Sharon Omer, Zhelezniakov Vladislav, Gat Yael, Falach Rotem, Narbayev Darya, Shiner Tamara, Walker Matthew P, Tauman Riva, Bregman Noa, Nir Yuval
Center for Human Sleep Science, Department of Psychology, University of California, Berkeley, Berkeley, California, USA.
Helen Wills Neuroscience Institute, University of California, Berkeley, Berkeley, California, USA.
Alzheimers Dement. 2025 May;21(5):e70247. doi: 10.1002/alz.70247.
INTRODUCTION: Alzheimer's disease (AD) disrupts human sleep architecture more severely than normal aging. However, it remains unclear how AD changes oscillatory neural activity during sleep, and whether such changes foreshadow cognitive decline in AD. METHODS: We used high-density electroencephalography sleep recordings in 55 participants: (1) 21 healthy older adults, (2) 28 patients with amnestic mild cognitive impairment (aMCI)-a prodromal AD stage, and (3) 6 AD patients. RESULTS: Cognitive performance robustly decreases with the slow wave (SW) trough amplitude and its synchronization across broad frontocentral cortical areas. Thus, across the AD spectrum, slow wave synchrony declines with cognition, as in normal aging, but at an accelerated pace. Moreover, delayed rapid eye movement (REM) sleep onset in aMCI and AD patients was associated with deficient SW activity, suggesting insufficiently restorative non-REM sleep. DISCUSSION: These findings suggest that impaired slow waves are closely linked to cognitive impairment and mark disrupted neural activity in AD progression. HIGHLIGHTS: Detailed analysis of high-density sleep electroencephalography was performed in amnestic mild cognitive impairment and Alzheimer's disease (AD) patients. Cognitive status robustly correlates with slow wave trough and its cortical spread. Delayed rapid eye movement sleep onset associated with AD correlates with diminished slow wave troughs. Impaired slow waves mark progressively disrupted neural activity in prodromal AD.
引言:阿尔茨海默病(AD)对人类睡眠结构的破坏比正常衰老更为严重。然而,目前尚不清楚AD如何改变睡眠期间的振荡神经活动,以及这些变化是否预示着AD患者的认知能力下降。 方法:我们对55名参与者进行了高密度脑电图睡眠记录:(1)21名健康老年人,(2)28名遗忘型轻度认知障碍(aMCI)患者——AD的前驱阶段,以及(3)6名AD患者。 结果:认知表现与慢波(SW)波谷振幅及其在广泛额中央皮质区域的同步性密切相关。因此,在整个AD谱系中,慢波同步性与认知能力一样,在正常衰老过程中会下降,但速度更快。此外,aMCI和AD患者快速眼动(REM)睡眠开始延迟与SW活动不足有关,这表明非快速眼动睡眠的恢复功能不足。 讨论:这些发现表明,慢波受损与认知障碍密切相关,并标志着AD进展过程中神经活动的破坏。 重点:对遗忘型轻度认知障碍和阿尔茨海默病(AD)患者进行了高密度睡眠脑电图的详细分析。认知状态与慢波波谷及其皮质扩散密切相关。与AD相关的快速眼动睡眠开始延迟与慢波波谷减少有关。慢波受损标志着前驱AD中神经活动的逐渐破坏。
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