Alzheimer’s disease and sleep–wake disturbances: Amyloid, astrocytes, and animal models

William M. Vanderheyden, Miranda M. Lim, Erik S. Musiek, Jason R. Gerstner

Research output: Contribution to journalArticle

10 Scopus citations

Abstract

Sleep–wake abnormalities are common in patients with Alzheimer’s disease, and can be a major reason for institutionalization. However, an emerging concept is that these sleep–wake disturbances are part of the causal pathway accelerating the neurodegenerative process. Recently, new findings have provided intriguing evidence for a positive feedback loop between sleep–wake dysfunction and β-amyloid (Aβ) aggregation. Studies in both humans and animal models have shown that extended periods of wakefulness increase Aβ levels and aggregation, and accumulation of Aβ causes fragmentation of sleep. This perspective is aimed at presenting evidence supporting causal links between sleep–wake dysfunction and aggregation of Aβ peptide in Alzheimer’s disease, and explores the role of astrocytes, a specialized type of glial cell, in this context underlying Alzheimer’s disease pathology. The utility of current animal models and the unexplored potential of alternative animal models for testing mechanisms involved in the reciprocal relationship between sleep disruption and Aβ are also discussed.

Original languageEnglish (US)
Pages (from-to)2901-2910
Number of pages10
JournalJournal of Neuroscience
Volume38
Issue number12
DOIs
StatePublished - Mar 21 2018

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Keywords

  • Beta-amyloid
  • Circadian rhythms
  • Glia
  • Neurodegeneration

ASJC Scopus subject areas

  • Neuroscience(all)

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