The DOI matches its Crossref record; 197 of the 197 references it cites were found in a registry or an index.
DNA damage in the oligodendrocyte lineage and its role in brain aging
Open accessAbstract
Myelination is a recent evolutionary addition that significantly enhances the speed of transmission in the neural network. Even slight defects in myelin integrity impair performance and enhance the risk of neurological disorders. Indeed, myelin degeneration is an early and well-recognized neuropathology that is age associated, but appears before cognitive decline. Myelin is only formed by fully differentiated oligodendrocytes, but the entire oligodendrocyte lineage are clear targets of the altered chemistry of the aging brain. As in neurons, unrepaired DNA damage accumulates in the postmitotic oligodendrocyte genome during normal aging, and indeed may be one of the upstream causes of cellular aging - a fact well illustrated by myelin co-morbidity in premature aging syndromes arising from deficits in DNA repair enzymes. The clinical and experimental evidence from Alzheimer's disease, progeroid syndromes, ataxia-telangiectasia and other conditions strongly suggest that oligodendrocytes may in fact be uniquely vulnerable to oxidative DNA damage. If this damage remains unrepaired, as is increasingly true in the aging brain, myelin gene transcription and oligodendrocyte differentiation is impaired. Delineating the relationships between early myelin loss and DNA damage in brain aging will offer an additional dimension outside the neurocentric view of neurodegenerative disease.
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“Ageing is often accompanied by a demyelination process, which is associated with increased levels of DNA oxidative damage in aged oligodendrocytes.147”
From Antiageing strategy for neurodegenerative diseases: from mechanisms to clinical advances (2025) · cites this paper as [147]
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“Other important brain cells affected by senescence are oligodendrocytes, which may lose their ability to myelinate and therefore disrupt axonal health and signaling capabilities when they become senescent [154].”
From DNA repair deficiency and senescence in concussed professional athletes involved in contact sports (2019) · cites this paper as [154]
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Metadata
- Authors
- Tse, K.-H., & Herrup, K.
- Affiliations
- Hong Kong University of Science and Technology (HK)
- Corresponding author
- Tse, Kai-Hei
- Venue
- Mechanisms of Ageing and Development
- Publisher
- Elsevier BV
- Published
- 2017-01
- Volume
- 161
- Issue
- Pt A
- Pages
- 37-50
- ISSN
- 0047-6374 (ISSN-L)
- PMC
- PMC5124419
- OpenAlex
- W2399828612
- Cited by
- 108
- References
- 195
- Citations by year
- 2026: 5 · 2025: 18 · 2024: 7 · 2023: 15 · 2022: 12 · 2021: 15 · 2020: 15 · 2019: 8 · 2018: 7 · 2017: 4
- FWCI
- 3.53
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Mechanisms of Ageing and Development (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Rare & Special e-Zone (The Hong Kong University of Science and Technology) (submittedVersion)
- Funders
- Research Grant Council, Hong Kong SAR (GRF16101315, GRF660813)
- National Key Basic Research Program of China (2013CB530900)
- National Institutes of Health of the United States (NS71022)
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- DNA damage, oligodendrocyte lineage, brain aging, myelination, myelin degeneration, oxidative DNA damage, DNA repair, cellular aging, premature aging syndromes, Alzheimer's disease, progeroid syndromes, ataxia telangiectasia, oligodendrocyte differentiation
- MeSH terms
- Aging, Alzheimer Disease, Animals, Brain, Cell Differentiation, DNA Damage, Humans, Neurons, Oligodendroglia
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