DNA damage-associated oligodendrocyte degeneration precedes amyloid pathology and contributes to Alzheimer’s disease and dementia
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INTRODUCTION: In looking for novel non-amyloid-based etiologies for Alzheimer's disease, we explore the hypothesis that age-related myelin loss is an attractive explanation for age-associated cognitive decline and dementia. METHODS: We performed a meta-analysis of data in the National Alzheimer's Coordinating Center database accompanied by quantitative histopathology of myelin and oligodendrocytes (OLs) in frontal cortices of 24 clinically characterized individuals. Pathological findings were further validated in an Alzheimer's disease mouse model and in culture. RESULTS: Myelin lesions increased with cognitive impairment in an amyloid-independent fashion with signs of degeneration appearing before neuronal loss. Myelinating OLs in the gray matter showed greater vulnerability than those in white matter, and the degenerative changes correlated with evidence of DNA damage. Similar results were found in myelinating OL cultures where DNA damage caused aberrant OL cell cycle re-entry and death. DISCUSSION: We present the first comprehensive analysis of the cell biology of early myelin loss in sporadic Alzheimer's disease.
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We previously showed that OL population in the frontal cortex diminishes in human dementia brain and in AD transgenic mouse model before any amyloid plaques are formed.
“Yet, we previously showed that OLs population in the frontal cortex diminish in human dementia brain and in AD transgenic mouse model before any amyloid plaques is formed (Tse et al. 2018).”
From Apolipoprotein E ε4 disrupts oligodendrocyte differentiation by interfering with astrocyte‐derived lipid transport (2023) · cites this paper as Tse et al. 2018
Studies using post-mortem human brain samples show that neurons, astrocytes, and oligodendrocytes accumulate DNA double-strand breaks (DSBs) early in the progression of AD.
“Studies using post-mortem human brain samples show that neurons, astrocytes, and oligodendrocytes accumulate DNA double-strand breaks (DSBs) early in the progression of AD”
From Neuronal DNA double-strand breaks lead to genome structural variations and 3D genome disruption in neurodegeneration (2023) · cites this paper as [7]
Neurons start accumulating DSBs early in the progression of AD.
“Neurons start accumulating DSBs early in the progression of AD”
From Neuronal DNA double-strand breaks lead to genome structural variations and 3D genome disruption in neurodegeneration (2023) · cites this paper as [7]
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Dileep, V., Boix, C. A., Mathys, H., Marco, A., Welch, G. M., Meharena, H. S., Loon, A., Jeloka, R., Peng, Z., Bennett, D. A., et al. (2023) · Cell · doi:10.1016/j.cell.2023.08.038 · Cited by 130 · see citing works
Contributions of DNA Damage to Alzheimer’s Disease
Lin, X., Kapoor, A., Gu, Y., Chow, M. J., Peng, J., Zhao, K., & Tang, D. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21051666 · Cited by 117 · see citing works
Thadathil, N., Delotterie, D. F., Xiao, J., Hori, R., McDonald, M. P., & Khan, M. M. (2021) · Molecular Neurobiology · doi:10.1007/s12035-020-02109-8 · Cited by 94 · see citing works
Mok, K. K., Yeung, S. H., Cheng, G. W., Ma, I. W., Lee, R. H., Herrup, K., & Tse, K. (2023) · Journal of Neurochemistry · doi:10.1111/jnc.15748 · Cited by 37 · see citing works
Self-citationSong, X., Aw, J. T. M., Ma, F., Cheung, M. F., Leung, D., & Herrup, K. (2021) · The Journal of Neuroscience · doi:10.1523/jneurosci.0845-21.2021 · Cited by 23 · see citing works
Self-citation
- Authors
- Tse, K., Cheng, A., Ma, F., & Herrup, K.
- Affiliations
- Hong Kong University of Science and Technology (HK)
- Corresponding author
- Tse, Kai‐Hei
- Venue
- Alzheimer's & Dementia
- Publisher
- Wiley
- Published
- 2018-01-09
- Volume
- 14
- Issue
- 5
- Pages
- 664-679
- ISSN
- 1552-5260 (ISSN-L)
- 1552-5279
- PMC
- PMC5938117
- OpenAlex
- W2784120777
- Cited by
- 56
- References
- 87
- Citations by year
- 2026: 11 · 2025: 7 · 2024: 3 · 2023: 7 · 2022: 7 · 2021: 9 · 2020: 10 · 2019: 1 · 2018: 1
- FWCI
- 0.69
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Alzheimer s & Dementia (publishedVersion, public-domain)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Rare & Special e-Zone (The Hong Kong University of Science and Technology) (submittedVersion)
- Funders
- National Institute on Aging (P30 AG019610, P30 AG013846, P50 AG008702, P50 AG025688, P50 AG047266, P30 AG010133, P50 AG005146, P50 AG005134, P50 AG016574, P50 AG005138, P30 AG008051, P30 AG013854, P30 AG008017, P30 AG010161, P50 AG047366, P30 AG010129, P50 AG016573, P50 AG016570, P50 AG005131, P50 AG023501, P30 AG035982, P30 AG028383, P30 AG010124, P50 AG005133, P50 AG005142, P30 AG012300, P50 AG005136, P50 AG033514, P50 AG005681, P50 AG047270, U01 AG016976)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, oligodendrocyte degeneration
- MeSH terms
- Aged, Animals, Cross-Sectional Studies, Dementia, Disease Models, Animal, DNA Damage, Frontal Lobe, Humans, Mice, Transgenic, Middle Aged, Oligodendroglia, Plaque, Amyloid, White Matter
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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