“Bi-Directional Relationship Between Sleep and Alzheimer’s Disease Pathology”

Hosted by the Center on Biological Rhythms and Sleep (COBRAS)

Abstract: Studies from the Holtzman lab and collaborators have found that the release of both amyloid-β (Aβ) and tau into the extracellular space of the brain is regulated dynamically by the sleep-wake cycle. In addition, chronic sleep deprivation in mouse models increased amyloid deposition and well as tauopathy whereas agents that promote sleep decrease these pathologies. Once Aβ and tau pathology accumulate, this is associated with disruption of the sleep-wake cycle. New data suggest that chronic sleep disruption enhances brain’s innate immune response and disrupts cellular metabolism which contributes to AD pathology accumulation. In addition, some of these effects appear to be APOE isoform-dependent.

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