Research articleChronic sleep fragmentation exacerbates amyloid β deposition in Alzheimer's disease model mice

- Sleep fragmentation resembling that in AD patients were induced in AD model mice.
- Sleep fragmentation exacerbated amyloid β (Aβ) deposition in the AD mouse brain.
- The severity of Aβ deposition correlated with the extent of sleep fragmentation.

Sleep fragmentation due to intermittent nocturnal arousal resulting in a reduction of total sleep time and sleep efficiency is a common symptom among people with Alzheimer's disease (AD) and elderly people with normal cognitive function. Although epidemiological studies have indicated an association between sleep fragmentation and elevated risk of AD, a relevant disease model to elucidate the underlying mechanisms was lacking owing to technical limitations. Here we successfully induced chronic sleep fragmentation in AD model mice using a recently developed running-wheel-based device and demonstrate that chronic sleep fragmentation increases amyloid β deposition. Notably, the severity of amyloid β deposition exhibited a significant positive correlation with the extent of sleep fragmentation. These findings provide a useful contribution to the development of novel treatments that decelerate the disease course of AD in the patients, or decrease the risk of developing AD in healthy elderly people through the improvement of sleep quality.