Evidence map›Paper›PMID 23025787›Full record

ArticleASN neuro2012

Astrogliosis during acute and chronic cuprizone demyelination and implications for remyelination.

Norah Hibbits, Jun Yoshino, Tuan Q Le, Regina C Armstrong

Open access · goldAbstract read
In one paragraph

Article in ASN neuro, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
3.3field-weighted citation impact, top 9% 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

66 citing papers in PubMed, 118 citations in OpenAlex.

  1. Article
  2. Article
  3. Cannabinoid CBCell communication and signaling : CCS · 2026
    Article
  4. Review
  5. Review
  6. Article
  7. Dysregulated Cholinergic Signaling Inhibits Oligodendrocyte Maturation Following Demyelination.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  8. Article
  9. Article
  10. Astrocytes: Lessons Learned from the Cuprizone Model.International journal of molecular sciences · 2023
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. The roles of microglia and astrocytes in myelin phagocytosis in the central nervous system.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
    Review
  16. Review
  17. Remyelination in Multiple Sclerosis: Findings in the Cuprizone Model.International journal of molecular sciences · 2022
    Review
  18. Review
  19. Article
  20. Review

6 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

4 authors at 2 institutions in 1 country.

Norah HibbitsNeuroscience Program, Uniformed Services University of Health Sciences 4301 Jones Bridge Road, Bethesda, MD 20814, USA.
Jun Yoshino
Tuan Q Le
Regina C Armstrong
Uniformed Services University of the Health Sciences · USColgate University · US

Funding

REMYELINATION AND AXON INTEGRITY IN CHRONIC DEMYELINATIONR01NS039293 · NINDS · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI ARMSTRONG, REGINA C · 2000 to 2010
$2.5M
NINDS NIH HHS NS39293NINDS NIH HHS R01 NS039293
6 · The paper itself

Abstract

In multiple sclerosis, microglia/macrophage activation and astrocyte reactivity are important components of the lesion environment that can impact remyelination. The current study characterizes these glial populations relative to expression of candidate regulatory molecules in cuprizone demyelinated corpus callosum. Importantly, periods of recovery after acute or chronic cuprizone demyelination are examined to compare conditions of efficient versus limited remyelination, respectively. Microglial activation attenuates after early demyelination. In contrast, astrocyte reactivity persists throughout demyelination and a 6-week recovery period following either acute or chronic demyelination. This astrocyte reaction is characterized by (a) early proliferation, (b) increased expression of GFAP (glial fibrillary acidic protein), Vim (vimentin), Fn1 (fibronectin) and CSPGs (chondroitin sulphate proteoglycans) and (c) elaboration of a dense network of processes. Glial processes elongated in the axonal plane persist throughout lesion areas during both the robust remyelination that follows acute demyelination and the partial remyelination that follows chronic demyelination. However, prolonged astrocyte reactivity with chronic cuprizone treatment does not progress to barrier formation, i.e. dense compaction of astrocyte processes to wall off the lesion area. Multiple candidate growth factors and inflammatory signals in the lesion environment show strong correlations with GFAP across the acute cuprizone demyelination and recovery time course, yet there is more divergence across the progression of chronic cuprizone demyelination and recovery. However, differential glial scar formation does not appear to be responsible for differential remyelination during recovery in the cuprizone model. The astrocyte phenotype and lesion characteristics in this demyelination model inform studies to identify triggers of non-remyelinating sclerosis in chronic multiple sclerosis lesions.

Indexed as

Demyelinating DiseasesAnimalsCell ProliferationChondroitin Sulfate ProteoglycansCicatrixCuprizoneDisease Models, AnimalGene Expression RegulationGlial Fibrillary Acidic ProteinGliosisMaleMiceMice, Inbred C57BLMonoamine Oxidase InhibitorsMyelin Basic ProteinStatistics as TopicChondroitin Sulfate ProteoglycansCuprizoneGlial Fibrillary Acidic ProteinMbp protein, mouseMonoamine Oxidase InhibitorsMyelin Basic Protein

Identifiers

PMID23025787
PMCPMC3483617
OpenAlexW2090699399

What OpenQuestion holds

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LicenceCC BY-NC
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.