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Research Articles, Neurobiology of Disease

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 7 August 2019, 39 (32) 6315-6324; DOI: https://doi.org/10.1523/JNEUROSCI.0503-19.2019
Joseph R. Winer
1Center for Human Sleep Science, Department of Psychology, University of California Berkeley, Berkeley, California 94720,
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Bryce A. Mander
1Center for Human Sleep Science, Department of Psychology, University of California Berkeley, Berkeley, California 94720, 2Department of Psychiatry and Human Behavior, University of California Irvine, Orange, California 92697,
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Randolph F. Helfrich
3Helen Wills Neuroscience Institute, University of California Berkeley, Berkeley, California 94720,
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Anne Maass
3Helen Wills Neuroscience Institute, University of California Berkeley, Berkeley, California 94720, 4German Center for Neurodegenerative Diseases, Magdeburg 39120, Germany, and
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Theresa M. Harrison
3Helen Wills Neuroscience Institute, University of California Berkeley, Berkeley, California 94720,
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Suzanne L. Baker
5Molecular Biophysics and Integrated Bioimaging, Lawrence Berkeley National Laboratory, Berkeley, California 94720
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Robert T. Knight
3Helen Wills Neuroscience Institute, University of California Berkeley, Berkeley, California 94720,
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William J. Jagust
3Helen Wills Neuroscience Institute, University of California Berkeley, Berkeley, California 94720, 5Molecular Biophysics and Integrated Bioimaging, Lawrence Berkeley National Laboratory, Berkeley, California 94720
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Matthew P. Walker
1Center for Human Sleep Science, Department of Psychology, University of California Berkeley, Berkeley, California 94720, 3Helen Wills Neuroscience Institute, University of California Berkeley, Berkeley, California 94720,
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Abstract

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 PET 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 <1 Hz 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 noninvasive, cost-effective, and scalable biomarkers (current and future forecasting) of AD pathology, and carry both therapeutic and public health implications.

SIGNIFICANCE STATEMENT 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 PET, the present study reveals human sleep signatures that 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.

  • aging
  • Alzheimer's disease
  • beta-amyloid
  • PET
  • sleep
  • tau
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The Journal of Neuroscience: 39 (32)
Journal of Neuroscience
Vol. 39, Issue 32
7 Aug 2019
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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, Matthew P. Walker
Journal of Neuroscience 7 August 2019, 39 (32) 6315-6324; DOI: 10.1523/JNEUROSCI.0503-19.2019

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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, Matthew P. Walker
Journal of Neuroscience 7 August 2019, 39 (32) 6315-6324; DOI: 10.1523/JNEUROSCI.0503-19.2019
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Keywords

  • aging
  • Alzheimer's disease
  • beta-amyloid
  • PET
  • sleep
  • tau

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