Evidence map›Paper›PMID 30454040›Full record

ReviewActa neuropathologica communications2018

The physiology of foamy phagocytes in multiple sclerosis.

Elien Grajchen, Jerome J A Hendriks, Jeroen F J Bogie

Open access · goldAbstract readReview
In one paragraph

Review in Acta neuropathologica communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

95 citing papers in PubMed, 128 citations in OpenAlex.

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  10. TNFR2 signaling shapes the sex-specific remyelinating properties of microglia after experimental stroke.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
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35 more citing papers are in PubMed but not listed here.

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.

Elien GrajchenBiomedical Research Institute, Hasselt University, Diepenbeek, Belgium/School of Life Sciences, Transnationale Universiteit Limburg, Diepenbeek, Belgium.
Jerome J A HendriksBiomedical Research Institute, Hasselt University, Diepenbeek, Belgium/School of Life Sciences, Transnationale Universiteit Limburg, Diepenbeek, Belgium.
Jeroen F J BogieBiomedical Research Institute, Hasselt University, Diepenbeek, Belgium/School of Life Sciences, Transnationale Universiteit Limburg, Diepenbeek, Belgium. Jeroen.bogie@uhasselt.be.ORCID 0000-0002-0016-1926
Hasselt University · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is a chronic disease of the central nervous system characterized by massive infiltration of immune cells, demyelination, and axonal loss. Active MS lesions mainly consist of macrophages and microglia containing abundant intracellular myelin remnants. Initial studies showed that these foamy phagocytes primarily promote MS disease progression by internalizing myelin debris, presenting brain-derived autoantigens, and adopting an inflammatory phenotype. However, more recent studies indicate that phagocytes can also adopt a beneficial phenotype upon myelin internalization. In this review, we summarize and discuss the current knowledge on the spatiotemporal physiology of foamy phagocytes in MS lesions, and elaborate on extrinsic and intrinsic factors regulating their behavior. In addition, we discuss and link the physiology of myelin-containing phagocytes to that of foamy macrophages in other disorders such atherosclerosis.

Indexed as

AnimalsDemyelinating DiseasesHumansMacrophagesMicrogliaMultiple SclerosisMyelin SheathPhagocytesMacrophageMicrogliaMultiple sclerosisNeuroinflammationPolarizationRemyelination

Identifiers

PMID30454040
PMCPMC6240956
OpenAlexW2900813984

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.