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

Trends Neurosci. 2016 Aug;39(8):552-566. doi: 10.1016/j.tins.2016.05.002. Epub 2016 Jun 17.


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.

Publication types

  • Review
  • Research Support, N.I.H., Extramural

MeSH terms

  • Aging / physiology*
  • Alzheimer Disease / diagnosis
  • Alzheimer Disease / physiopathology*
  • Alzheimer Disease / therapy*
  • Animals
  • Humans
  • Sleep / drug effects
  • Sleep / physiology*