Evidence map›Paper›PMID 35948371›Full record

ReviewWIREs mechanisms of disease2023

Neurodegeneration in multiple sclerosis.

Gabrielle M Mey, Kedar R Mahajan, Tara M DeSilva

Open access · hybridAbstract readReview
In one paragraph

Review in WIREs mechanisms of disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 7 pooled it
20.0field-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

88 citing papers in PubMed, 7 syntheses or guidelines pooled it, 144 citations in OpenAlex.

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  13. Investigating theResearch in pharmaceutical sciences · 2026
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28 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 2 institutions in 1 country.

Gabrielle M MeyDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, and Case Western Reserve University, Cleveland, Ohio, USA.ORCID 0000-0002-3952-849X
Kedar R MahajanDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, and Case Western Reserve University, Cleveland, Ohio, USA.ORCID 0000-0002-0339-9876
Tara M DeSilvaDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, and Case Western Reserve University, Cleveland, Ohio, USA.ORCID 0000-0002-1212-5762
Cleveland Clinic Lerner College of Medicine · USCleveland Clinic · US

Funding

RESOURCE/SERVICE CORE C - MOLECULAR INFORMATICS MODULEP30EY025585 · NEI · CLEVELAND CLINIC LERNER COM-CWRU · PI BELA ANAND-APTE · 2016 to 2026
$7.7M
Mechanisms of Activity-Dependent Myelination in the Visual SystemR01EY025687 · NEI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DESILVA, TARA MARIA · 2015 to 2019
$2.4M
Mechanisms of retinal degeneration in neuroinflammatory demyelinating diseasesR01EY032342 · NEI · CLEVELAND CLINIC LERNER COM-CWRU · PI DESILVA, TARA MARIA · 2021 to 2024
$1.6M
Cole Eye Institute Vision Science Training ProgramT32EY024236 · NEI · CLEVELAND CLINIC LERNER COM-CWRU · PI ANAND-APTE, BELA · 2015 to 2025
$1.0M
Thalamic MRI, histopathologic, and clinical correlations in multiple sclerosisK23NS109328 · NINDS · CLEVELAND CLINIC LERNER COM-CWRU · PI MAHAJAN, KEDAR · 2018 to 2022
$919k
NEI NIH HHS P30 EY025585NEI NIH HHS R01 EY025687NEI NIH HHS R01 EY032342NEI NIH HHS T32 EY024236NINDS NIH HHS K23 NS109328
6 · The paper itself

Abstract

Axonal loss in multiple sclerosis (MS) is a key component of disease progression and permanent neurologic disability. MS is a heterogeneous demyelinating and neurodegenerative disease of the central nervous system (CNS) with varying presentation, disease courses, and prognosis. Immunomodulatory therapies reduce the frequency and severity of inflammatory demyelinating events that are a hallmark of MS, but there is minimal therapy to treat progressive disease and there is no cure. Data from patients with MS, post-mortem histological analysis, and animal models of demyelinating disease have elucidated patterns of MS pathogenesis and underlying mechanisms of neurodegeneration. MRI and molecular biomarkers have been proposed to identify predictors of neurodegeneration and risk factors for disease progression. Early signs of axonal dysfunction have come to light including impaired mitochondrial trafficking, structural axonal changes, and synaptic alterations. With sustained inflammation as well as impaired remyelination, axons succumb to degeneration contributing to CNS atrophy and worsening of disease. These studies highlight the role of chronic demyelination in the CNS in perpetuating axonal loss, and the difficulty in promoting remyelination and repair amidst persistent inflammatory insult. Regenerative and neuroprotective strategies are essential to overcome this barrier, with early intervention being critical to rescue axonal integrity and function. The clinical and basic research studies discussed in this review have set the stage for identifying key propagators of neurodegeneration in MS, leading the way for neuroprotective therapeutic development. This article is categorized under: Immune System Diseases > Molecular and Cellular Physiology Neurological Diseases > Molecular and Cellular Physiology.

Indexed as

Multiple SclerosisNeurodegenerative DiseasesAnimalsAxonsCentral Nervous SystemDisease Progressionaxonal injurydemyelinating diseasesmultiple sclerosisneurodegenerationneuroinflammation

Identifiers

PMID35948371
PMCPMC9839517
OpenAlexW4291019740

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.