Normandie Univ, UNICAEN, PSL Université, EPHE, INSERM, U1077, CHU de Caen, GIP Cyceron, NIMH « Neuropsychologie et Imagerie de la Mémoire Humaine », Caen, France; Normandie Univ, UNICAEN, INSERM, U1237, PhIND "Physiopathology and Imaging of Neurological Disorders", Institut Blood and Brain @ Caen-Normandie, Cyceron, Caen, France.
Normandie Univ, UNICAEN, PSL Université, EPHE, INSERM, U1077, CHU de Caen, GIP Cyceron, NIMH « Neuropsychologie et Imagerie de la Mémoire Humaine », Caen, France.
Ageing Res Rev. 2021 Mar;66:101252. doi: 10.1016/j.arr.2020.101252. Epub 2021 Jan 5.
Ageing is characterized by a progressive decline of sleep quality. Sleep difficulties are increasingly recognized as a risk factor for Alzheimer's disease (AD), and have been associated with cognitive decline. However, the brain substrates underlying this association remain unclear. In this review, our objective was to provide a comprehensive overview of the relationships between sleep changes and brain structural, functional and molecular integrity, including amyloid and tau pathologies in cognitively unimpaired older adults. We especially discuss the topography and causality of these associations, as well as the potential underlying mechanisms. Taken together, current findings converge to a link between several sleep parameters, amyloid and tau levels in the CSF, and neurodegeneration in diffuse frontal, temporal and parietal areas. However, the existing literature remains heterogeneous, and the specific sleep changes associated with early AD pathological changes, in terms of topography and neuroimaging modality, is not clearly established yet. Notably, if slow wave sleep disruption seems to be related to frontal amyloid deposition, the brain correlates of sleep-disordered breathing and REM sleep disruption remain unclear. Moreover, sleep parameters associated with tau- and FDG-PET imaging are largely unexplored. Lastly, whether sleep disruption is a cause or a consequence of brain alterations remains an open question.
衰老的特点是睡眠质量逐渐下降。睡眠困难越来越被认为是阿尔茨海默病 (AD) 的一个风险因素，并与认知能力下降有关。然而，这种关联的大脑基础仍不清楚。在这篇综述中，我们的目的是全面概述睡眠变化与大脑结构、功能和分子完整性之间的关系，包括认知正常的老年人中的淀粉样蛋白和 tau 病理学。我们特别讨论了这些关联的拓扑结构和因果关系，以及潜在的潜在机制。总之，目前的研究结果表明，几个睡眠参数、CSF 中的淀粉样蛋白和 tau 水平以及弥漫性额叶、颞叶和顶叶区域的神经退行性变之间存在关联。然而，现有文献仍然存在异质性，并且与早期 AD 病理变化相关的特定睡眠变化，就拓扑结构和神经影像学方式而言，尚未明确确定。值得注意的是，如果慢波睡眠中断似乎与额叶淀粉样蛋白沉积有关，那么睡眠呼吸紊乱和 REM 睡眠中断的大脑相关性仍不清楚。此外，与 tau 和 FDG-PET 成像相关的睡眠参数在很大程度上尚未得到探索。最后，睡眠中断是大脑改变的原因还是结果，这仍然是一个悬而未决的问题。
