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本文引用的文献

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Aging Impairs Cerebrovascular Reactivity at Preserved Resting Cerebral Arteriolar Tone and Vascular Density in the Laboratory Rat.衰老损害实验大鼠静息脑小动脉张力和血管密度保持不变时的脑血管反应性。
Front Aging Neurosci. 2019 Nov 8;11:301. doi: 10.3389/fnagi.2019.00301. eCollection 2019.
2
Increased mitochondrial NADPH oxidase 4 (NOX4) expression in aging is a causative factor in aortic stiffening.衰老过程中线粒体 NADPH 氧化酶 4（NOX4）表达增加是导致主动脉僵硬的一个原因。
Redox Biol. 2019 Sep;26:101288. doi: 10.1016/j.redox.2019.101288. Epub 2019 Aug 2.
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Glochidion zeylanicum leaf extracts exhibit lifespan extending and oxidative stress resistance properties in Caenorhabditis elegans via DAF-16/FoxO and SKN-1/Nrf-2 signaling pathways.厚鳞柯叶提取物通过 DAF-16/FoxO 和 SKN-1/Nrf-2 信号通路延长秀丽隐杆线虫寿命并增强其抗氧化应激能力。
Phytomedicine. 2019 Nov;64:153061. doi: 10.1016/j.phymed.2019.153061. Epub 2019 Jul 31.
4
Evidence for sleep-dependent synaptic renormalization in mouse pups.睡眠依赖性突触再调整在小鼠幼仔中的证据。
Sleep. 2019 Oct 21;42(11). doi: 10.1093/sleep/zsz184.
5
Bioinformatic prediction of critical genes and pathways involved in longevity in Drosophila melanogaster.生物信息学预测参与黑腹果蝇长寿的关键基因和途径。
Mol Genet Genomics. 2019 Dec;294(6):1463-1475. doi: 10.1007/s00438-019-01589-1. Epub 2019 Jul 20.
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Aging-induced elevation in circulating complement C1q level is associated with arterial stiffness.衰老导致循环补体 C1q 水平升高与动脉僵硬有关。
Exp Gerontol. 2019 Sep;124:110650. doi: 10.1016/j.exger.2019.110650. Epub 2019 Jul 4.
7
Acute and Chronic Sleep Deprivation-Related Changes in N-methyl-D-aspartate Receptor-Nitric Oxide Signalling in the Rat Cerebral Cortex with Reference to Aging and Brain Lateralization.急性和慢性睡眠剥夺相关的大鼠大脑皮质中 N-甲基-D-天冬氨酸受体-一氧化氮信号的改变，以及与衰老和大脑偏侧性的关系。
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8
Sleep Deprivation by Exposure to Novel Objects Increases Synapse Density and Axon-Spine Interface in the Hippocampal CA1 Region of Adolescent Mice.暴露于新异物体致睡眠剥夺增加青春期小鼠海马 CA1 区突触密度和轴突-棘突界面。
J Neurosci. 2019 Aug 21;39(34):6613-6625. doi: 10.1523/JNEUROSCI.0380-19.2019. Epub 2019 Jul 1.
9
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Geroscience. 2019 Jun;41(3):341-349. doi: 10.1007/s11357-019-00078-y. Epub 2019 Jun 17.
10
Melatonin modifies SOX2 cell proliferation in dentate gyrus and modulates SIRT1 and MECP2 in long-term sleep deprivation.褪黑素可改变齿状回中SOX2细胞的增殖，并在长期睡眠剥夺中调节SIRT1和MECP2。
Neural Regen Res. 2019 Oct;14(10):1787-1795. doi: 10.4103/1673-5374.257537.

睡眠、大脑血管健康与衰老。

Sleep, brain vascular health and ageing.

机构信息

Department of Pharmacology, JSS College of Pharmacy, JSS Academy of Higher Education & Research, Mysuru, Karnataka, 570015, India.

Centre for Experimental Pharmacology and Toxicology, Central Animal Facility, JSS Academy of Higher Education & Research, Mysuru, Karnataka, 570015, India.

出版信息

Geroscience. 2020 Oct;42(5):1257-1283. doi: 10.1007/s11357-020-00235-8. Epub 2020 Aug 3.

DOI:10.1007/s11357-020-00235-8
PMID:32748314
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7525637/
Abstract

Sleep maintains the function of the entire body through homeostasis. Chronic sleep deprivation (CSD) is a prime health concern in the modern world. Previous reports have shown that CSD has profound negative effects on brain vasculature at both the cellular and molecular levels, and that this is a major cause of cognitive dysfunction and early vascular ageing. However, correlations among sleep deprivation (SD), brain vascular changes and ageing have barely been looked into. This review attempts to correlate the alterations in the levels of major neurotransmitters (acetylcholine, adrenaline, GABA and glutamate) and signalling molecules (Sirt1, PGC1α, FOXO, P66, PARP1) in SD and changes in brain vasculature, cognitive dysfunction and early ageing. It also aims to connect SD-induced loss in the number of dendritic spines and their effects on alterations in synaptic plasticity, cognitive disabilities and early vascular ageing based on data available in scientific literature. To the best of our knowledge, this is the first article providing a pathophysiological basis to link SD to brain vascular ageing.

摘要

睡眠通过体内平衡维持全身的功能。慢性睡眠剥夺（CSD）是现代社会的主要健康关注点。先前的报告表明，CSD 在细胞和分子水平上对脑脉管系统有深远的负面影响，这是认知功能障碍和早期血管老化的主要原因。然而，睡眠剥夺（SD）、脑血管变化和衰老之间的相关性几乎没有被研究过。本综述试图将主要神经递质（乙酰胆碱、肾上腺素、GABA 和谷氨酸）和信号分子（Sirt1、PGC1α、FOXO、P66、PARP1）在 SD 中的水平变化与脑脉管系统、认知功能障碍和早期衰老的变化相关联。它还旨在根据科学文献中的现有数据，将 SD 引起的树突棘数量减少及其对突触可塑性、认知障碍和早期血管老化的影响联系起来。据我们所知，这是第一篇提供病理生理学基础将 SD 与脑血管老化联系起来的文章。