Mitochondrial Aβ A potential cause of metabolic dysfunction in Alzheimer's disease
Abstract
Deficits in mitochondrial function are a characteristic finding in Alzheimer's disease (AD), though the mechanism remains to be clarified. Recent studies revealed that amyloid beta peptide (Abeta) gains access into mitochondrial matrix, which was much more pronounced in both AD brain and transgenic mutant APP mice than in normal controls. Abeta progressively accumulates in mitochondria and mediates mitochondrial toxicity. Interaction of mitochondrial Abeta with mitochondrial enzymes such as amyloid beta binding alcohol dehydrogenase (ABAD) exaggerates mitochondrial stress by inhibiting the enzyme activity, releasing reactive oxygen species (ROS), and affecting glycolytic, Krebs cycle and/or the respiratory chain pathways through the accumulation of deleterious intermediate metabolites. The pathways proposed may play a key role in the pathogenesis of this devastating neurodegenerative disorder, Alzheimer's disease.
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While aberrant Aβ42 accumulation begins in endosomes, mitochondrial Aβ may be a critical contributor in the pathological cascade leading to neuronal dysfunction and pathology in AD.
“Thus, while aberrant Aβ42 accumulation begins in endosomes, mitochondrial Aβ may be a critical contributor in the pathological cascade leading to neuronal dysfunction and pathology in AD [33, 103, 149].”
From Intraneuronal β-amyloid accumulation and synapse pathology in Alzheimer’s disease (2010) · cites this paper as [33]
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Type II Diabetes and Metabolic Syndrome as Risk Factors for Alzheimer’s Disease
Farooqui, A. A. (2017) · Elsevier eBooks · doi:10.1016/b978-0-12-809937-7.00005-7
Diagnosis and Treatment of Alzheimer’s Disease in Elderly and Senile Age
Myakotnykh, V. S. (2019) · Advances in Gerontology · doi:10.1134/s207905701904012x
Small Molecular Weight Compounds Antagonistic to Amyloid Peptide25-35
Williams, W. R. (2021) · Journal of Biosciences and Medicines · doi:10.4236/jbm.2021.91004
“Aβ accumulates within mitochondria and inhibits processes within the respiratory chain [43].”
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Mitochondria, neurosteroids and biological rhythms : implications in health and disease states
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Ferroptosis and Pyroptosis: Association with Three Types of Neurodegenerative Diseases
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Structure and function of Scaptodrosophila lebanonensis alcohol dehydrogenase
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- Authors
- Chen, X., & Yan, S. D.
- Affiliations
- St. Louis VA Medical Center (US)
- Columbia University (US)
- ORCID
- Chen, Xi
- Venue
- IUBMB Life
- Publisher
- Wiley
- Published
- 2006-12
- Volume
- 58
- Issue
- 12
- Pages
- 686-694
- ISSN
- 1521-6543 (ISSN-L)
- OpenAlex
- W2062519141
- Cited by
- 96
- References
- 0
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 3 · 2023: 4 · 2022: 2 · 2021: 4 · 2020: 2 · 2019: 6 · 2018: 5 · 2017: 6 · 2016: 7 · 2015: 8 · 2014: 4 · 2013: 3 · 2012: 7
- FWCI
- 3.76
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- IUBMB Life (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (AG 16736, P01AG017490, P01 AG 17490, R01AG016736)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, amyloid-beta, mitochondrial dysfunction, mitochondrial toxicity, reactive oxygen species, glycolysis, TCA cycle, electron transport chain, APP transgenic mice, metabolic dysfunction
- MeSH terms
- Alzheimer Disease, Electron Transport, Energy Metabolism, Enzymes, Humans, Mitochondria, 3-Hydroxyacyl CoA Dehydrogenases, Amyloid beta-Peptides
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