Evidence map›Paper›PMID 30484905›Full record

ArticleGlia2019

The formation of a glial scar does not prohibit remyelination in an animal model of multiple sclerosis.

Michaela Tanja Haindl, Ulrike Köck, Milena Zeitelhofer-Adzemovic, Franz Fazekas, Sonja Hochmeister

Open access · hybridAbstract read
In one paragraph

Article in Glia, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 43 citations in OpenAlex.

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  20. Neuromodulation of Glial Function During Neurodegeneration.Frontiers in cellular neuroscience · 2020
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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

5 authors at 3 institutions in 2 countries.

Michaela Tanja HaindlDepartment of Neurology, Medical University of Graz, Graz, Austria.
Ulrike KöckCenter for Brain Research, Medical University of Vienna, Vienna, Austria.
Milena Zeitelhofer-AdzemovicDepartment of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
Franz FazekasDepartment of Neurology, Medical University of Graz, Graz, Austria.
Sonja HochmeisterDepartment of Neurology, Medical University of Graz, Graz, Austria.ORCID 0000-0002-3925-6455
Medical University of Graz · ATKarolinska Institutet · SEMedical University of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of astrocytes in the pathophysiology of multiple sclerosis (MS) is discussed controversially. Especially the formation of the glial scar is often believed to act as a barrier for remyelination. At the same time, astrocytes are known to produce factors that influence oligodendrocyte precursor cell (OPC) survival. To explore these mechanisms, we investigated the astrocytic reaction in an animal model induced by immunization with myelin oligodendrocyte glycoprotein (MOG) in Dark Agouti (DA) rats, which mimics most of the histological features of MS. We correlated the astroglial reaction by immunohistochemistry (IHC) for glial fibrillary acidic protein (GFAP) to the remyelination capacity by in situ hybridization for mRNA of proteolipid protein (PLP), indicative of OPCs, over the full course of the disease. PLP mRNA peaked in early remyelinating lesions while the amount of GFAP positive astrocytes was highest in remyelinated lesions. In shadow plaques, we found at the same time all features of a glial scar and numbers of OPCs and mature oligodendrocytes, which were nearly equal to that in unaffected white matter areas. To assess the plaque environment, we furthermore quantitatively analyzed factors expressed by astrocytes previously suggested to influence remyelination. From our data, we conclude that remyelination occurs despite an abundant glial reaction in this animal model. The different patterns of astrocytic factors and the occurrence of different astrocytic phenotypes during lesion evolution furthermore indicate a finely regulated, balanced astrocytic involvement leading to successful repair.

Indexed as

AnimalsBrainEncephalomyelitis, Autoimmune, ExperimentalGliosisMaleMyelin SheathNeurogliaRatsRemyelinationSpinal Cordastrocytesglial scarmultiple sclerosisoligodendrocyte precursor cellsremyelinationshadow plaque

Identifiers

PMID30484905
PMCPMC6588096
OpenAlexW2902635016

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Registered trials

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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.