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[睡眠与痴呆症]

[Sleep and dementia].

作者信息

Mayer Geert, Stenmanns Carla, Doeppner Thorsten R, Hermann Dirk M, Gronewold Janine

机构信息

Philipps-Universität Marburg, Marburg, Deutschland.

, Privatweg 2, 34582, Borken, Deutschland.

出版信息

Z Gerontol Geriatr. 2023 Nov;56(7):556-560. doi: 10.1007/s00391-023-02237-5. Epub 2023 Sep 7.

Abstract

Aging is associated with changes in sleep structure and cerebral deposition of amyloid beta and tau proteins. Sleep disturbances precede the onset of dementia by years. Comorbid sleep disorders, such as insomnia and sleep-disordered breathing, a family history of dementia and epigenetic factors can contribute to the development of dementia. This article explores the question of the interaction between sleep and dementia based on the existing literature. Alterations caused by slow wave sleep lead to changes in the glymphatic clearance of amyloid beta, tau proteins and other proteins. Transient and chronic sleep disorders cause disturbances in the brain areas responsible for cognition and behavior. Sleep-regulating brain areas are the first to be affected in the neurodegenerative process and accelerate the risk of dementia. Circadian age-related changes in amyloid beta and tau proteins affect the amount and depth of sleep and vice versa. Amyloid beta in cerebrospinal fluid shows an inverse correlation with sleep. Orexins modulate amyloid beta and sleep.

摘要

衰老与睡眠结构的变化以及β-淀粉样蛋白和tau蛋白在大脑中的沉积有关。睡眠障碍在痴呆症发病前数年就已出现。共病的睡眠障碍,如失眠和睡眠呼吸紊乱、痴呆症家族史以及表观遗传因素都可能导致痴呆症的发展。本文基于现有文献探讨睡眠与痴呆症之间的相互作用问题。慢波睡眠引起的改变会导致β-淀粉样蛋白、tau蛋白和其他蛋白质的类淋巴清除率发生变化。短暂性和慢性睡眠障碍会导致负责认知和行为的脑区出现紊乱。调节睡眠的脑区在神经退行性过程中最先受到影响,并加速痴呆症的风险。与年龄相关的β-淀粉样蛋白和tau蛋白的昼夜节律变化会影响睡眠的量和深度,反之亦然。脑脊液中的β-淀粉样蛋白与睡眠呈负相关。食欲素调节β-淀粉样蛋白和睡眠。

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