Sleep and Alzheimer disease pathology--a bidirectional relationship.
Sleep and Alzheimer disease pathology--a bidirectional relationship.
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DOI：
10.1038/nrneurol.2013.269
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发表时间：
2014-02
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除年龄和遗传因素外，其他因素可能会增加患阿尔茨海默病（AD）的风险。淀粉样β（Aβ）肽在脑中的积累似乎启动了AD发病机制中的一系列关键事件。此外，有证据表明，睡眠-觉醒周期直接影响大脑中Aβ的水平。在实验模型中，睡眠剥夺会增加可溶性Aβ的浓度，导致Aβ的慢性积累，而睡眠延长则会产生相反的效果。此外，一旦Aβ积累，就会增加觉醒和改变睡眠模式。具有早期Aβ沉积但仍具有正常认知功能的个体报告睡眠异常，由于AD而患有非常轻度痴呆的个体也报告睡眠异常。因此，睡眠和神经退行性疾病可能在许多方面相互影响，对AD的诊断和治疗具有重要意义。
Factors other than age and genetics may increase the risk of developing Alzheimer disease (AD). Accumulation of the amyloid-β (Aβ) peptide in the brain seems to initiate a cascade of key events in the pathogenesis of AD. Moreover, evidence is emerging that the sleep–wake cycle directly influences levels of Aβ in the brain. In experimental models, sleep deprivation increases the concentration of soluble Aβ and results in chronic accumulation of Aβ, whereas sleep extension has the opposite effect. Furthermore, once Aβ accumulates, increased wakefulness and altered sleep patterns develop. Individuals with early Aβ deposition who still have normal cognitive function report sleep abnormalities, as do individuals with very mild dementia due to AD. Thus, sleep and neurodegenerative disease may influence each other in many ways that have important implications for the diagnosis and treatment of AD.