Evidence map›Paper›PMID 33807572›Full record

ReviewCells2021

Oligodendrocyte Dysfunction in Amyotrophic Lateral Sclerosis: Mechanisms and Therapeutic Perspectives.

Stefano Raffaele, Marta Boccazzi, Marta Fumagalli

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 3% 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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 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

3 authors at 1 institution in 1 country.

Stefano RaffaeleDepartment of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, 20133 Milan, Italy.ORCID 0000-0002-2734-5418
Marta BoccazziDepartment of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, 20133 Milan, Italy.ORCID 0000-0003-0844-1030
Marta FumagalliDepartment of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, 20133 Milan, Italy.ORCID 0000-0002-0158-842X
University of Milan · IT

Funding

Fondazione AriSLA GPR17ALS-1Italian Ministry of University and Research (MIUR) "Department of excellence" 2018-2022Italian Multiple Sclerosis Foundation (FISM) 2019_BS_006
6 · The paper itself

Abstract

Myelin is the lipid-rich structure formed by oligodendrocytes (OLs) that wraps the axons in multilayered sheaths, assuring protection, efficient saltatory signal conduction and metabolic support to neurons. In the last few years, the impact of OL dysfunction and myelin damage has progressively received more attention and is now considered to be a major contributing factor to neurodegeneration in several neurological diseases, including amyotrophic lateral sclerosis (ALS). Upon OL injury, oligodendrocyte precursor cells (OPCs) of adult nervous tissue sustain the generation of new OLs for myelin reconstitution, but this spontaneous regeneration process fails to successfully counteract myelin damage. Of note, the functions of OPCs exceed the formation and repair of myelin, and also involve the trophic support to axons and the capability to exert an immunomodulatory role, which are particularly relevant in the context of neurodegeneration. In this review, we deeply analyze the impact of dysfunctional OLs in ALS pathogenesis. The possible mechanisms underlying OL degeneration, defective OPC maturation, and impairment in energy supply to motor neurons (MNs) have also been examined to provide insights on future therapeutic interventions. On this basis, we discuss the potential therapeutic utility in ALS of several molecules, based on their remyelinating potential or capability to enhance energy metabolism.

Indexed as

Amyotrophic Lateral SclerosisHumansOligodendrogliaamyotrophic lateral sclerosis (ALS)glial cellsGPR17 receptormonocarboxylate transporter 1 (MCT1)neurodegenerative diseaseoligodendrocyte precursor cells (OPCs)oligodendrocytesregenerative medicineremyelination

Identifiers

PMID33807572
PMCPMC8000560
OpenAlexW3133832441

What Socratic 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 Socratic graph.