Purpose of review: Suboptimal sleep has been reported as both a comorbidity and risk factor for the development of Alzheimer's disease. Previous research suggests that beta-amyloid (Aβ) may be central to this association, with reports indicating a bi-directional relationship between sleep and Aβ. Here, we review recent animal and human studies investigating the relationship between sleep and measures of Aβ, and explore the potential mechanisms underlying this association.
Recent findings: Two recent animal studies have provided further support for a bi-directional relationship between sleep and Aβ. In addition, five recent human studies support the notion that higher brain Aβ is linked to poor sleep in cognitively healthy individuals. One of the recent human studies utilized polysomnography to link brain Aβ to a disruption in slow wave activity during sleep, which in turn was associated with decreased hippocampal-dependent memory.
Summary: Recent findings indicate that poor sleep is a risk factor for brain Aβ deposition, and Aβ deposition contributes to sleep disruption. Through the conduct of more mechanistic studies, and both longitudinal and intervention human studies, we can further elucidate the clearly complex nature of the relationship between sleep and Aβ.