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Publication Detail
The Reciprocal Interaction Between Sleep and Alzheimer’s Disease
  • Publication Type:
  • Authors:
    Harris SS, Schwerd-Kleine T, Lee BI, Busche MA
  • Publisher:
    Springer, Cham
  • Publication date:
  • Pagination:
    169, 188
  • Volume:
  • Series:
    Advances in Experimental Medicine and Biology, vol 1344
  • ISBN-13:
  • Status:
  • Book title:
    Circadian Clock in Brain Health and Disease
  • Language:
  • Keywords:
    Alzheimer’s disease, Amyloid-beta, Clinical, Learning and memory, Sleep impairment, Sleep-wake cycle, Slow-wave sleep, Tau, Translational, Aged, Alzheimer Disease, Amyloid beta-Peptides, Basal Forebrain, Humans, Neurodegenerative Diseases, Sleep
  • Notes:
    This version is the author accepted manuscript. For information on re-use, please refer to the publisher’s terms and conditions.
It is becoming increasingly recognized that patients with a variety of neurodegenerative diseases exhibit disordered sleep/wake patterns. While sleep impairments have typically been thought of as sequelae of underlying neurodegenerative processes in sleep-wake cycle regulating brain regions, including the brainstem, hypothalamus, and basal forebrain, emerging evidence now indicates that sleep deficits may also act as pathophysiological drivers of brain-wide disease progression. Specifically, recent work has indicated that impaired sleep can impact on neuronal activity, brain clearance mechanisms, pathological build-up of proteins, and inflammation. Altered sleep patterns may therefore be novel (potentially reversible) dynamic functional markers of proteinopathies and modifiable targets for early therapeutic intervention using non-invasive stimulation and behavioral techniques. Here we highlight research describing a potentially reciprocal interaction between impaired sleep and circadian patterns and the accumulation of pathological signs and features in Alzheimer's disease, the most prevalent neurodegenerative disease in the elderly.
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