Journal of Alzheimer's disease : JADMay 28, 2017

Does Poor Sleep Increase the Risk of Alzheimer's Disease?

Circadian Biology Weekly Brief ↗PubMed ↗DOI ↗

Updated Apr 1, 2026

Abstract

25-40% of patients with mild-to-moderate Alzheimer's disease experience sleep disturbances.

Sleep disturbances may indicate underlying neurodegeneration in Alzheimer's disease.
A history of sleep disruption could be a potential risk factor for developing Alzheimer's disease.
Emerging evidence suggests that disruptions in the sleep-wake cycle are linked to increased amyloid-beta (Aβ) deposition.
Enhanced Aβ accumulation may be one mechanism through which sleep disturbances contribute to Alzheimer's development.
Other potential mechanisms include brain hypoxia, oxidative stress, circadian rhythm disturbances, overexpression of orexins, and blood-brain barrier impairment.
Further research is needed to clarify the relationship between sleep disturbances and the risk of developing Alzheimer's disease.

Simplified

Sleep disturbances are routinely encountered in Alzheimer's disease (AD) and affect about 25-40% of patients in the mild-to-moderate stages of the disease. In many, sleep pathology may represent a symptom of the underlying neurodegeneration. However, a history of sleep disruption occurring years prior to onset of cognitive symptoms could represent a potential risk factor for AD. The aim of the present narrative review was to evaluate current evidence linking sleep disturbances with AD development and to understand the mechanisms that may contribute to this. Although the mechanisms by which poor sleep may contribute to AD genesis is not fully understood, emerging evidence linking disturbances in the sleep wake cycle with Aβ deposition is shedding light on the relationship between sleep pathology and the subsequent development of AD. Aβ burden appears to be enhanced by sleep-wake cycle disruptions and is suspected as being an important mechanism by which sleep disruptions contribute in AD development. Other mechanisms triggered by sleep disruption may also be involved in AD development, such as brain hypoxia, oxidative stress, circadian activity rhythms disturbances, overexpression of orexins, and blood-brain barrier impairment. Further understanding of the link between sleep disturbances and future development of AD is still needed before sleep disturbances are clearly marked as a preventable risk factor for AD. In these circumstances, early lifestyle interventions to help increase the quantity and quality of sleep may have a favorable outcome on decreasing the incidence of AD and this needs to be investigated further.

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Does Poor Sleep Increase the Risk of Alzheimer's Disease?

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