Center for Human Sleep Science, Department of Psychology, University of California Berkeley, Berkeley, California 94720,
Center for Human Sleep Science, Department of Psychology, University of California Berkeley, Berkeley, California 94720.
J Neurosci. 2019 Aug 7;39(32):6315-6324. doi: 10.1523/JNEUROSCI.0503-19.2019. Epub 2019 Jun 17.
Recent proposals suggest that sleep may be a factor associated with accumulation of two core pathological features of Alzheimer's disease (AD): tau and β-amyloid (Aβ). Here we combined PET measures of Aβ and tau, electroencephalogram sleep recordings, and retrospective sleep evaluations to investigate the potential utility of sleep measures in predicting AD pathology in male and female older adults. Regression analyses revealed that the severity of impaired slow oscillation-sleep spindle coupling predicted greater medial temporal lobe tau burden. Aβ burden was not associated with coupling impairment but instead predicted the diminished amplitude of <1 Hz slow-wave-activity, results that were statistically dissociable from each other. Additionally, comparisons of AD pathology and retrospective, self-reported changes in sleep duration demonstrated that changes in sleep across the lifespan can predict late-life Aβ and tau burden. Thus, quantitative and qualitative features of human sleep represent potential noninvasive, cost-effective, and scalable biomarkers (current and future forecasting) of AD pathology, and carry both therapeutic and public health implications. Several studies have linked sleep disruption to the progression of Alzheimer's disease (AD). Tau and β-amyloid (Aβ), the primary pathological features of AD, are associated with both objective and subjective changes in sleep. However, it remains unknown whether late life tau and Aβ burden are associated with distinct impairments in sleep physiology or changes in sleep across the lifespan. Using polysomnography, retrospective questionnaires, and tau- and Aβ-specific PET, the present study reveals human sleep signatures that dissociably predict levels of brain tau and Aβ in older adults. These results suggest that a night of polysomnography may aid in evaluating tau and Aβ burden, and that treating sleep deficiencies within decade-specific time windows may serve in delaying AD progression.
最近的研究表明，睡眠可能是阿尔茨海默病（AD）两种核心病理特征——tau 和 β-淀粉样蛋白（Aβ）累积的相关因素。在这里，我们结合了 Aβ 和 tau 的正电子发射断层扫描（PET）测量、脑电图睡眠记录和回顾性睡眠评估，以研究睡眠测量在预测男性和女性老年人 AD 病理方面的潜在效用。回归分析显示，慢波睡眠纺锤波耦合受损的严重程度预测了内侧颞叶 tau 负荷的增加。Aβ 负担与耦合损伤无关，但预测了<1Hz 慢波活动的幅度减小，这些结果在统计学上是可分离的。此外，AD 病理和回顾性、自我报告的睡眠持续时间变化的比较表明，整个生命周期的睡眠变化可以预测晚年的 Aβ 和 tau 负担。因此，人类睡眠的定量和定性特征代表了 AD 病理的潜在非侵入性、具有成本效益和可扩展的生物标志物（当前和未来预测），并具有治疗和公共卫生意义。有几项研究将睡眠中断与阿尔茨海默病（AD）的进展联系起来。tau 和 β-淀粉样蛋白（Aβ）是 AD 的主要病理特征，与睡眠的客观和主观变化都有关。然而，目前尚不清楚晚年 tau 和 Aβ 负担是否与睡眠生理学的不同损伤或整个生命周期的睡眠变化有关。使用多导睡眠图、回顾性问卷以及 tau 和 Aβ 特异性正电子发射断层扫描（PET），本研究揭示了可分离预测老年人大脑 tau 和 Aβ 水平的人类睡眠特征。这些结果表明，一夜多导睡眠图可能有助于评估 tau 和 Aβ 负担，并且在特定的十年时间窗口内治疗睡眠缺陷可能有助于延缓 AD 的进展。
