Lucey Brendan P, Bateman Randall J
Department of Neurology, Washington University School of Medicine, St. Louis, MO, USA.
Department of Neurology, Washington University School of Medicine, St. Louis, MO, USA; Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO, USA; Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO, USA.
Neurobiol Aging. 2014 Sep;35 Suppl 2:S29-34. doi: 10.1016/j.neurobiolaging.2014.03.035. Epub 2014 May 15.
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive cognitive decline that is a growing public health crisis with a prevalence projected to more than double in the next 20 years. Sleep is frequently impaired in individuals with AD. Further, recent studies have linked numerous age-related sleep disturbances such as poor sleep efficiency and sleep apnea, to future risk of cognitive impairment. Aggregation of amyloid-β (Aβ) into extracellular plaques in the brain is a key step in AD pathogenesis and likely begins 20 years before the onset of dementia. Aβ concentrations in both humans and mouse models show Aβ concentrations rise during wakefulness and fall during sleep, that is, an Aβ diurnal pattern. There is evidence in animal models that changes in sleep time alter Aβ deposition, suggesting that sleep may play a role in AD pathogenesis. A hypothetical model for the role of sleep and the Aβ diurnal pattern in AD pathogenesis is proposed.
阿尔茨海默病（AD）是一种神经退行性疾病，其特征是进行性认知衰退，这是一个日益严重的公共卫生危机，预计在未来20年患病率将增加一倍以上。AD患者经常存在睡眠障碍。此外，最近的研究将许多与年龄相关的睡眠障碍，如睡眠效率低下和睡眠呼吸暂停，与未来认知障碍的风险联系起来。淀粉样β蛋白（Aβ）在大脑中聚集成细胞外斑块是AD发病机制中的关键步骤，可能在痴呆症发作前20年就开始了。人类和小鼠模型中的Aβ浓度均显示，Aβ浓度在清醒时升高，在睡眠时下降，即Aβ昼夜模式。动物模型中有证据表明，睡眠时间的变化会改变Aβ沉积，这表明睡眠可能在AD发病机制中起作用。本文提出了一个关于睡眠和Aβ昼夜模式在AD发病机制中作用的假设模型。
