http://www.frontiersin.org/neuroscience/agingneuroscience/paper/10.3389/fnagi.2010.00024/

Vollständiger Abstract

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<h4>Background</h4>Sleep deprivation is a modifiable risk factor for Alzheimer's disease (AD). Plasma amyloid-β (Aβ) and phosphorylated tau (P-tau) are closely related to cerebral AD pathology and serve as peripheral biomarkers. Our previous work showed that acute sleep deprivation elevated plasma Aβ 40 in healthy adults. Here we conducted an exploratory analysis to examine the effects of sleep deprivation and subsequent recovery on plasma total tau (T-tau) and P-tau181 levels.<h4>Methods</h4>Twenty healthy adults underwent 24 h of total sleep deprivation followed by daytime naps and a full night of recovery. Venous blood was drawn at 12 predefined time points. Plasma T-tau and P-tau181 were measured by enzyme-linked immunosorbent assay (ELISA).<h4>Results</h4>Plasma T-tau increased by 35.09% (<i>P</i> = 0.018) after 24 h of sleep deprivation, and decreased by 37.78% (<i>P</i> = 0.005) after sleep recovery. The rise in T-tau was positively correlated with wakefulness duration (β = 0.629, <i>P</i> < 0.001). In contrast, no significant changes in plasma P-tau181 were detected with sleep deprivation or recovery under the present experimental conditions.<h4>Conclusion</h4>Under an experimental protocol of 24-h sleep deprivation followed by recovery sleep, transient elevation of plasma T-tau (but not P-tau181) was observed in healthy young adults in this exploratory study. These findings indicate that conditions involving short-term sleep loss are associated with fluctuations in a nonspecific plasma marker of neuronal activity.

Abstract: PubMed · Datensatz