Sleep and Alzheimer disease pathology--a bidirectional relationship
Yo-El S Ju1, Brendan P Lucey1, David M Holtzman1
1Washington University School of Medicine, Department of Neurology, Washington University, 660 South Euclid Avenue, Box 8111, St Louis, MO 63110, USA.
Nature Reviews. Neurology
|December 25, 2013
Summary
Sleep disturbances may increase Alzheimer disease (AD) risk by affecting amyloid-β (Aβ) peptide levels. Addressing sleep issues could offer new avenues for AD diagnosis and treatment.
Area of Science:
- Neuroscience
- Sleep Medicine
- Alzheimer's Disease Research
Background:
- Alzheimer disease (AD) pathogenesis involves amyloid-β (Aβ) peptide accumulation.
- Factors beyond age and genetics may contribute to AD risk.
- Emerging evidence links the sleep-wake cycle to brain Aβ levels.
Purpose of the Study:
- To investigate the relationship between the sleep-wake cycle and amyloid-β (Aβ) peptide levels in the brain.
- To explore the bidirectional influence between sleep disturbances and Alzheimer disease (AD) progression.
Main Methods:
- Utilized experimental models to assess the impact of sleep deprivation and extension on soluble Aβ concentrations.
- Examined sleep patterns in individuals with early Aβ deposition and mild AD dementia.
Main Results:
- Sleep deprivation in experimental models led to increased soluble Aβ and chronic Aβ accumulation.
- Sleep extension demonstrated an inverse effect on Aβ levels.
- Individuals with early Aβ deposition and mild AD dementia reported sleep abnormalities.
Conclusions:
- The sleep-wake cycle significantly influences Aβ levels, impacting AD pathogenesis.
- A bidirectional relationship exists between Aβ accumulation and sleep disturbances in AD.
- Sleep modulation presents potential implications for AD diagnosis and therapeutic strategies.
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