Abstract
Alzheimer’s disease (AD) is the most common form of dementia and affects over 45 million people worldwide. Both type-2-diabetes (T2D), a metabolic condition associated with aging, and disrupted sleep are implicated in the pathogenesis of AD, but how sleep and metabolism interact to affect AD progression remains unclear. In the healthy brain, sleep/wake cycles are a well-coordinated interaction between metabolic and neuronal activity, but when disrupted, are associated with a myriad of health-related issues, including metabolic syndrome, cardiovascular disease, T2D, and AD. Therefore, this review will explore our current understanding of the relationship between metabolism, sleep, and AD-related pathology to identify the causes and consequences of disease progression in AD. Moreover, sleep disturbances and metabolic dysfunction could serve as potential therapeutic targets to mitigate the increased risk of AD in individuals with T2D or offer a novel approach for treating AD.
Highlights
Alzheimer’s disease (AD) is severe neurodegenerative disorder characterized by the accumulation of extracellular amyloid plaques and intracellular neurofibrillary tau tangles (NFT), with detectable pathology occurring 15–20 years prior to the onset of clinical symptoms [as reviewed in Holtzman et al (2011)]
We summarize the current understanding of the interplay between metabolism, sleep, and AD pathophysiology with an emphasis on disrupted sleep as a modifiable lifestyle characteristic contributing to increased risk of both AD and T2D
Chronic hyperinsulinemia is thought to lead to lower insulin levels in the brain, which could explain why treating with insulin has been shown to cause memory improvements (Craft et al, 1996; Kern et al, 2001; Rerger et al, 2008). These studies suggest that both abnormal peripheral glucose metabolism and insulin resistance, akin to that seen in T2D, can accelerate AD pathogenesis through alterations in both neuronal and metabolic activity
Summary
Alzheimer’s disease (AD) is severe neurodegenerative disorder characterized by the accumulation of extracellular amyloid plaques and intracellular neurofibrillary tau tangles (NFT), with detectable pathology occurring 15–20 years prior to the onset of clinical symptoms [as reviewed in Holtzman et al (2011)]. It is still unclear how alterations in glucose availability and glycemic variability can modify the relationship between neuronal and metabolic activity to influence AD-related pathology and dementia.
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