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阿尔茨海默病发病机制中睡眠-淀粉样蛋白相互作用之外的研究进展。

Beyond the sleep-amyloid interactions in Alzheimer's disease pathogenesis.

机构信息

Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts.

Graduate Program for Neuroscience, Boston University School of Medicine , Boston, Massachusetts.

出版信息

J Neurophysiol. 2019 Jul 1;122(1):1-4. doi: 10.1152/jn.00118.2019. Epub 2019 Mar 13.

DOI:10.1152/jn.00118.2019
PMID:30864847
Abstract

Cognitive impairment in older adults is associated with sleep and circadian rhythm disturbances. Numerous studies have linked disrupted sleep and circadian rhythms with amyloid-β (Aβ), a key pathological hallmark in Alzheimer's disease (AD). While previous evidence suggests that Aβ initiates AD pathogenesis, tau, another major hallmark of AD, seems to drive neurodegeneration. Recent studies imply that sleep-wake cycles affect brain tau more significantly than Aβ levels, leading to accelerated AD progression and cognitive decline. The study of sleep disturbances in AD is shedding light on our understanding of the mechanism underlying sleep disturbances in AD and dementia.

摘要

老年人认知障碍与睡眠和昼夜节律紊乱有关。大量研究表明,睡眠和昼夜节律紊乱与淀粉样蛋白-β(Aβ)有关,Aβ是阿尔茨海默病(AD)的关键病理标志。虽然先前的证据表明 Aβ引发了 AD 的发病机制,但另一个 AD 的主要标志——tau 似乎会导致神经退行性变。最近的研究表明,睡眠-觉醒周期对大脑 tau 的影响比 Aβ水平更为显著,导致 AD 进展和认知能力下降加速。AD 中睡眠障碍的研究揭示了我们对 AD 和痴呆症中睡眠障碍机制的理解。

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