Evidence map›Paper›PMID 30143572›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2018

Experimental Traumatic Brain Injury Identifies Distinct Early and Late Phase Axonal Conduction Deficits of White Matter Pathophysiology, and Reveals Intervening Recovery.

Christina M Marion, Kryslaine L Radomski, Nathan P Cramer, Zygmunt Galdzicki, Regina C Armstrong

Registry-linked trialOpen access · hybridAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06163833 (MATRIx), which is not on this map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
7.7field-weighted citation impact, top 2% 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.

NCT06163833 phase2recruitingnot on this mapstarted 2023, after this paper: background citation

MATRIx: MesenchymAl Stromal Cells for Traumatic bRain Injury

TypeinterventionalSponsorFondazione IRCCS San Gerardo dei TintoriRan2023 to 2026Enrolled78ConditionsTraumatic Brain Injury With Loss of ConsciousnessArmsMesenchymal stromal cell low dosage-80*10^6 cells, Mesenchymal stromal cell low dosage-160*10^6 cells, Placebo-storage solution
3 · Its place in the literature

Who cites it

60 citing papers in PubMed, 113 citations in OpenAlex.

  1. Article
  2. Research progress on biomarkers of traumatic brain injury.Animal models and experimental medicine · 2026
    Review
  3. Article
  4. Article
  5. Frontiers in neuroscience · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
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  20. Review
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

5 authors at 2 institutions in 2 countries.

Christina M MarionCenter for Neuroscience and Regenerative Medicine.ORCID 0000-0003-0381-4109
Kryslaine L RadomskiCenter for Neuroscience and Regenerative Medicine.ORCID 0000-0001-9624-623X
Nathan P CramerCenter for Neuroscience and Regenerative Medicine.
Zygmunt GaldzickiCenter for Neuroscience and Regenerative Medicine.
Regina C ArmstrongCenter for Neuroscience and Regenerative Medicine, regina.armstrong@usuhs.edu.ORCID 0000-0001-7296-6750
Uniformed Services University of the Health Sciences · USInstitut thématique Génétique, génomique et bioinformatique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traumatic brain injury (TBI) patients often exhibit slowed information processing speed that can underlie diverse symptoms. Processing speed depends on neural circuit function at synapses, in the soma, and along axons. Long axons in white matter (WM) tracts are particularly vulnerable to TBI. We hypothesized that disrupted axon-myelin interactions that slow or block action potential conduction in WM tracts may contribute to slowed processing speed after TBI. Concussive TBI in male/female mice was used to produce traumatic axonal injury in the corpus callosum (CC), similar to WM pathology in human TBI cases. Compound action potential velocity was slowed along myelinated axons at 3 d after TBI with partial recovery by 2 weeks, suggesting early demyelination followed by remyelination. Ultrastructurally, dispersed demyelinated axons and disorganized myelin attachment to axons at paranodes were apparent within CC regions exhibiting traumatic axonal injury. Action potential conduction is exquisitely sensitive to paranode abnormalities. Molecular identification of paranodes and nodes of Ranvier detected asymmetrical paranode pairs and abnormal heminodes after TBI. Fluorescent labeling of oligodendrocyte progenitors in

Indexed as

Action PotentialsAnimalsAxonsBrain Injuries, TraumaticCorpus CallosumDisease Models, AnimalFemaleMaleMice, Inbred C57BLMyelin SheathOligodendrogliaWhite Matteraxon damageCLARITYmyelinnerve conductionnode of Ranvierparanode

Identifiers

PMID30143572
PMCPMC6181309
OpenAlexW2888223086

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.