Mitochondrial DNA damage in a mouse model of Alzheimer's disease decreases amyloid beta plaque formation
Open accessAbstract
Mitochondrial DNA (mtDNA) damage and the generation of reactive oxygen species have been associated with and implicated in the development and progression of Alzheimer's disease. To study how mtDNA damage affects reactive oxygen species and amyloid beta (Aβ) pathology in vivo, we generated an Alzheimer's disease mouse model expressing an inducible mitochondrial-targeted endonuclease (Mito-PstI) in the central nervous system. Mito-PstI cleaves mtDNA causing mostly an mtDNA depletion, which leads to a partial oxidative phosphorylation defect when expressed during a short period in adulthood. We found that a mild mitochondrial dysfunction in adult neurons did not exacerbate Aβ accumulation and decreased plaque pathology. Mito-PstI expression altered the cleavage pathway of amyloid precursor protein without increasing oxidative stress in the brain. These data suggest that mtDNA damage is not a primary cause of Aβ accumulation.
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Brains of mice engineered to overproduce mutant APP and PS1 in the setting of less COX holoenzyme show reduced plaque deposition, less fibrillar Aβ, and less oxidative stress than APP-PS1 mice that can freely produce COX.
“The brains of these mice show reduced plaque deposition, less fibrillar Aβ, and less oxidative stress than APP-PS1 mice that can freely produce COX [175, 176].”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [176]
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References 74 · Cited by 47
- Authors
- Pinto, M., Pickrell, A. M., Fukui, H., & Moraes, C. T.
- Affiliations
- University of Miami (US)
- Corresponding author
- Moraes, Carlos T.
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2013-10
- Volume
- 34
- Issue
- 10
- Pages
- 2399-2407
- ISSN
- 0197-4580 (ISSN-L)
- PMC
- PMC4020357
- OpenAlex
- W2092011963
- Cited by
- 47
- References
- 74
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 2 · 2023: 7 · 2022: 4 · 2021: 6 · 2020: 2 · 2019: 1 · 2018: 3 · 2017: 4 · 2016: 3 · 2015: 2 · 2014: 5 · 2013: 3
- FWCI
- 3.01
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neurobiology of Aging (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (1R01AG036871, 1R01NS079965, 5R01EY010804, 5T32NS007492, 5T32NS007459)
- American Heart Association (11Pre7610007)
- Lois Pope LIFE Fellowship
- 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
- mitochondrial DNA damage, Alzheimer's disease, amyloid plaques, amyloid precursor protein cleavage, mtDNA depletion, oxidative phosphorylation, mitochondrial dysfunction, reactive oxygen species, oxidative stress, mouse model
- MeSH terms
- Alzheimer Disease, Animals, Brain, Disease Models, Animal, DNA Damage, DNA, Mitochondrial, Endonucleases, Mice, Inbred C57BL, Mice, Transgenic, Amyloid beta-Peptides, Reactive Oxygen Species, Plaque, Amyloid
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