The sleep-wake cycle and Alzheimer's disease: what do we know?

The sleep-wake cycle and Alzheimer's disease: what do we know?
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DOI:
10.2217/nmt.14.33
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发表时间:
2014
影响因子:
2.6
通讯作者:
Holtzman DM
Holtzman DM
中科院分区:
其他
文献类型:
--
作者:
Lim MM;Gerstner JR;Holtzman DM

文献摘要

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睡眠-觉醒障碍是阿尔茨海默病(AD)的一种高度流行且经常致残的特征。AD的主要特征包括淀粉样蛋白斑块的形成,其与淀粉样蛋白-β(Aβ)肽的细胞外积累相关。来自动物和人类研究的证据表明,Aβ病理学可能会破坏睡眠-觉醒周期,因为随着Aβ的积累,会出现更多的睡眠-觉醒碎片。此外,最近在动物和人类研究中的研究表明,睡眠-觉醒周期本身可能影响阿尔茨海默病的发病和进展。在实验模型中,慢性睡眠剥夺增加了淀粉样斑块的沉积,而睡眠延长导致斑块减少。在这篇综述中,我们讨论了睡眠-觉醒周期与AD病理和行为之间相互关系的可能机制,并提出了目前治疗AD睡眠障碍的方法。
Sleep–wake disturbances are a highly prevalent and often disabling feature of Alzheimer’s disease (AD). A cardinal feature of AD includes the formation of amyloid plaques, associated with the extracellular accumulation of the amyloid-β (Aβ) peptide. Evidence from animal and human studies suggests that Aβ pathology may disrupt the sleep–wake cycle, in that as Aβ accumulates, more sleep–wake fragmentation develops. Furthermore, recent research in animal and human studies suggests that the sleep–wake cycle itself may influence Alzheimer’s disease onset and progression. Chronic sleep deprivation increases amyloid plaque deposition, and sleep extension results in fewer plaques in experimental models. In this review geared towards the practicing clinician, we discuss possible mechanisms underlying the reciprocal relationship between the sleep–wake cycle and AD pathology and behavior, and present current approaches to therapy for sleep disorders in AD.