Alzheimer's disease (AD) is a devastating and irreversible cognitive impairment and the most common type of dementia. Along with progressive cognitive impairment, dysfunction of the circadian rhythms also plays a pivotal role in the progression of AD. A mutual relationship among circadian rhythms, sleep, and AD has been well-recommended. The etiopathogenesis of the disturbances of the circadian system and AD share some general features that also unlock the outlook of observing them as a mutually dependent pathway. Indeed, the burden of amyloid β (Aβ), neurofibrillary tangles (NFTs), neuroinflammation, oxidative stress, and dysfunction of circadian rhythms may lead to AD. Aging can alter both sleep timings and quality that can be strongly disrupted in AD. Increased production of Aβ and reduced Aβ clearance are caused by a close interplay of Aβ, sleep disturbance and raised wakefulness. Besides Aβ, the impact of tau pathology is possibly noteworthy to the sleep deprivation found in AD. Hence, this review is focused on the primary mechanistic complexities linked to disruption of circadian rhythms, sleep deprivation, and AD. Furthermore, this review also highlights the potential therapeutic strategies to abate AD pathogenesis.

阿尔茨海默氏病（AD）是毁灭性且不可逆的认知障碍，是最常见的痴呆类型。除了进行性认知障碍外，昼夜节律的功能障碍在AD的进展中也起着关键作用。昼夜节律，睡眠和AD之间的相互关系已被很好地推荐。昼夜节律系统和AD的紊乱的病因病因具有一些共同的特征，这些特征也开启了将它们视为相互依赖的途径的前景。确实，淀粉样蛋白β（Aβ），神经原纤维缠结（NFT），神经发炎，氧化应激和昼夜节律紊乱的负担可能导致AD。衰老会改变睡眠时间和睡眠质量，这可能会严重破坏AD。Aβ的紧密相互作用导致Aβ产量增加和Aβ清除率降低，睡眠障碍和清醒。除了Aβ外，tau病理学的影响可能还值得注意于AD中的睡眠剥夺。因此，本综述的重点是与昼夜节律紊乱，睡眠剥夺和AD相关的主要机制的复杂性。此外，本综述还重点介绍了减轻AD发病机理的潜在治疗策略。