Spousal Dementia Caregivers: Risk for Accelerated Aging

配偶痴呆症照顾者：加速衰老的风险

基本信息

批准号：
10642931
负责人：
Lisa Michelle Christian
金额：
$ 109.69万
依托单位：
OHIO STATE UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
2020
资助国家：
美国
起止时间：
2020-09-15 至 2025-05-31
项目状态：
未结题

来源：
https://reporter.nih.gov/project-details/10642931
关键词：
Acceleration Address Age Aging Bacterial Translocation Behavior Behavioral Biological Aging Biological Markers CD8-Positive T-Lymphocytes CDKN2A gene Caregiver Burden Caregivers Caring Chronic Chronic stress Chronology Clinic Cytomegalovirus Data Dementia Dementia caregivers Dimensions Disease Distress Eligibility Determination Endotoxins Epigenetic Process Family Practice Gender Health Health Benefit Home Immune system Immunologics Impairment Individual Inflammaging Inflammation Intake Intestinal permeability Leaky Gut Length Longevity Memory Memory Disorders Mental Depression Meta-Analysis Methodology Molecular Moods Morbidity - disease rate Nature Ohio Outcome Pathway interactions Persons Process Research Risk Risk Behaviors Sampling Source Spouse Caregiver Spouses Stress Support Groups Telomere Shortening Testing Time Visit Woman care recipients caregiver stress caregiving clinically significant dementia caregiving depressive symptoms design follow-up frailty frontier healthspan immune function innovation insight men mortality novel prospective recruit secondary analysis seropositive social relationships sociodemographics stressor telomere

项目摘要

Project Summary/Abstract Many studies have shown that providing care for a spouse with dementia can be quite stressful, leading to a heightened risk for depression, multiple negative health outcomes, frailty, and early mortality. Stress- and depression-related immune system alterations are seen as a key pathway to poorer health in caregivers. However, the health impacts of caregiver stress have been questioned in recent years, based on newer evidence that caregiving may benefit health and extend lifespan. Furthermore, even though caregivers have typically had poorer immune function than noncaregiving controls, the clinical significance of these differences has been questioned. These discrepant findings reflect both methodological and conceptual issues that this project will address. Three molecular aging biomarkers (telomere length, p16INK4a expression, and epigenetic age) have each been associated with multiple diseases and disorders. Their combined use will provide an innovative way to quantify the long-term health risks of caregiving, allowing us to ask novel questions: Does caregiving accelerate aging? Can caregiving-related distress propel molecular aging and shorten health span (the length of time that a person is healthy—not just alive)? We will also assess three stress-sensitive pathways relevant to molecular aging: inflammation, intestinal permeability, and cytomegalovirus serostatus and reactivation. Drawing on behavioral, immunological, and molecular aging research, this transdisciplinary study will assess concurrent and prospective relationships related to key caregiving risk-related dimensions (gender, social relationships, caregiving intensity/burden, and benefit finding), and these aging biomarkers. Spousal dementia caregivers and sociodemographically-comparable married noncaregivers will be evaluated at study intake and then again one and two years later. This design will provide longitudinal data to assess changes in caregiving, depression, key risk behaviors, aging biomarkers, and the stress-sensitive pathways related to molecular aging. We have three specific aims: 1) To characterize the concurrent and prospective differences between caregivers and noncaregivers on the molecular aging biomarkers, inflammation, and mood. 2) To assess the relationships among the molecular aging biomarkers. 3) This exploratory aim addresses the relative contributions of key risk-related dimensions to depression, accelerated increases in aging biomarkers, and inflammation. This proposal describes a distinctly novel methodology that will provide a way to test innovative and original hypotheses about the ways that spousal dementia caregiving impacts lifespan and health span. The interactions between behavior and molecular aging represent an important new frontier for understanding how caregiving (and other chronic stressors) can accelerate or slow aging. This cutting edge research will help illuminate the mechanisms through which caregiving and depression influence health and longevity.

项目摘要/摘要许多研究表明，为配偶提供痴呆症的护理可能很大，领先抑郁症的风险增加，多种负面健康结果，脆弱和早期死亡率。压力- 与抑郁症相关的免疫系统的改变被视为健康状况较差的关键途径照顾者。但是，近年来，护理人员压力的健康影响受到质疑在更新的证据证明护理可能会受益并延长寿命。此外，即使护理人员的免疫功能通常比非关注控制较差，这是临床意义这些差异已受到质疑。这些差异发现既反映了方法论和该项目将解决的概念问题。三个分子老化的生物标志物（端粒长度，p16ink4a表达和表观遗传年龄）每个与多种疾病和疾病有关。他们的合并用途将提供一种创新的方式量化护理人员的长期健康风险，使我们提出新颖的问题：护理是否可以照顾加速衰老？可以照顾相关的遇险促进分子衰老和缩短健康跨度（一个人健康的时间长度，而不是还活着）？我们还将评估三种应力敏感途径与分子衰老有关：感染，肠道通透性和巨细胞病毒血清和重新激活。借助行为，免疫学和分子衰老研究，该跨学科研究将评估与关键护理风险相关维度有关的并发和前瞻性关系（性别，社会关系，照料强度/负担和利益发现）以及这些老化的生物标志物。配偶痴呆症护理人员和社交人口统计学上可行的已婚非保养者将是在研究摄入量进行评估，然后在一年后再次进行评估。该设计将提供纵向数据评估护理，抑郁，关键风险行为，衰老生物标志物和应激敏感的变化与分子衰老有关的途径。我们有三个具体的目标：1）表征并发和看护人和非照料者在分子衰老生物标志物上的预期差异，炎症和心情。 2）评估分子老化生物标志物之间的关系。 3）这个探索目的解决了关键风险相关方面对抑郁的相对贡献，衰老的生物标志物和炎症加速增加。该建议描述了一种明显的新方法，该方法将提供一种测试创新和的方法关于配偶痴呆症护理影响寿命和健康跨度的方式的原始假设。这行为与分子老化之间的相互作用代表了理解的重要新领域护理（和其他慢性压力源）如何加速或缓慢衰老。这项尖端研究将帮助照亮护理和抑郁影响健康和寿命的机制。