Cited by 212Parkinson's Disease Mechanisms and TreatmentsRedox biology and oxidative stressNuclear Receptors and Signaling

The role of free radicals in the aging brain and Parkinson’s Disease: Convergence and parallelism

Open access
Kumar, Hemant, Lim, Hyung-Woo, More, Sandeep Vasant, Kim, Byung-Wook, Koppula, Sushruta, Kim, In Su, Choi, Dong-Kug·2012·International Journal of Molecular Sciences

Abstract

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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  1. [126]Aloisi F Cytokine Production Neuroglia Kettenmann H. Ransom B.R. Oxford University Press New York, NY, USA 2005 285 301

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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)
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
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

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