Sleep as a potential biomarker of tau and β-amyloid burden in the human brain
Joseph R. Winer, Bryce A. Mander, Randolph F. Helfrich, Anne Maass, Theresa M. Harrison, Suzanne L. Baker, Robert T. Knight, William J. Jagust and Matthew P. Walker
Journal of Neuroscience 17 June 2019, 0503-19; DOI: https://doi.org/10.1523/JNEUROSCI.0503-19.2019
A new paper from Matthew Walker et al.
Science Daily has a longish discussion/summary of this paper that might be a good substitute for actually reading it: https://www.sciencedaily.com/releases/2019/06/190627114105.htm
Here's the summary from the Journal of Neuroscience link:
Recent proposals suggest that sleep may be a factor associated with accumulation of two core pathological features of Alzheimer's disease (AD): tau and β-amyloid (Aβ). Here we combined positron emission tomography measures of Aβ and tau, electroencephalogram sleep recordings, and retrospective sleep evaluations to investigate the potential utility of sleep measures in predicting in vivo AD pathology in male and female older adults. Regression analyses revealed that the severity of impaired slow oscillation-sleep spindle coupling predicted greater medial temporal lobe tau burden. Aβ burden was not associated with coupling impairment, but instead predicted the diminished amplitude of <1Hz slow-wave-activity—results that were statistically dissociable from each other. Additionally, comparisons of AD pathology and retrospective, self-reported changes in sleep duration demonstrated that changes in sleep across the lifespan can predict late-life Aβ and tau burden. Thus, quantitative and qualitative features of human sleep represent potential non-invasive, cost-effective and scalable biomarkers (current and future-forecasting) of AD pathology, and carry both therapeutic and public-health implications.
Several studies have linked sleep disruption to the progression of Alzheimer's disease (AD). Tau and β-amyloid (Aβ), the primary pathological features of AD, are associated with both objective and subjective changes in sleep. However it remains unknown whether late life tau and Aβ burden are associated with distinct impairments in sleep physiology or changes in sleep across the lifespan. Using polysomnography, retrospective questionnaires, and tau- and Aβ-specific positron emission tomography, the present study reveals human sleep signatures which dissociably predict levels of brain tau and Aβ in older adults. These results suggest that a night of polysomnography may aid in evaluating tau and Aβ burden, and that treating sleep deficiencies within decade-specific time windows may serve in delaying AD progression.
I wonder if "retrospective sleep evaluations" are more trustworthy than the somewhat discredited diet questionnaires that nutritional epidemiologists use.