Spatial correlation between brain aerobic glycolysis and amyloid-β (Aβ) deposition
Open accessAbstract
Amyloid-β (Aβ) plaque deposition can precede the clinical manifestations of dementia of the Alzheimer type (DAT) by many years and can be associated with changes in brain metabolism. Both the Aβ plaque deposition and the changes in metabolism appear to be concentrated in the brain's default-mode network. In contrast to prior studies of brain metabolism which viewed brain metabolism from a unitary perspective that equated glucose utilization with oxygen consumption, we here report on regional glucose use apart from that entering oxidative phosphorylation (so-called "aerobic glycolysis"). Using PET, we found that the spatial distribution of aerobic glycolysis in normal young adults correlates spatially with Aβ deposition in individuals with DAT and cognitively normal participants with elevated Aβ, suggesting a possible link between regional aerobic glycolysis in young adulthood and later development of Alzheimer pathology.
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Brain aerobic glycolysis was previously found to be highest in regions most vulnerable to amyloid deposition.
“Similarly, brain AG was previously found to be highest in regions most vulnerable to amyloid deposition”
From Aerobic glycolysis in the human brain is associated with development and neotenous gene expression (2014) · cites this paper as Vlassenko et al., 2010
Aerobic glycolysis identifies regions most vulnerable to amyloid-beta deposition in Alzheimer's disease.
“Further, AG identifies regions most vulnerable to amyloid-beta deposition in Alzheimer’s disease”
From Aerobic glycolysis in the human brain is associated with development and neotenous gene expression (2014) · cites this paper as Vlassenko et al., 2010
Young ApoE4 carriers showed increased brain activity in default network regions, as well as in the hippocampus and the temporal lobe, possibly due to increased aerobic glycolysis.
“Young ApoE4 carriers showed increased brain activity in default network regions, as well as in the hippocampus and the temporal lobe, possibly due to increased aerobic glycolysis.34”
From ApoE4-dependent lysosomal cholesterol accumulation impairs mitochondrial homeostasis and oxidative phosphorylation in human astrocytes (2023) · cites this paper as [34]
Abundant data from human and cell-based studies either suggest or demonstrate bioenergetic factors regulate both APP processing and Aβ production.
“Whether Aβ changes precede either age-related or AD-related brain bioenergetic changes is less clear-cut, especially since abundant data from human and cell-based studies either suggest or demonstrate bioenergetic factors regulate both APP processing and Aβ production [95–100].”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [99]
Whether Aβ changes precede either age-related or AD-related brain bioenergetic changes is less clear-cut.
“Whether Aβ changes precede either age-related or AD-related brain bioenergetic changes is less clear-cut, especially since abundant data from human and cell-based studies either suggest or demonstrate bioenergetic factors regulate both APP processing and Aβ production [95–100].”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [99]
Brain plaque deposition anatomically corresponds to the fMRI-defined default mode network (DMN), a brain region characterized by relatively high glycolysis rates.
“Brain plaque deposition anatomically corresponds to the functional magnetic resonance imaging (fMRI)-defined default mode network (DMN), a brain region characterized by relatively high glycolysis rates [69, 99, 136].”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [99]
Bioenergetic metabolism affects APP processing and Aβ production.
“Bioenergetic metabolism certainly affects APP processing and Aβ production.”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [99]
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- Authors
- Vlassenko, A. G., Vaishnavi, S. N., Couture, L., Sacco, D., Shannon, B. J., Mach, R. H., Morris, J. C., Raichle, M. E., & Mintun, M. A.
- Affiliations
- Washington University in St. Louis (US)
- Departments of aRadiology,
- Neurology,
- Corresponding author
- Mintun, Mark A.
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2010-09-13
- Volume
- 107
- Issue
- 41
- Pages
- 17763-17767
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC2955133
- OpenAlex
- W2137243283
- Cited by
- 404
- References
- 84
- Citations by year
- 2026: 20 · 2025: 21 · 2024: 15 · 2023: 21 · 2022: 26 · 2021: 22 · 2020: 24 · 2019: 20 · 2018: 28 · 2017: 41 · 2016: 20 · 2015: 23 · 2014: 28 · 2013: 33 · 2012: 28
- FWCI
- 20.41
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5p20mh077967-04, AG05681, AG003991)
- National Institute on Aging (P50AG005681, P01AG003991)
- National Institute of Mental Health (P20MH-077967)
- National Institute of Neurological Disorders and Stroke (F30NS057901, P30NS048056, P50NS006833)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Medical Imaging Techniques and Applications
- Keywords
- aerobic glycolysis, amyloid-beta deposition, Alzheimer's disease, default mode network, brain glucose metabolism, oxidative phosphorylation, spatial correlation, young adults, positron emission tomography
- MeSH terms
- Adult, Alzheimer Disease, Amyloid, Brain, Female, Glucose, Glycolysis, Humans, Male, Oxygen, Positron-Emission Tomography
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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