Evidence map›Paper›PMID 30098384›Full record

ReviewNeuroscience letters2018

Stroke in CNS white matter: Models and mechanisms.

Miguel Alejandro Marin, S Thomas Carmichael

Abstract readReview
In one paragraph

Review in Neuroscience letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. White matter injury after brain ischemia.Experimental neurology · 2026
    Review
  2. Article
  3. Article
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  6. Article
  7. Review
  8. Article
  9. The Ties That Bind: Glial Transplantation in White Matter Ischemia and Vascular Dementia.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Roles Played by the NaNeurochemical research · 2020
    Article
  18. Severe white matter damage in SHANK3 deficiency: a human and translational study.Annals of clinical and translational neurology · 2020
    Article
  19. 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

2 authors.

Miguel Alejandro MarinDepartment of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, CA, 9009, United States. Electronic address: Mamarin@mednet.ucla.edu.
S Thomas CarmichaelDepartment of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, CA, 9009, United States. Electronic address: SCarmichael@mednet.ucla.edu.

Funding

Mechanisms of White Matter Repair in Subcortical White Matter IschemiaR37NS102185 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CARMICHAEL, STANLEY THOMAS · 2018 to 2024
$2.8M
Mechanisms of Neuronal Regeneration after Stroke in a Novel Neurovascular NicheR01NS053957 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CARMICHAEL, STANLEY THOMAS · 2006 to 2010
$1.8M
Mechanisms of Neural Repair in White Matter StrokeR01NS071481 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CARMICHAEL, STANLEY THOMAS · 2010 to 2014
$1.7M
Mechanisms of Axonal Sprouting After StrokeR01NS045729 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CARMICHAEL, STANLEY THOMAS · 2004 to 2007
$1.1M
NINDS NIH HHS R01 NS045729NINDS NIH HHS R01 NS053957NINDS NIH HHS R01 NS071481NINDS NIH HHS R37 NS102185
6 · The paper itself

Abstract

White matter stroke (WMS) is a debilitating disorder, which is characterized by the formation of ischemic lesions along subcortical white matter tracts of the central nervous system. Initial infarction during the early stages of the disease is often asymptomatic and is thus considered a form of silent stroke. However, over time lesions accumulate, resulting in severe cognitive and motor decline of which there are no known therapies. Functional imaging and post mortem analysis of patients demonstrates a loss of oligodendrocytes and the subsequent damage of myelin as a primary hallmark of WMS lesions. Though the adult mammalian brain maintains the capacity to regenerate adult oligodendrocytes, this process is blocked in the infarcted white matter thereby preventing remyelination. Recent evidence suggests that activation of neural circuits via motor training or direct stimulation drives oligodendrogenesis and de novo myelin synthesis, opening a potential avenue for therapy in WMS.

Indexed as

Disease Models, AnimalAnimalsBrainHumansOligodendrogliaRemyelinationStrokeWhite MatterIschemiaMyelinOligodendrocyteOligodendrocyte precursor cellVascular dementia

Identifiers

PMID30098384
PMCPMC6981238

What OpenQuestion holds

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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.