Association of Sleep and β-Amyloid Pathology Among Older Cognitively Unimpaired Adults.
Association of Sleep and β-Amyloid Pathology Among Older Cognitively Unimpaired Adults.
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DOI：
10.1001/jamanetworkopen.2021.17573
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发表时间：
2021-07-01
影响因子：
13.8
通讯作者：
Mackin RS
中科院分区：
文献类型：
--
作者：
Insel PS;Mohlenhoff BS;Neylan TC;Krystal AD;Mackin RS
在认知功能未受损的老年人中，白天和夜间睡眠与β淀粉样蛋白（Aβ）病理之间的关联程度和发病时间是什么？在这项对4425名认知未受损参与者的横断面研究中，夜间睡眠每增加1小时，Aβ正电子发射断层扫描标准化摄取值比值就会出现统计学显著性降低，而白天睡眠则会增加Aβ的局部蓄积。这种关联发生在早期，在显著的Aβ积累或认知障碍之前，并且发生在大脑的特定区域。如果较长的睡眠时间导致淀粉样蛋白水平降低，则增加睡眠时间的治疗可能会减少Aβ蓄积，并有助于延迟与Aβ沉积相关的认知功能障碍的发作。睡眠中断通常发生在神经退行性疾病的进展中。有必要对认知功能未受损的成年人进行大规模、特征明确的神经影像学研究，以阐明睡眠与新出现的β淀粉样蛋白（Aβ）病理学之间的关联程度和发病时间。在老年认知未受损成人中评价日间和夜间睡眠持续时间与局部Aβ病理学之间的相关性。在这项横断面研究中，筛选数据收集于2014年4月1日至2017年12月31日之间，来自65至85岁的健康，认知未受损的成年人，他们接受了florbetapir F 18正电子发射断层扫描（PET），具有APOE基因型信息，在简易精神状态检查中得分在25至30之间，并且在无症状阿尔茨海默病（A4）研究中的抗淀粉样蛋白治疗的临床痴呆评级为0。数据分析于2019年12月1日至2021年5月10日进行。自我报告的白天和夜间睡眠时间。局部Aβ病理学，通过florbetapir PET标准化摄取值比率测量。在4425名认知未受损的参与者中获得了淀粉样蛋白PET和睡眠持续时间信息（平均[SD]年龄，71.3 [4.7]岁; 2628名[59.4%]女性; 1509名[34.1%]测试Aβ阳性）。夜间睡眠每增加1小时，Aβ标准摄取值比值降低0.005（F1，4419 = 5.0; P = 0.03），内侧眶额Aβ降低0.009（F1，4419 = 17.4; P < .001），前扣带回Aβ减少0.011（F1，4419 = 15.9; P < .001）。当限制对Aβ检测阴性的参与者进行分析时，夜间睡眠与内侧眶额Aβ降低0.006（F1，2910 = 16.9; P <0.001）和前扣带回Aβ降低0.005（F1，2910 = 7.6; P = 0.03）相关。在Aβ检测阴性的参与者中，白天睡眠与楔前叶Aβ增加0.013（F1，2910 = 7.3; P = 0.03）和后扣带回Aβ增加0.024（F1，2910 = 14.2; P = 0.001）相关。在这项横断面研究中，随着夜间睡眠时间减少，Aβ沉积风险增加发生在认知障碍或显著Aβ沉积之前的早期。白天睡眠可能与早期Aβ蓄积的风险增加相关，并且似乎不能纠正夜间睡眠的丧失，这表明睡眠在预防Aβ蓄积方面具有昼夜节律依赖性。改善睡眠的治疗可以减少早期Aβ积累，并有助于延迟与早期阿尔茨海默病相关的认知功能障碍的发作。这项横断面研究评估了白天和夜间睡眠时间与老年认知未受损成年人局部β-淀粉样蛋白病理学之间的关系。
What is the magnitude and time of onset of the association between daytime and nighttime sleep with β-amyloid (Aβ) pathology in cognitively unimpaired older adults? In this cross-sectional study of 4425 cognitively unimpaired participants, each additional hour of nighttime sleep was associated with a statistically significant reduction of Aβ positron emission tomographic standardized uptake value ratio, whereas daytime sleep was associated with increased regional accumulation of Aβ. The association occurs early, before significant Aβ accumulation or cognitive impairment, and in specific regions of the brain. If longer sleep duration leads to reduced amyloid levels, treatments increasing sleep duration may reduce Aβ accumulation and aid in delaying the onset of cognitive dysfunction associated with Aβ deposition. Disrupted sleep commonly occurs with progressing neurodegenerative disease. Large, well-characterized neuroimaging studies of cognitively unimpaired adults are warranted to clarify the magnitude and onset of the association between sleep and emerging β-amyloid (Aβ) pathology. To evaluate the associations between daytime and nighttime sleep duration with regional Aβ pathology in older cognitively unimpaired adults. In this cross-sectional study, screening data were collected between April 1, 2014, and December 31, 2017, from healthy, cognitively unimpaired adults 65 to 85 years of age who underwent florbetapir F 18 positron emission tomography (PET), had APOE genotype information, scored between 25 and 30 on the Mini-Mental State Examination, and had a Clinical Dementia Rating of 0 for the Anti-Amyloid Treatment in Asymptomatic Alzheimer Disease (A4) Study. Data analysis was performed from December 1, 2019, to May 10, 2021. Self-reported daytime and nighttime sleep duration. Regional Aβ pathology, measured by florbetapir PET standardized uptake value ratio. Amyloid PET and sleep duration information was acquired on 4425 cognitively unimpaired participants (mean [SD] age, 71.3 [4.7] years; 2628 [59.4%] female; 1509 [34.1%] tested Aβ positive). Each additional hour of nighttime sleep was associated with a 0.005 reduction of global Aβ standardized uptake value ratio (F1, 4419 = 5.0; P = .03), a 0.009 reduction of medial orbitofrontal Aβ (F1, 4419 = 17.4; P < .001), and a 0.011 reduction of anterior cingulate Aβ (F1, 4419 = 15.9; P < .001). When restricting analyses to participants who tested Aβ negative, nighttime sleep was associated with a 0.006 reduction of medial orbitofrontal Aβ (F1,2910 = 16.9; P < .001) and a 0.005 reduction of anterior cingulate Aβ (F1,2910 = 7.6; P = .03). Daytime sleep was associated with a 0.013 increase of precuneus Aβ (F1,2910 = 7.3; P = .03) and a 0.024 increase of posterior cingulate Aβ (F1,2910 = 14.2; P = .001) in participants who tested Aβ negative. In this cross-sectional study, the increased risk of Aβ deposition with reduced nighttime sleep duration occurred early, before cognitive impairment or significant Aβ deposition. Daytime sleep may be associated with an increase in risk for early Aβ accumulation and did not appear to be corrective for loss of nighttime sleep, demonstrating a circadian rhythm dependence of sleep in preventing Aβ accumulation. Treatments that improve sleep may reduce early Aβ accumulation and aid in delaying the onset of cognitive dysfunction associated with early Alzheimer disease. This cross-sectional study evaluates the associations between daytime and nighttime sleep duration with regional β-amyloid pathology in older cognitively unimpaired adults.
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影响因子：
11.2
作者：
Lucey BP;Hicks TJ;McLeland JS;Toedebusch CD;Boyd J;Elbert DL;Patterson BW;Baty J;Morris JC;Ovod V;Mawuenyega KG;Bateman RJ
通讯作者：
Bateman RJ
DOI：
10.1126/science.abb8739
发表时间：
2020-10-02
期刊：
Science (New York, N.Y.)
影响因子：
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作者：
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通讯作者：
Goldman SA
影响因子：
4.8
作者：
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通讯作者：
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DOI：
10.1126/science.1180962
发表时间：
2009-11-13
期刊：
Science (New York, N.Y.)
影响因子：
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作者：
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通讯作者：
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DOI：
10.1126/science.aah4968
发表时间：
2016-11-25
期刊：
Science (New York, N.Y.)
影响因子：
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作者：
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通讯作者：
Holtzman DM