Evidence map›Paper›PMID 31399729›Full record

ReviewNature reviews. Drug discovery2019

Progressive multiple sclerosis: from pathophysiology to therapeutic strategies.

Simon Faissner, Jason R Plemel, Ralf Gold, V Wee Yong

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Drug discovery, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 265 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
265citing papers in PubMed, 4 pooled it
35.4field-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

265 citing papers in PubMed, 4 syntheses or guidelines pooled it, 443 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Role of lipoic acid in multiple sclerosis.CNS neuroscience & therapeutics · 2022
    Pooled it
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  13. Observational
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205 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

4 authors at 3 institutions in 2 countries.

Simon FaissnerDepartment of Neurology, St. Josef-Hospital, Ruhr-University Bochum, Bochum, Germany. simon.faissner@rub.de.ORCID http://orcid.org/0000-0002-3412-762X
Jason R PlemelDepartment of Medicine, University of Alberta, Edmonton, Alberta, Canada.ORCID http://orcid.org/0000-0003-1385-1464
Ralf GoldDepartment of Neurology, St. Josef-Hospital, Ruhr-University Bochum, Bochum, Germany.
V Wee YongHotchkiss Brain Institute and Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta, Canada. vyong@ucalgary.ca.ORCID http://orcid.org/0000-0002-2600-3563
University of Calgary · CASt. Josef-Hospital · DEUniversity of Alberta · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system that involves demyelination and axonal degeneration. Although substantial progress has been made in drug development for relapsing-remitting MS, treatment of the progressive forms of the disease, which are characterized clinically by the accumulation of disability in the absence of relapses, remains unsatisfactory. This unmet clinical need is related to the complexity of the pathophysiological mechanisms involved in MS progression. Chronic inflammation, which occurs behind a closed blood-brain barrier with activation of microglia and continued involvement of T cells and B cells, is a hallmark pathophysiological feature. Inflammation can enhance mitochondrial damage in neurons, which, consequently, develop an energy deficit, further reducing axonal health. The growth-inhibitory and inflammatory environment of lesions also impairs remyelination, a repair process that might protect axons from degeneration. Moreover, neurodegeneration is accelerated by the altered expression of ion channels on denuded axons. In this Review, we discuss the current understanding of these disease mechanisms and highlight emerging therapeutic strategies based on these insights, including those targeting the neuroinflammatory and degenerative aspects as well as remyelination-promoting approaches.

Indexed as

Drug DevelopmentAnimalsDemyelinating DiseasesDisease ProgressionHumansInflammationMultiple SclerosisNeurodegenerative Diseases

Identifiers

PMID31399729
OpenAlexW2967983128

What OpenQuestion holds

Textmetadata
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.