Evidence map›Paper›PMID 28229330›Full record

ReviewMolecular neurobiology2018

The Involvement of the Myelin-Associated Inhibitors and Their Receptors in CNS Plasticity and Injury.

Anthony G Boghdadi, Leon Teo, James A Bourne

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

38 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Oxygen and the Spark of Human Brain Evolution: Complex Interactions of Metabolism and Cortical Expansion across Development and Evolution.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024
    Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Pathophysiology and Therapeutic Approaches for Spinal Cord Injury.International journal of molecular sciences · 2022
    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

3 authors at 1 institution in 1 country.

Anthony G BoghdadiAustralian Regenerative Medicine Institute, Monash University, 15 Innovation Walk (Building 75), Clayton, VIC, 3800, Australia.
Leon TeoAustralian Regenerative Medicine Institute, Monash University, 15 Innovation Walk (Building 75), Clayton, VIC, 3800, Australia.
James A BourneAustralian Regenerative Medicine Institute, Monash University, 15 Innovation Walk (Building 75), Clayton, VIC, 3800, Australia. james.bourne@monash.edu.
Australian Regenerative Medicine Institute · AU

Funding

National Health and Medical Research Council APP1077677National Health and Medical Research Council APP108197
6 · The paper itself

Abstract

The limited capacity for the central nervous system (CNS) to repair itself was first described over 100 years ago by Spanish neuroscientist Ramon Y. Cajal. However, the exact mechanisms underlying this failure in neuronal regeneration remain unclear and, as such, no effective therapeutics yet exist. Numerous studies have attempted to elucidate the biochemical and molecular mechanisms that inhibit neuronal repair with increasing evidence suggesting that several inhibitory factors and repulsive guidance cues active during development actually persist into adulthood and may be contributing to the inhibition of repair. For example, in the injured adult CNS, there are various inhibitory factors that impede the outgrowth of neurites from damaged neurons. One of the most potent of these neurite outgrowth inhibitors is the group of proteins known as the myelin-associated inhibitors (MAIs), present mainly on the membranes of oligodendroglia. Several studies have shown that interfering with these proteins can have positive outcomes in CNS injury models by promoting neurite outgrowth and improving functional recovery. As such, the MAIs, their receptors, and downstream effectors are valid drug targets for the treatment of CNS injury. This review will discuss the current literature on MAIs in the context of CNS development, plasticity, and injury. Molecules that interfere with the MAIs and their receptors as potential candidates for the treatment of CNS injury will additionally be introduced in the context of preclinical and clinical trials.

Indexed as

AnimalsCentral Nervous SystemCentral Nervous System DiseasesHumansMyelin-Associated GlycoproteinMyelin ProteinsMyelin SheathNerve RegenerationNeuritesNeuronal PlasticityNeuronsNogo Receptor 1Myelin-Associated GlycoproteinMyelin ProteinsNogo Receptor 1RTN4R protein, humanGlycoproteinNeurite outgrowth inhibitorNeuroplasticityOligodendrocyteStroke

Identifiers

PMID28229330
OpenAlexW2591018839

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.