Alzheimer Caregiver Coping: Mental and Physical Health

阿尔茨海默病护理人员应对：心理和身体健康

• 批准号: 6533785
• 负责人: IGOR GRANT
• 金额: $ 61.26万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN DIEGO
• 依托单位国家: 美国
• 财政年份: 1997
• 资助国家: 美国
• 起止时间: 1997-09-30 至 2006-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6533785
• 关键词: Alzheimer's disease; adrenal medulla; aging; arousal; behavioral /social science research tag; beta adrenergic receptor; blood chemistry; caregivers; catecholamines; cell adhesion molecules; clinical research; coping; disease /disorder proneness /risk; epinephrine; flow cytometry; human old age (65+); human subject; hypertension; longitudinal human study; polysomnography; psychological stressor; questionnaires; sleep apnea; social psychology; von Willebrand factor

The experiences of elderly caregivers of Alzheimer relatives (CG) can be viewed as a model of chronic human stress in aging. Our work in the past funding cycle has been guided by the notion that such stress is accompanied by increased sympathoadrenalmedullary (SAM) activation whose cardiovascular and molecular responses may be amplified by superimposed stressors such as excessive care demands relative to respite received ("vulnerable CG"). The results to date indicate heightened basal circulating epinephrine (E) in vulnerable CG, altered L-selectin cell adhesion molecule (CAM) expression, down- regulation of beta-adrenergic receptors of lymphocytes, but no systematic changes in heart rate or blood pressure variability. Vulnerable CG who received a two week respite intervention demonstrated lessened circulating E in response to stressors compared to wait-listed CG, but there were no systematic treatment-related changes in other variables. Pilot data revealed: 1) increased expression of procoagulation factors (especially D-Dimer) which correlated with amount of sleep disturbance and level of catecholamines; 2) Vulnerable CG had less total sleep time and more awakenings than nonvulnerable CG. In the proposed research we wish to refine our understanding of the molecular changes underlying chronic and acute stress in elderly caregiving. The basic theory is that the chronic stress of caregiving yields a state of relative SAM arousal reflected in greater resting and stressor-related releases of catecholamines. As outcome variables of chronic and acute stressors related to caregiving, we shall focus on coagulation factors and cellular adhesion molecules, each of which has been associated with heightened risk of cardiovascular morbidity and mortality. The general hypothesis is that elderly caregivers, versus noncaregiving controls (NC) will have greater SAM arousal and greater expression of coagulation and adhesion molecules. It is posited further that those caregivers who have background medical risks (history of cardiovascular disease or hypertension), and who experienced superimposed stressors, such as excessive caregiving demands, or other negative life events, will be selectively vulnerable to these physiological changes. Disturbed sleep environment is posited to be one of the pathways whereby caregiving stressors are translated into SAM arousal and molecular changes. The study design calls for recruitment of 120 elderly caregivers (CG) and 60 noncaregiving controls (NC). Laboratory-derived speech stressor tasks will be used to probe differences in SAM responsivity to speech stressors between CG and NC, as well as CG at several levels of "mismatch" between caregiving demand and respite received. At-home polysomnography and actigraphy will monitor sleep disruption, sleep disorders (e.g., sleep apnea), and circadian activity variation. In the longitudinal phase, subjects will be re-evaluated annually to determine if hypothesized recovery of SAM arousability occurs in those CG who have placed their spouse, or whose spouse has died. The results of this research should bring us closer to understanding the physiological and molecular mechanisms underlying increased morbidity in elderly persons under chronic stress.

老年人亲戚（CG）的老年护理人员的经历可以看作是衰老中慢性人类压力的模型。 我们在过去的融资周期中的工作一直受到这样的指导：这种压力伴随着交感神经肾上腺素（SAM）激活的增加，其心血管和分子反应可能会被叠加压力的叠加压力（例如相对于喘息的过度护理需求）扩大（“脆弱的CG”）。 迄今为止的结果表明，在脆弱的CG中，基础循环肾上腺素（E）的增强，L-选择素细胞粘附分子（CAM）表达改变，淋巴细胞的β-肾上腺素能受体的下调，但没有系统性变化心率或血压变化。与等待上市的CG相比，接受了两周暂息干预的脆弱的CG表现出对压力源的循环E的减少，但其他变量没有系统的治疗相关变化。 试点数据显示：1）与睡眠障碍和儿茶酚胺水平相关的突发凝因子（尤其是D-二聚体）的表达增加； 2）脆弱的CG的总睡眠时间较少，而觉醒的比不可侵蚀的CG。在拟议的研究中，我们希望完善我们对老年护理中慢性和急性应激的分子变化的理解。 基本理论是，护理的慢性应激产生的相对Sam唤醒状态反映在儿茶酚胺的更大静止和压力相关的释放中。作为与护理有关的慢性和急性应激源的结果变量，我们将重点关注凝血因子和细胞粘附分子，每个分子都与心血管发病率和死亡率的升高有关。 一般的假设是，老年护理人员与非护理对照组（NC）将具有更大的SAM唤醒和更大的凝结和粘附分子表达。 进一步认为，那些具有背景医疗风险的看护人（心血管疾病或高血压病史），并且经历了叠加的压力源（例如过度的照顾需求或其他负面生活事件），将有选择性地容易受到这些生理变化的影响。 扰动的睡眠环境被认为是将护理应激源转化为SAM唤醒和分子变化的途径之一。该研究设计要求招募120名老年护理人员（CG）和60个非护理控制（NC）。 实验室衍生的语音压力任务将用于探测SAM对CG和NC之间语音压力源的反应性差异，以及在照料需求和收到的喘息之间的几个级别的“不匹配”级别的CG。 在家的多摄影术和动作法将监测睡眠破坏，睡眠障碍（例如睡眠呼吸暂停）和昼夜节律活动变化。 在纵向阶段，将每年重新评估受试者，以确定在放置配偶或配偶死亡的CG的那些CG中是否会发生假设的SAM唤醒性。 这项研究的结果应该使我们更加了解慢性压力下老年人发病率增加的生理和分子机制。