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.
Original language | English |
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Article number | 258 |
Journal | Frontiers in Aging Neuroscience |
Volume | 11 |
DOIs | |
State | Published - Sep 20 2019 |
Bibliographical note
Funding Information:The authors would like to thank their colleagues for the careful review and critique of this manuscript. Funding. We would like to acknowledge the following grants: 1K01AG050719 (SM), R01AG061805 (SM), NCDRC Pilot Award (SM), and the Wake Forest University Alzheimer’s Disease Research Center (P30 AG049638), which is funded by the National Institute on Aging.
Publisher Copyright:
© Copyright © 2019 Carroll and Macauley.
Keywords
- Alzheimer’s disease
- glucose
- insulin
- metabolism
- sleep
- type-2-diabetes
ASJC Scopus subject areas
- Aging
- Cognitive Neuroscience