Evidence map›Paper›PMID 30577457›Full record

ReviewCells2018

Can We Design a Nogo Receptor-Dependent Cellular Therapy to Target MS?

Min Joung Kim, Jung Hee Kang, Paschalis Theotokis, Nikolaos Grigoriadis, Steven Petratos

Abstract readReview
In one paragraph

Review in Cells, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Article
  2. Review
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  6. Article
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  8. 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.

Min Joung KimDepartment of Neuroscience, Central Clinical School, Monash University, Prahran, VIC 3004, Australia. erica.kim@monash.edu.
Jung Hee KangDepartment of Neuroscience, Central Clinical School, Monash University, Prahran, VIC 3004, Australia. jungheekang427@gmail.com.
Paschalis TheotokisB' Department of Neurology, Laboratory of Experimental Neurology and Neuroimmunology, AHEPA University Hospital, Stilponos Kiriakides str. 1, 54636 Thessaloniki, Macedonia, Greece. ptheotokis@gmail.com.
Nikolaos GrigoriadisB' Department of Neurology, Laboratory of Experimental Neurology and Neuroimmunology, AHEPA University Hospital, Stilponos Kiriakides str. 1, 54636 Thessaloniki, Macedonia, Greece. grigoria@med.auth.gr.
Steven PetratosDepartment of Neuroscience, Central Clinical School, Monash University, Prahran, VIC 3004, Australia. steven.petratos@monash.edu.ORCID 0000-0003-1211-4577

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The current landscape of therapeutics designed to treat multiple sclerosis (MS) and its pathological sequelae is saturated with drugs that modify disease course and limit relapse rates. While these small molecules and biologicals are producing profound benefits to patients with reductions in annualized relapse rates, the repair or reversal of demyelinated lesions with or without axonal damage, remains the principle unmet need for progressive forms of the disease. Targeting the extracellular pathological milieu and the signaling mechanisms that drive neurodegeneration are potential means to achieve neuroprotection and/or repair in the central nervous system of progressive MS patients. The Nogo-A receptor-dependent signaling mechanism has raised considerable interest in neurological disease paradigms since it can promulgate axonal transport deficits, further demyelination, and extant axonal dystrophy, thereby limiting remyelination. If specific therapeutic regimes could be devised to directly clear the Nogo-A-enriched myelin debris in an expedited manner, it may provide the necessary CNS environment for neurorepair to become a clinical reality. The current review outlines novel means to achieve neurorepair with biologicals that may be directed to sites of active demyelination.

Indexed as

Cell- and Tissue-Based TherapyNogo ReceptorsAxonsHumansMultiple SclerosisMyelin SheathNeuroaxonal DystrophiesNogo ProteinsRemyelinationNogo ProteinsNogo Receptorsaxonal dystrophyinflammatory demyelinationmultiple sclerosismyelin debrisNogo-ANogo receptorremyelination

Identifiers

PMID30577457
PMCPMC6357095

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.