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Samuel Gobraeil Gina Rizq

Abstract

Introduction: Alzheimer’s disease (AD) is the most common neurodegenerative disorder, impacting 55 million people worldwide. With rates on the rise, research is continually being conducted to find potential causes, that are leading to its growing prevalence. There is growing evidence showing a bidirectional relationship between sleep and AD, where poor sleep contributes to the development of AD, and conversely, AD pathology impairs patients’ sleep quality and quantity. 


Methods: A narrative review was conducted in a systematic fashion using the databases PubMed, Embase and the Cochrane Library. After performing a literature search, high-quality relevant sources are selected, and important data is extracted and analyzed to explore the relationship between AD and lack of sleep. 


Results: A bi-directional relationship was suggested based off evidence which was gathered from longitudinal studies and cross-sectional studies. As well as experimental studies which was focused on the mechanisms of AD, including Tau protein aggregation and beta-amyloid accumulation.


Discussion: Results showed that there could be a potential bi-directional relationship when discussing AD and sleep.  In AD, metabolic waste known as beta-amyloid creates neurotoxic plaques which form in the spaces between the neurons. Studies suggest that Aβ has an important role to play in sleep as increased sleep disturbances are present with Aβ accumulation.  Conversely, after losing one night of sleep there is an increase in beta-amyloid, highlighting the role of sleep in metabolite clearance. Another AD protein associated with sleep is Tau. Poor sleep is associated with clumping of Tau, forming toxic tangles inside neurons which injure tissues nearby and contributes to cognitive impairment. However, it still difficult to conclude the directionality of sleep and AD due to limitations on the current technologies used to detect amyloid-beta and Tau.


Conclusion: This narrative review concludes that a bi-directional relationship may be present between sleep abnormalities and AD. Management of poor sleep quality should be further considered as a potential prophylactic intervention against AD. 

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Section
Review