Evidence map›Paper›PMID 28790913›Full record

ReviewFrontiers in aging neuroscience2017

The Dual Role of Microglia in ALS: Mechanisms and Therapeutic Approaches.

Maria Concetta Geloso, Valentina Corvino, Elisa Marchese, Alessia Serrano, Fabrizio Michetti, Nadia D'Ambrosi

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in aging neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed, 2 pooled it
14.2field-weighted citation impact, top 1% 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

133 citing papers in PubMed, 2 syntheses or guidelines pooled it, 246 citations in OpenAlex.

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73 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

6 authors at 2 institutions in 1 country.

Maria Concetta GelosoInstitute of Anatomy and Cell Biology, Università Cattolica del Sacro CuoreRome, Italy.
Valentina CorvinoInstitute of Anatomy and Cell Biology, Università Cattolica del Sacro CuoreRome, Italy.
Elisa MarcheseInstitute of Anatomy and Cell Biology, Università Cattolica del Sacro CuoreRome, Italy.
Alessia SerranoInstitute of Anatomy and Cell Biology, Università Cattolica del Sacro CuoreRome, Italy.
Fabrizio MichettiInstitute of Anatomy and Cell Biology, Università Cattolica del Sacro CuoreRome, Italy.
Nadia D'AmbrosiDepartment of Biology, University of Rome Tor VergataRome, Italy.
Università Cattolica del Sacro Cuore · ITUniversity of Rome Tor Vergata · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by a non-cell autonomous motor neuron loss. While it is generally believed that the disease onset takes place inside motor neurons, different cell types mediating neuroinflammatory processes are considered deeply involved in the progression of the disease. On these grounds, many treatments have been tested on ALS animals with the aim of inhibiting or reducing the pro-inflammatory action of microglia and astrocytes and counteract the progression of the disease. Unfortunately, these anti-inflammatory therapies have been only modestly successful. The non-univocal role played by microglia during stress and injuries might explain this failure. Indeed, it is now well recognized that, during ALS, microglia displays different phenotypes, from surveillant in early stages, to activated states, M1 and M2, characterized by the expression of respectively harmful and protective genes in later phases of the disease. Consistently, the inhibition of microglial function seems to be a valid strategy only if the different stages of microglia polarization are taken into account, interfering with the reactivity of microglia specifically targeting only the harmful pathways and/or potentiating the trophic ones. In this review article, we will analyze the features and timing of microglia activation in the light of M1/M2 phenotypes in the main mice models of ALS. Moreover, we will also revise the results obtained by different anti-inflammatory therapies aimed to unbalance the M1/M2 ratio, shifting it towards a protective outcome.

Indexed as

amyotrophic lateral sclerosisanti-inflammatory drugsgenetic modifiersM1/M2 microgliamutant SOD1 miceneuroinflammation

Identifiers

PMID28790913
PMCPMC5524666
OpenAlexW2738927545

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.