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Trends Neurosci. 2016 Aug;39(8):552-66. doi: 10.1016/j.tins.2016.05.002. Epub 2016 Jun 17.

Sleep: A Novel Mechanistic Pathway, Biomarker, and Treatment Target in the Pathology of Alzheimer's Disease?

Author information

  • 1Sleep and Neuroimaging Laboratory University of California, Berkeley, CA 94720-1650, USA. Electronic address: bamander@berkeley.edu.
  • 2Sleep and Neuroimaging Laboratory University of California, Berkeley, CA 94720-1650, USA.
  • 3Helen Wills Neuroscience Institute, University of California, Berkeley, CA 94720-1650, USA; Molecular Biophysics and Bioimaging Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA.
  • 4Sleep and Neuroimaging Laboratory University of California, Berkeley, CA 94720-1650, USA; Helen Wills Neuroscience Institute, University of California, Berkeley, CA 94720-1650, USA. Electronic address: mpwalker@berkeley.edu.

Abstract

Sleep disruption appears to be a core component of Alzheimer's disease (AD) and its pathophysiology. Signature abnormalities of sleep emerge before clinical onset of AD. Moreover, insufficient sleep facilitates accumulation of amyloid-β (Aβ), potentially triggering earlier cognitive decline and conversion to AD. Building on such findings, this review has four goals: evaluating (i) associations and plausible mechanisms linking non-rapid-eye-movement (NREM) sleep disruption, Aβ, and AD; (ii) a role for NREM sleep disruption as a novel factor linking cortical Aβ to impaired hippocampus-dependent memory consolidation; (iii) the potential diagnostic utility of NREM sleep disruption as a new biomarker of AD; and (iv) the possibility of sleep as a new treatment target in aging, affording preventative and therapeutic benefits.

KEYWORDS:

Alzheimer's disease; aging; amyloid-β; cognitive decline; sleep

PMID:
27325209
PMCID:
PMC4967375
[Available on 2017-08-01]
DOI:
10.1016/j.tins.2016.05.002
[PubMed - in process]
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