脑脊液
内科学
内分泌学
白蛋白
睡眠剥夺
睡眠(系统调用)
血浆
医学
阿尔茨海默病
疾病
昼夜节律
操作系统
计算机科学
作者
Haiyan Liu,Nicolas R. Barthélemy,Vitaliy Ovod,James G. Bollinger,Yingxin He,Samir L. Chahin,Brendan Androff,Randall J. Bateman,Brendan P. Lucey
摘要
Abstract Introduction Sleep deprivation increases cerebrospinal fluid (CSF) amyloid beta (Aβ) and tau levels; however, sleep's effect on Aβ and tau in plasma is unknown. Methods In a cross‐over design, CSF Aβ and tau concentrations were measured in five cognitively normal individuals who had blood and CSF collected every 2 hours for 36 hours during sleep‐deprived and normal sleep control conditions. Results Aβ40, Aβ42, unphosphorylated tau threonine181 (T181), unphosphorylated tau threonine‐217 (T217), and phosphorylated T181 (pT181) concentrations increased ∼35% to 55% in CSF and decreased ∼5% to 15% in plasma during sleep deprivation. CSF/plasma ratios of all Alzheimer's disease (AD) biomarkers increased during sleep deprivation while the CSF/plasma albumin ratio, a measure of blood–CSF barrier permeability, decreased. CSF and plasma Aβ42/40, pT181/T181, and pT181/Aβ42 ratios were stable longitudinally in both groups. Discussion These findings show that sleep loss alters some plasma AD biomarkers by lowering brain clearance mechanisms and needs to be taken into account when interpreting individual plasma AD biomarkers but not ratios.
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