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Winer JR, Mander BA, Helfrich RF, Maass A, Harrison TM, Baker SL, Knight RT, Jagust WJ, Walker MP. Sleep as a Potential Biomarker of Tau and β-Amyloid Burden in the Human Brain. J Neurosci. 2019 Aug 7;39(32):6315-6324. Epub 2019 Jun 17 PubMed.
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University of Wisonsin
This paper from Winer et al. provides a convincing contribution to the growing literature that objective and subjective measures of sleep are associated with Alzheimer’s disease pathology. In this case, lower amplitude of slow-wave activity (specifically in the 1Hz and below frequency range) was associated with amyloid burden as measured with amyloid PET, and disrupted coupling between slow oscillations and sleep spindles was related to tau pathology in the medial temporal lobe, also measured with PET.
Furthermore, participants completed a questionnaire reporting their estimated average sleep duration in each decade of life. Focusing on sleep duration in midlife and older age (decade intervals from the participants’ 40s to 70s) the researchers determined that self-reported changes in sleep duration were associated with both amyloid and tau pathology. While self-reported measures may have some limitations, it is still interesting to note that midlife decreases in sleep duration (i.e., when participants were in their 50s) appeared to be associated with later life amyloid pathology. This finding underscores the notion that midlife may be a critical time period when trajectories of brain pathology are determined, and may be a time frame when interventions should be implemented to ensure beneficial effects on trajectories of aging. Studies are needed to prospectively test whether treating sleep dysfunction attenuates the accumulation of Alzheimer’s disease pathology.
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