Sleep Disturbance Forecasts β-Amyloid Accumulation across Subsequent Years.
Sleep Disturbance Forecasts β-Amyloid Accumulation across Subsequent Years.
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DOI：
10.1016/j.cub.2020.08.017
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发表时间：
2020-11-02
期刊：
影响因子：
--
通讯作者：
Walker MP
中科院分区：
文献类型：
--
作者：
Winer JR;Mander BA;Kumar S;Reed M;Baker SL;Jagust WJ;Walker MP
啮齿动物和人类的实验性睡眠-觉醒中断会因果地调节β-淀粉样蛋白(A-β)的动力学(例如)。这导致了一种假设，即除了横断面关联之外，睡眠结构和生理受损可能代表Aβ随着时间积累的速度的预期生物标记物。在这里，我们测试了这样一种假设，即非快速眼动、睡眠慢波活动和睡眠质量(效率)的初始基线测量可以提供对随后几年Aβ积累率的未来预测敏感性。对一组临床正常的老年人进行客观睡眠多导睡眠监测，并用[11C]PIB正电子发射断层扫描对Aβ积聚进行纵向追踪。低于1赫兹的NREM SWA的比例和睡眠效率的测量都可以预测随后Aβ随时间沉积的速度(斜率)，当考虑到其他感兴趣的辅助因素(例如，年龄、性别、睡眠呼吸暂停)时，这些相关性仍然很强。此外，这些测量是特定的，因此没有其他宏观和微生理结构的睡眠指标表现出这样的敏感性。我们的数据支持客观睡眠标记物可能是一组生物标记物的一部分，这些生物标记物在统计上预测人脑皮质Aβ沉积的纵向轨迹。因此，睡眠可能是一种潜在的负担得起、可扩展、可重复和非侵入性的工具，用于在阿尔茨海默病(AD)的认知症状之前量化Aβ病理进展。Winer等人。证明睡眠生理学的客观指标可以预测健康老年人随后的β-淀粉样蛋白堆积。基线时慢波活动减少和睡眠效率低下都与皮质β-淀粉样斑块沉积速度加快有关。
Experimental sleep-wake disruption in rodents and humans causally modulates β-amyloid (Aβ) dynamics (e.g.,). This leads to the hypothesis that, beyond cross-sectional associations, impaired sleep structure and physiology could represent prospective biomarkers of the speed with which Aβ accumulates over time. Here, we test the hypothesis that initial baseline measures of non-rapid eye movement (NREM) sleep slow-wave activity (SWA) and sleep quality (efficiency) provide future forecasting sensitivity to the rate of Aβ accumulation over subsequent years. A cohort of clinically normal older adults was assessed using objective sleep polysomnography in combination with longitudinal tracking of Aβ accumulation with [11C]PiB positron emission tomography (PET) imaging. Both the proportion of NREM SWA below 1 Hz and the measure of sleep efficiency predicted the speed (slope) of subsequent Aβ deposition over time, and these associations remained robust when taking into account additional cofactors of interest (e.g., age, sex, sleep apnea). Moreover, these measures were specific, such that no other macro- and microphysiological architecture metrics of sleep demonstrated such sensitivity. Our data support the proposal that objective sleep markers could be part of a set of biomarkers that statistically forecast the longitudinal trajectory of cortical Aβ deposition in the human brain. Sleep may therefore represent a potentially affordable, scalable, repeatable, and non-invasive tool for quantifying of Aβ pathological progression, prior to cognitive symptoms of Alzheimer’s disease (AD). Winer et al. demonstrate that objective measures of sleep physiology forecast subsequent β-amyloid accumulation in healthy older adults. Reduced slow-wave activity and low sleep efficiency at baseline are both associated with accelerated rate of cortical β-amyloid plaque deposition.
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DOI：
10.1126/science.1180962
发表时间：
2009-11-13
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Kang JE;Lim MM;Bateman RJ;Lee JJ;Smyth LP;Cirrito JR;Fujiki N;Nishino S;Holtzman DM
通讯作者：
Holtzman DM
影响因子：
3
作者：
Dvorak, Dino;Fenton, Andre A.
通讯作者：
Fenton, Andre A.
影响因子：
16.6
作者：
Hadoux, Xavier;Hui, Flora;van Wijngaarden, Peter
通讯作者：
van Wijngaarden, Peter
影响因子：
9.9
作者：
Doraiswamy, P. Murali;Sperling, Reisa A.;Pontecorvo, Michael J.
通讯作者：
Pontecorvo, Michael J.
影响因子：
16.2
作者：
Helfrich RF;Mander BA;Jagust WJ;Knight RT;Walker MP
通讯作者：
Walker MP