Evidence map›Paper›PMID 27235538›Full record

ReviewMechanisms of ageing and development2017

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

Kai-Hei Tse, Karl Herrup

Open access · greenAbstract readReview
In one paragraph

Review in Mechanisms of ageing and development, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

68 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Dying oligodendrocytes persist without mitochondria.bioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. Review
  6. Glial Cells and Aging: From the CNS to the Cerebellum.International journal of molecular sciences · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Oligodendrocyte Maturation Alters the Cell Death Mechanisms That Cause Demyelination.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  18. Article
  19. Review
  20. Article

8 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Kai-Hei TseDivision of Life Science, The Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong. Electronic address: frankitse@ust.hk.
Karl HerrupDivision of Life Science, The Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong.
Hong Kong University of Science and Technology · HK

Funding

The function of ATM protein in the biology of the adult neuron CNS:R01NS071022 · NINDS · RUTGERS, THE STATE UNIV OF N.J. · PI PLUMMER, MARK R. · 2010 to 2014
$2.0M
NINDS NIH HHS R01 NS071022
6 · The paper itself

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.

Indexed as

DNA DamageAgingAlzheimer DiseaseAnimalsBrainCell DifferentiationHumansNeuronsOligodendrogliaAging brainAlzheimer’s diseaseDNA damageOligodendrocyteProgeriod syndromesWhite matter

Identifiers

PMID27235538
PMCPMC5124419
OpenAlexW2399828612

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.