Evidence map›Paper›PMID 38395617›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2024

Oligodendrocyte Maturation Alters the Cell Death Mechanisms That Cause Demyelination.

Timothy W Chapman, Yasmine Kamen, Enrique T Piedra, Robert A Hill

Open access · greenAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
9.5field-weighted citation impact, top 1% 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

24 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Cannabinoid CBCell communication and signaling : CCS · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Dying oligodendrocytes persist without mitochondria.bioRxiv : the preprint server for biology · 2026
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Transient Upregulation of Procaspase-3 during Oligodendrocyte Fate Decisions.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  18. Review
  19. Article
  20. Article
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

4 authors at 1 institution in 1 country.

Timothy W ChapmanDepartment of Biological Sciences, Dartmouth College, Hanover, New Hampshire 03755.
Yasmine KamenDepartment of Biological Sciences, Dartmouth College, Hanover, New Hampshire 03755.ORCID 0000-0003-1867-7397
Enrique T PiedraDepartment of Biological Sciences, Dartmouth College, Hanover, New Hampshire 03755.
Robert A HillDepartment of Biological Sciences, Dartmouth College, Hanover, New Hampshire 03755 robert.hill@dartmouth.edu.ORCID 0000-0001-6080-8712
Dartmouth College · US

Funding

Glial Mechanisms Governing the Removal and Repair of Degenerating MyelinR01NS122800 · NINDS · DARTMOUTH COLLEGE · PI HILL, ROBERT A. · 2021 to 2025
$2.3M
NINDS NIH HHS R01 NS122800
6 · The paper itself

Abstract

Myelinating oligodendrocytes die in human disease and early in aging. Despite this, the mechanisms that underly oligodendrocyte death are not resolved and it is also not clear whether these mechanisms change as oligodendrocyte lineage cells are undergoing differentiation and maturation. Here, we used a combination of intravital imaging, single-cell ablation, and cuprizone-mediated demyelination, in both female and male mice, to discover that oligodendrocyte maturation dictates the dynamics and mechanisms of cell death. After single-cell phototoxic damage, oligodendrocyte precursor cells underwent programmed cell death within hours, differentiating oligodendrocytes died over several days, while mature oligodendrocytes took weeks to die. Importantly cells at each maturation stage all eventually died but did so with drastically different temporal dynamics and morphological features. Consistent with this, cuprizone treatment initiated a caspase-3-dependent form of rapid cell death in differentiating oligodendrocytes, while mature oligodendrocytes never activated this executioner caspase. Instead, mature oligodendrocytes exhibited delayed cell death which was marked by DNA damage and disruption in poly-ADP-ribose subcellular localization. Thus, oligodendrocyte maturation plays a key role in determining the mechanism of death a cell undergoes in response to the same insult. This means that oligodendrocyte maturation is important to consider when designing strategies for preventing cell death and preserving myelin while also enhancing the survival of new oligodendrocytes in demyelinating conditions.

Indexed as

CuprizoneDemyelinating DiseasesAnimalsApoptosisCell DifferentiationFemaleHumansMaleMiceMice, Inbred C57BLMyelin SheathOligodendrogliaCuprizonecell deathdemyelinationgliamyelinoligodendrocyte

Identifiers

PMID38395617
PMCPMC10977033
OpenAlexW4392094192

What OpenQuestion holds

Textmetadata
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.