Effect of energy shortage and oxidative stress on amyloid precursor protein metabolism in COS cells
Abstract
The present study investigates the influence of energy related metabolic stress on amyloid precursor protein (APP) non-amyloidogenic secretory processing in COS cells. The effect of glucose deprivation on soluble APP (sAPP) secretion has been evaluated: incubation of COS cells with 50 mM 2-deoxy-D-glucose (2-DG) in glucose free medium was able to reduce sAPP secretion (-26%). Sodium azide (NaN3), an inhibitor of cytochrome c oxidase (complex IV of the mitochondrial electron transfer chain) decreased sAPP release in a concentration dependent way (maximum -75%). Treatment of COS cells with the antioxidant glutathione (GSH) fully antagonized the inhibitory effect of azide (1 mM) and elicited sAPP release over basal level. These results suggest that the inhibition of energy metabolism can influence APP processing leading to a decreased secretion of non-amyloidogenic fragments of APP.
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Mitochondria directly influence other AD-associated pathologies, particularly APP and Aβ homeostasis.
“Data also argue mitochondria directly influence other AD-associated pathologies, and particularly APP and Aβ homeostasis.”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [51]
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 [96]
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 [96]
COX inhibition and ATP depletion both reduced non-amyloidogenic, α secretase-mediated APP processing in cell culture experiments.
“This was directly demonstrated in cell culture experiments in which COX inhibition and ATP depletion both reduced non-amyloidogenic, α secretase-mediated APP processing [95, 96, 98].”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [96]
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 [96]
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References 26 · Cited by 89
- Authors
- Gasparini, L., Racchi, M., Benussi, L., Curti, D., Binetti, G., Bianchetti, A., Trabucchi, M., & Govoni, S.
- Affiliations
- Centro San Giovanni di Dio Fatebenefratelli (IT)
- University of Pavia (IT)
- University of Rome Tor Vergata (IT)
- Corresponding author
- Gasparini, Laura
- ORCID
- Venue
- Neuroscience Letters
- Publisher
- Elsevier BV
- Published
- 1997-08
- Volume
- 231
- Issue
- 2
- Pages
- 113-117
- ISSN
- 0304-3940 (ISSN-L)
- OpenAlex
- W2005748599
- Cited by
- 89
- References
- 26
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 1 · 2023: 5 · 2022: 2 · 2021: 2 · 2020: 5 · 2019: 4 · 2018: 5 · 2017: 3 · 2016: 5 · 2015: 2 · 2014: 2 · 2013: 2 · 2012: 2
- FWCI
- 3.46
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience Letters (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- amyloid precursor protein, energy metabolism, oxidative stress, glucose deprivation, 2-deoxyglucose, sodium azide, cytochrome c oxidase inhibition, glutathione, COS cells, mitochondrial electron transport chain
- MeSH terms
- Animals, Antimetabolites, Azides, Electron Transport Complex IV, Deoxyglucose, Energy Metabolism, Enzyme Inhibitors, Glucose, L-Lactate Dehydrogenase, Amyloid beta-Protein Precursor, Oxidative Stress, COS Cells, Sodium Azide
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