The Interaction Between Sleep and Metabolism in Alzheimer’s Disease: Cause or Consequence of Disease?
Open accessAbstract
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.
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Lactate levels in the interstitial fluid were higher in patients than in unaffected individuals.
“Lactate levels in the interstitial fluid were higher in patients than those in unaffected individuals.29”
From ApoE4-dependent lysosomal cholesterol accumulation impairs mitochondrial homeostasis and oxidative phosphorylation in human astrocytes (2023) · cites this paper as [29]
The “Glucose Metabolism and Neuronal Activity in AD” section (page unavailable) reports increased interstitial-fluid lactate after induced hyperglycemia in rodents, with a greater effect in mice with substantial amyloid pathology. It does not report higher interstitial-fluid lactate in patients than in unaffected people; the cited comparison changes both the population and condition. (LLM, conf=0.82)
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Cited by
Sorted by citations
Lee, H., Cho, S., Kim, M.-J., Park, Y. J., Cho, E., Jo, Y. S., Kim, Y.-S., Lee, J. Y., Thoudam, T., Woo, S.-H., et al. (2023) · Cell Reports · doi:10.1016/j.celrep.2023.113183 · Cited by 93 · see citing works
- Authors
- Carroll, C. M., & Macauley, S. L.
- Affiliations
- Wake Forest University Health Sciences (US)
- Corresponding author
- Macauley, Shannon L.
- Venue
- Frontiers in Aging Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2019-09-20
- Volume
- 11
- Pages
- 258-258
- ISSN
- 1663-4365 (ISSN-L)
- PMC
- PMC6764218
- OpenAlex
- W2970438846
- Cited by
- 32
- References
- 21
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 4 · 2023: 8 · 2022: 3 · 2021: 3 · 2020: 3
- FWCI
- 0.38
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Aging Neuroscience (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Wake Forest University
- National Institute on Aging (R01AG061805, P30AG049638, K01AG050719)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
- Keywords
- Alzheimer's disease, sleep, metabolism, type 2 diabetes, sleep disruption, metabolic dysfunction, metabolic syndrome, disease progression, therapeutic target, aging
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