Resumen
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.
| Idioma original | English |
|---|---|
| Número de artículo | 258 |
| Publicación | Frontiers in Aging Neuroscience |
| Volumen | 11 |
| DOI | |
| Estado | Published - sept 20 2019 |
Nota bibliográfica
Publisher Copyright:© Copyright © 2019 Carroll and Macauley.
Financiación
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.
| Financiadores | Número del financiador |
|---|---|
| NCDRC | |
| National Institute on Aging | |
| Alzheimer's Disease Research Center, Wake Forest School of Medicine | P30 AG049638 |
| Alzheimer's Disease Research Center, Wake Forest School of Medicine |
ODS de las Naciones Unidas
Este resultado contribuye a los siguientes Objetivos de Desarrollo Sostenible
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Good health and well being
ASJC Scopus subject areas
- Aging
- Cognitive Neuroscience
Huella
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