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Social Isolation and Sleep Disturance in Aging: Inflammatory Mechanisms

Social Isolation and Sleep Disturance in Aging: Inflammatory Mechanisms
衰老过程中的社会孤立和睡眠障碍:炎症机制
批准号:
8316190
负责人:
Michael R Irwin
金额:
$39.12万
依托单位国家:
美国
项目类别:
财政年份:
2009
资助国家:
美国
项目状态:
已结题
起止时间:
2009-09-15 至 2014-08-31

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中文摘要
翻译
摘要 社会孤立的老年人全因死亡的风险增加, 特定的传染病、肿瘤和心血管疾病。然而,神经生物学和基因组学 这些影响的机制在很大程度上仍未被探索。我们的初步研究发现, 主观的社会隔离与睡眠障碍有关, 炎症本研究的主要目的是评估老年人的主观社会隔离, 成年人和这种社会隔离对睡眠的稳态调节的后果, 炎症生物学动力学鉴于我们的发现,细胞和基因组激活炎症 标记物发生沿着主观社会隔离以及睡眠障碍,这项研究将测试 自然主义和实验性睡眠缺失对社会联系感觉的影响, 在社会隔离与社会整合的老年人中炎症的细胞和基因组标志物。 本研究的目的是:1)确定社会隔离人群中睡眠障碍的性质和严重程度, 老年人; 2)评估社会隔离老年人炎症的细胞和基因组标志物 成年人;和3)检查睡眠丧失和恢复睡眠对行为症状的贡献 以及与社会隔离的老年人中炎症的细胞和基因组标志物。了解 社会隔离对睡眠的稳态调节的影响, 观察和实验研究设计对识别心理生物学 可能推动社会隔离和健康之间联系的途径。鉴于睡眠不足会导致 促炎细胞因子活性升高, 睡眠和细胞因子可能会导致前馈循环,其中睡眠中断和细胞因子水平升高, 促炎性细胞因子产生了一个恶性循环,加剧了睡眠, 社会脱节这项研究的结果对开发具有直接的临床意义。 针对睡眠障碍的干预措施,可能对以下疾病的发病率和结局产生影响: 主观上与社会隔离的老年人。
英文摘要
ABSTRACT Older adults who are socially isolated have increased risk of all-cause mortality, and several specific infectious, neoplastic, and cardiovascular diseases. However, the neurobiologic and genomic mechanisms of these effects remain largely unexplored. Our preliminary studies have found that subjective social isolation is associated with sleep disturbance as well as increases in markers of inflammation. The over-arching objective of this study is to evaluate subjective social isolation in older adults and the consequences of such social isolation for the homeostatic regulation of sleep and inflammatory biology dynamics. Given our findings that cellular and genomic activation of inflammatory markers occurs along with subjective social isolation as well as sleep disturbance, this study will test the consequences of naturalistic and experimental sleep loss on feelings of social connection and cellular and genomic markers of inflammation in socially isolated vs. socially integrated older adults. The study aims are: 1) to determine the nature and severity of disordered sleep in socially isolated older adults; 2) to evaluate cellular and genomic markers of inflammation in socially isolated older adults; and 3) to examine the contribution of sleep loss and recovery sleep to behavioral symptoms and cellular and genomic markers of inflammation in socially isolated older adults. Understanding the consequences of social isolation for the homeostatic regulation of sleep within the framework of an observational and experimental research design has implications for identifying the psychobiological pathways that might drive the link between social isolation and health. Given that sleep loss induces elevations in proinflammatory cytokine activity, dysregulation of the bi-directional relationship between sleep and cytokines may result in a feed-forward loop in which disrupted sleep and elevated proinflammatory cytokines create a vicious cycle exacerbating sleep and contributing to feelings of social disconnection. Results of this study have immediate clinical implications for the development of interventions that target disordered sleep with potential effects on morbidity and outcomes in subjectively socially isolated older adults.
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