The role of free radicals in the aging brain and Parkinson’s Disease: Convergence and parallelism
Open accessAbstract
Free radical production and their targeted action on biomolecules have roles in aging and age-related disorders such as Parkinson's disease (PD). There is an age-associated increase in oxidative damage to the brain, and aging is considered a risk factor for PD. Dopaminergic neurons show linear fallout of 5-10% per decade with aging; however, the rate and intensity of neuronal loss in patients with PD is more marked than that of aging. Here, we enumerate the common link between aging and PD at the cellular level with special reference to oxidative damage caused by free radicals. Oxidative damage includes mitochondrial dysfunction, dopamine auto-oxidation, α-synuclein aggregation, glial cell activation, alterations in calcium signaling, and excess free iron. Moreover, neurons encounter more oxidative stress as a counteracting mechanism with advancing age does not function properly. Alterations in transcriptional activity of various pathways, including nuclear factor erythroid 2-related factor 2, glycogen synthase kinase 3β, mitogen activated protein kinase, nuclear factor kappa B, and reduced activity of superoxide dismutase, catalase and glutathione with aging might be correlated with the increased incidence of PD.
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Altered glial cell activity is a major source of free radicals under altered neurological conditions.
“Altered glial cell activity is a major source of free radicals under altered neurological conditions [78],”
From Beneficial Effects of Spirulina Consumption on Brain Health (2022) · cites this paper as [78]
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- Authors
- Kumar, H., Lim, H.-W., More, S. V., Kim, B.-W., Koppula, S., Kim, I. S., & Choi, D.-K.
- Affiliations
- Konkuk University (KR)
- Corresponding author
- Choi, Dong-Kug
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2012-08-21
- Volume
- 13
- Issue
- 8
- Pages
- 10478-10504
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC3431873
- OpenAlex
- W2138898590
- Cited by
- 212
- References
- 220
- Citations by year
- 2026: 4 · 2025: 15 · 2024: 9 · 2023: 16 · 2022: 29 · 2021: 18 · 2020: 18 · 2019: 15 · 2018: 17 · 2017: 14 · 2016: 8 · 2015: 16 · 2014: 11 · 2013: 21 · 2012: 1
- FWCI
- 2.25
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Konkuk University
- Ministry of Knowledge Economy
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- free radicals, Parkinson's disease, brain aging, oxidative stress, oxidative damage, dopaminergic neurons, mitochondrial dysfunction, alpha-synuclein aggregation, glial activation, calcium signaling, free iron, NF-κB, Nrf2, glycogen synthase kinase-3β, mitogen-activated protein kinase, superoxide dismutase, catalase, glutathione
- MeSH terms
- Aging, Animals, Brain, Free Radicals, Humans, Oxidation-Reduction, Parkinson Disease, Oxidative Stress
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.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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