Due to worldwide demographic change, the number of older persons in the population is increasing. Aging is accompanied by changes of sleep structure, deposition of beta-amyloid (Aß) and tau proteins and vascular changes and can turn into mild cognitive impairment (MCI) as well as dementia. Sleep disorders are discussed both as a risk factor for and as a consequence of MCI/dementia. Cross-sectional and longitudinal population-based as well as case–control studies revealed sleep disorders, especially sleep-disorderded breathing (SDB) and excessive or insufficient sleep durations, as risk factors for all-cause MCI/dementia. Regarding different dementia types, SDB was especially associated with vascular dementia while insomnia/insufficient sleep was related to an increased risk of Alzheimer’s disease (AD). Scarce and still inconsistent evidence suggests that therapy of sleep disorders, especially continuous positive airway pressure (CPAP) in SDB, can improve cognition in patients with sleep disorders with and without comorbid dementia and delay onset of MCI/dementia in patients with sleep disorders without previous cognitive impairment. Regarding potential pathomechanisms via which sleep disorders lead to MCI/dementia, disturbed sleep, chronic sleep deficit and SDB can impair glymphatic clearance of beta-amyloid (Aß) and tau which lead to amyloid deposition and tau aggregation resulting in changes of brain structures responsible for cognition. Orexins are discussed to modulate sleep and Aß pathology. Their diurnal fluctuation is suppressed by sleep fragmentation and the expression suppressed at the point of hippocampal atrophy, contributing to the progression of dementia. Additionally, sleep disorders can lead to an increased vascular risk profile and vascular changes such as inflammation, endothelial dysfunction and atherosclerosis which can foster neurodegenerative pathology. There is ample evidence indicating that changes of sleep structure in aging persons can lead to dementia and also evidence that therapy of sleep disorder can improve cognition. Therefore, sleep disorders should be identified and treated early.

中文翻译：

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睡眠障碍与全因 MCI/痴呆和不同类型痴呆的关联——临床证据、潜在的病理机制和治疗选择：叙述性综述

由于世界范围内的人口变化，人口中老年人的数量正在增加。衰老伴随着睡眠结构的变化、β-淀粉样蛋白 (Aß) 和 tau 蛋白的沉积以及血管变化，并可能转变为轻度认知障碍 (MCI) 以及痴呆症。睡眠障碍既是 MCI/痴呆的危险因素，也是 MCI/痴呆的后果。基于人群的横断面和纵向研究以及病例对照研究表明，睡眠障碍，尤其是睡眠呼吸障碍 (SDB) 和睡眠时间过多或不足，是全因 MCI/痴呆的危险因素。对于不同的痴呆类型，SDB与血管性痴呆尤其相关，而失眠/睡眠不足则与阿尔茨海默病（AD）的风险增加有关。缺乏且仍然不一致的证据表明，睡眠障碍的治疗，尤其是 SDB 中的持续气道正压通气 (CPAP)，可以改善患有或不患有痴呆症的睡眠障碍患者的认知，并延迟既往无睡眠障碍的睡眠障碍患者的 MCI/痴呆的发作。认知障碍。关于睡眠障碍导致 MCI/痴呆的潜在病理机制，睡眠障碍、慢性睡眠不足和 SDB 会损害 β-淀粉样蛋白 (Aß) 和 tau 的类淋巴清除率，从而导致淀粉样蛋白沉积和 tau 聚集，从而导致大脑结构发生变化，从而导致认识。人们讨论了食欲素调节睡眠和 Aß 病理学。它们的昼夜波动受到睡眠碎片化的抑制，并且在海马萎缩时表达受到抑制，从而导致痴呆症的进展。此外，睡眠障碍会导致血管风险增加和血管变化，例如炎症、内皮功能障碍和动脉粥样硬化，从而促进神经退行性病变。有大量证据表明，老年人睡眠结构的变化可能导致痴呆，也有证据表明，睡眠障碍的治疗可以改善认知能力。因此，睡眠障碍应及早发现并治疗。