Evidence map›Paper›PMID 36497029›Full record

ReviewCells2022

Modulation of the Microglial Nogo-A/NgR Signaling Pathway as a Therapeutic Target for Multiple Sclerosis.

Danica Nheu, Olivia Ellen, Sining Ye, Ezgi Ozturk, Maurice Pagnin, Stephen Kertadjaja, Paschalis Theotokis, Nikolaos Grigoriadis, Catriona McLean, Steven Petratos

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

13 citing papers in PubMed, 13 citations in OpenAlex.

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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

10 authors at 3 institutions in 2 countries.

Danica NheuDepartment of Neuroscience, Central Clinical School, Monash University, Prahran, VIC 3004, Australia.
Olivia EllenDepartment of Neuroscience, Central Clinical School, Monash University, Prahran, VIC 3004, Australia.
Sining YeDepartment of Neuroscience, Central Clinical School, Monash University, Prahran, VIC 3004, Australia.
Ezgi OzturkDepartment of Neuroscience, Central Clinical School, Monash University, Prahran, VIC 3004, Australia.
Maurice PagninDepartment of Neuroscience, Central Clinical School, Monash University, Prahran, VIC 3004, Australia.
Stephen KertadjajaDepartment of Neuroscience, Central Clinical School, Monash University, Prahran, VIC 3004, Australia.ORCID 0000-0001-5784-7868
Paschalis TheotokisLaboratory of Experimental Neurology and Neuroimmunology, Department of Neurology, AHEPA University Hospital, Stilponos Kiriakides str. 1, 54636 Thessaloniki, Greece.ORCID 0000-0001-8607-6695
Nikolaos GrigoriadisLaboratory of Experimental Neurology and Neuroimmunology, Department of Neurology, AHEPA University Hospital, Stilponos Kiriakides str. 1, 54636 Thessaloniki, Greece.
Catriona McLeanDepartment of Anatomical Pathology, Alfred Hospital, Prahran, VIC 3004, Australia.ORCID 0000-0002-0302-5727
Steven PetratosDepartment of Neuroscience, Central Clinical School, Monash University, Prahran, VIC 3004, Australia.ORCID 0000-0003-1211-4577
Monash University · AUAHEPA University Hospital · GRThe Alfred Hospital · AU

Funding

MS Australia ID#212-058
6 · The paper itself

Abstract

Current therapeutics targeting chronic phases of multiple sclerosis (MS) are considerably limited in reversing the neural damage resulting from repeated inflammation and demyelination insults in the multi-focal lesions. This inflammation is propagated by the activation of microglia, the endogenous immune cell aiding in the central nervous system homeostasis. Activated microglia may transition into polarized phenotypes; namely, the classically activated proinflammatory phenotype (previously categorized as M1) and the alternatively activated anti-inflammatory phenotype (previously, M2). These transitional microglial phenotypes are dynamic states, existing as a continuum. Shifting microglial polarization to an anti-inflammatory status may be a potential therapeutic strategy that can be harnessed to limit neuroinflammation and further neurodegeneration in MS. Our research has observed that the obstruction of signaling by inhibitory myelin proteins such as myelin-associated inhibitory factor, Nogo-A, with its receptor (NgR), can regulate microglial cell function and activity in pre-clinical animal studies. Our review explores the microglial role and polarization in MS pathology. Additionally, the potential therapeutics of targeting Nogo-A/NgR cellular mechanisms on microglia migration, polarization and phagocytosis for neurorepair in MS and other demyelination diseases will be discussed.

Indexed as

MicrogliaMultiple SclerosisAnimalsInflammationMyelin ProteinsNogo ProteinsSignal TransductionMyelin ProteinsNogo Proteinsalternatively activated microgliaclassically activated microgliamicrogliamicroglial polarizationmultiple sclerosismyelin debrisNogo-ANogo receptor

Identifiers

PMID36497029
PMCPMC9737582
OpenAlexW4310211215

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.