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

William M. Vanderheyden, Miranda M. Lim, Erik S. Musiek and Jason R. Gerstner. Journal of Neuroscience, Volume 38, Issue 12, 21 March 2018, Pages 2901-2910 Read More


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. © 2018 the authors.

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Posted on April 4, 2018
Posted in: Clocks & Sleep, HPAN, Neurodegeneration, Publications Authors: