Abstract
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.
Keywords
- Sleep impairment
- Sleep-wake cycle
- Slow-wave sleep
- Learning and memory
- Alzheimer’s disease
- Amyloid-beta
- Tau
- Clinical
- Translational
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Acknowledgements
SSH, TSK, BIL, and MAB are supported by the UK Dementia Research Institute which receives its funding from DRI Ltd, funded by the Medical Research Council, Alzheimer’s Society and Alzheimer Research UK. We acknowledge the donors of Alzheimer’s Disease Research, a program of BrightFocus Foundation, for support of this research (Grant Number: A2019112S). SSH is further supported by a UK DRI Pilot Studies programme award. MAB is further supported by a UKRI Future Leaders Fellowship (Grant Number: MR/S017003/1).
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Harris, S.S., Schwerd-Kleine, T., Lee, B.I., Busche, M.A. (2021). The Reciprocal Interaction Between Sleep and Alzheimer’s Disease. In: Engmann, O., Brancaccio, M. (eds) Circadian Clock in Brain Health and Disease. Advances in Experimental Medicine and Biology, vol 1344. Springer, Cham. https://doi.org/10.1007/978-3-030-81147-1_10
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