Abstract
Sleep has a major role in learning, memory consolidation, and metabolic function. Although it is known that sleep restriction increases the accumulation of amyloid β peptide (Aβ) and the risk to develop Alzheimer’s disease (AD), the mechanism behind these effects remains unknown. In this review, we discuss how chronic sleep restriction induces metabolic and cognitive impairments that could result in the development of AD in late life. Here, we integrate evidence regarding mechanisms whereby metabolic signaling becomes disturbed after short or chronic sleep restriction in the context of cognitive impairment, particularly in the accumulation of Aβ in the brain. We also discuss the role of the blood-brain barrier in sleep restriction with an emphasis on the transport of metabolic signals into the brain and Aβ clearance. This review presents the unexplored possibility that the alteration of peripheral metabolic signals induced by sleep restriction, especially insulin resistance, is responsible for cognitive deficit and, subsequently, implicated in AD development.
Highlights
Sleep is a reversible physiological process characterized by the loss of consciousness, reduction in locomotor activity, and decreased response to external stimuli
Free Fatty Acids The sleeping period is accompanied by several hours of fasting, in which the main energy substrate is provided by free fatty acids (FFA) that are released into the circulation from the white adipose tissue (Shostak et al, 2013; Kumar Jha et al, 2015)
Based on the evidence presented, we propose that chronic sleep restriction induces peripheral low-grade inflammation and insulin resistance leading to hyperglycemia which together alter the BBB function (Figure 2)
Summary
Sleep is a reversible physiological process characterized by the loss of consciousness, reduction in locomotor activity, and decreased response to external stimuli. The decrease of REM sleep and SWS is observed in aging (Roffwarg et al, 1966; Li et al, 2018) This fact is relevant in the context of cognitive functions because both REM sleep and SWS are essential for learning and memory consolidation (Ackermann and Rasch, 2014; Boyce et al, 2017). Voluntary sleep restriction is a prevalent problem in modern society (Potter et al, 2016) that affects neurobehavioral and physiological functioning It contributes to the development of a range of negative health outcomes, including cardiovascular diseases, type 2 diabetes, and neurodegenerative diseases (Kincheski et al, 2017; Chattu et al, 2018). We propose that chronic sleep restriction may induce the most common neurodegenerative disease worldwide Alzheimer’s disease (AD), by impairing brain insulin signaling
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