atherosclerosis, as well as protocols to assess other known and emerging CHD risk factors at a baseline time point (Time 1) and at a follow-up time point 3-years later (Time 2). Aim 1 tests whether stressor-evoked functional connectivity between the anterior cingulate cortex, anterior insula, and amygdala predicts the progression of preclinical atherosclerosis (as measured by carotid intima-media thickness and adventitial diameter) after accounting for known cardiovascular risk factors. Aim 2 tests whether stressor-evoked blood pressure reactivity partially mediates the associations between stressor-evoked functional connectivity and the progression of preclinical atherosclerosis. Aim 3 tests whether the functional connectivity between the anterior cingulate cortex, anterior insula, and amygdala during the cognitive reappraisal of negative emotional stimuli associates with preclinical atherosclerosis at Time 1 and progression to Time 2.
描述(由申请人提供):一个人对急性心理压力源表现出夸张的血压反应的倾向与颈动脉临床前动脉粥样硬化的风险增加有关,颈动脉是冠状动脉心脏病(CHD)导致过早残疾和死亡的已知预测因素。该 R01 (HL089850) 支持的先前工作已经描述了调节应激诱发的血压反应的大脑系统网络的特征,包括扣带皮层、岛叶和杏仁核的细分。其他横断面研究表明,这些大脑系统中压力源诱发的功能活动与临床前颈动脉粥样硬化有关。该延续项目通过测试组织假设来扩展 HL089850,即扣带皮层、岛叶和杏仁核中压力源诱发的功能活动可预测临床前动脉粥样硬化的 3 年纵向进展。它还通过测试新的假设来扩展 HL089850,即在调节负面情绪体验期间扣带皮层、岛叶和杏仁核活动的个体差异也解释了临床前动脉粥样硬化的横截面和纵向变化。为了测试从这些假设得出的具体预测,将在男性和女性(年龄 30-50 岁)的社区样本中追求三个特定目标,这些样本无临床心血管疾病症状,并且具有已知的人口统计学、人体测量学、生物学、和心理社会心血管危险因素。参与者将在功能性磁共振成像 (fMRI) 会议中完成一系列心理压力反应和情绪调节任务,并同时进行外周生理监测。他们还将完成无创颈动脉超声方案以评估临床前动脉粥样硬化,以及在基线时间点(时间 1)和 3 年随访时间点评估其他已知和新出现的 CHD 危险因素的方案稍后(时间 2)。目标 1 在考虑已知的心血管危险因素后,测试压力源诱发的前扣带皮层、前岛叶和杏仁核之间的功能连接是否可以预测临床前动脉粥样硬化的进展(通过颈动脉内膜中层厚度和外膜直径测量)。目标 2 测试压力源诱发的血压反应性是否部分介导压力源诱发的功能连接与临床前动脉粥样硬化进展之间的关联。目标 3 测试在负面情绪刺激的认知重新评估过程中,前扣带皮层、前岛叶和杏仁核之间的功能连接是否与时间 1 和进展到时间 2 的临床前动脉粥样硬化相关。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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Peter J Gianaros其他文献
Peter J Gianaros的其他文献
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{{ truncateString('Peter J Gianaros', 18)}}的其他基金
Midlife cardiovascular stress physiology and preclinical cerebrovascular disease
中年心血管应激生理学与临床前脑血管疾病
- 批准号:
10720054 - 财政年份:2023
- 资助金额:
$ 50.34万 - 项目类别:
Metabolic and Inflammatory Pathways of Midlife Neurocognitive Disparities
中年神经认知差异的代谢和炎症途径
- 批准号:
10200027 - 财政年份:2017
- 资助金额:
$ 50.34万 - 项目类别:
Metabolic and Inflammatory Pathways of Midlife Neurocognitive Disparities
中年神经认知差异的代谢和炎症途径
- 批准号:
9531344 - 财政年份:2017
- 资助金额:
$ 50.34万 - 项目类别:
Metabolic and Inflammatory Pathways of Midlife Neurocognitive Disparities
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- 批准号:
9975001 - 财政年份:2017
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Metabolic and Inflammatory Pathways of Midlife Neurocognitive Disparities
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9754817 - 财政年份:2017
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$ 50.34万 - 项目类别:
Central Mechanisms for Cardioprotective Behavioral Effects of W-3 Fatty Acids
W-3 脂肪酸心脏保护行为作用的核心机制
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7861036 - 财政年份:2010
- 资助金额:
$ 50.34万 - 项目类别:
Central Mechanisms for Cardioprotective Behavioral Effects of W-3 Fatty Acids
W-3 脂肪酸心脏保护行为作用的核心机制
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8021782 - 财政年份:2010
- 资助金额:
$ 50.34万 - 项目类别:
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