The oxidative damage theory of aging
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The 'oxidative damage theory of aging' postulates that age-related functional losses are caused by the gradual accumulation of ROS and general oxidative damage to macromolecules, and that ROS reduction and oxidative damage repair attenuate the rate of aging and increase lifespan.
“The “oxidative damage theory of aging” [206] thus postulates that: (1) age-related functional losses are caused by the gradual accumulation of ROS and general oxidative damage to macromolecules, and that (2) ROS reduction and oxidative damage repair attenuate the rate of aging and increases lifespan.”
From Nrf2 and Oxidative Stress: A General Overview of Mechanisms and Implications in Human Disease (2022) · cites this paper as [206]
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Sequence Analysis of the Entire Mitochondrial Genome in Parkinson's Disease
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Nrf2 and Oxidative Stress: A General Overview of Mechanisms and Implications in Human Disease
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Aging Hallmarks and Progression and Age-Related Diseases: A Landscape View of Research Advancement
Tenchov, R., Sasso, J. M., Wang, X., & Zhou, Q. A. (2024) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.3c00531 · Cited by 276 · see citing works
Aging causes partial loss of basal forebrain but no loss of pontine reticular cholinergic neurons
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- Authors
- Lin, M. T., & Flint Beal, M.
- Affiliations
- Cornell University (US)
- Venue
- Clinical Neuroscience Research
- Publisher
- Elsevier BV
- Published
- 2003-01
- Volume
- 2
- Issue
- 5-6
- Pages
- 305-315
- ISSN
- 1566-2772 (ISSN-L)
- OpenAlex
- W1983478218
- Cited by
- 89
- References
- 120
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 5 · 2023: 12 · 2022: 9 · 2021: 2 · 2020: 5 · 2019: 1 · 2018: 1 · 2017: 1 · 2016: 6 · 2015: 4 · 2014: 3 · 2013: 1 · 2012: 6
- FWCI
- 1.04
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Clinical Neuroscience Research (publishedVersion)
- Funders
- National Institute on Aging
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- oxidative damage, mitochondrial DNA mutations, superoxide dismutase, methionine sulfoxide reductase, caloric restriction, 4-phenylbutyric acid, lifespan extension, cytochrome oxidase activity, brain aging, DNA damage accumulation
About these checks
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.
Statistics and arithmetic are recomputed, not judged.
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