Cited by 108Neurogenesis and neuroplasticity mechanismsDNA Repair MechanismsGenetics, Aging, and Longevity in Model Organisms

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DNA damage in the oligodendrocyte lineage and its role in brain aging

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Tse, Kai-Hei, Herrup, Karl·2017·Mechanisms of Ageing and Development

DOI 10.1016/j.mad.2016.05.006PMC PMC5124419

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Abstract

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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Authors: Tse, K.-H., & Herrup, K.
Affiliations: Hong Kong University of Science and Technology (HK)
Corresponding author: Tse, Kai-Hei
ORCID: Tse, Kai-Hei
Herrup, Karl
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)
DOI: 10.1016/j.mad.2016.05.006
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
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
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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DNA damage in the oligodendrocyte lineage and its role in brain aging

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