Evidence map›Paper›PMID 32696271›Full record

ReviewDrugs in R&D2020

Fingolimod as a Treatment in Neurologic Disorders Beyond Multiple Sclerosis.

Pablo Bascuñana, Luisa Möhle, Mirjam Brackhan, Jens Pahnke

Open access · goldAbstract readReview
In one paragraph

Review in Drugs in R&D, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

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  17. Fatty acid elongation by ELOVL6 hampers remyelination by promoting inflammatory foam cell formation during demyelination.Proceedings of the National Academy of Sciences of the United States of America · 2023
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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

4 authors at 2 institutions in 3 countries.

Pablo BascuñanaDepartment of Neuro-/Pathology, University of Oslo (UiO) and Oslo University Hospital (OUS), Oslo, Norway. pablo.bascunana@medisin.uio.no.ORCID http://orcid.org/0000-0003-2186-8899
Luisa MöhleDepartment of Neuro-/Pathology, University of Oslo (UiO) and Oslo University Hospital (OUS), Oslo, Norway.
Mirjam BrackhanDepartment of Neuro-/Pathology, University of Oslo (UiO) and Oslo University Hospital (OUS), Oslo, Norway.
Jens PahnkeDepartment of Neuro-/Pathology, University of Oslo (UiO) and Oslo University Hospital (OUS), Oslo, Norway. jens.pahnke@medisin.uio.no.
Oslo University Hospital · NOLatvia University of Life Sciences and Technologies · LV

Funding

Deutsche Forschungsgemeinschaft (DE) DFG PA930/12Helse Sør-Øst RHF 2016062Helse Sør-Øst RHF 2019054Helse Sør-Øst RHF 2019055Horizon 2020 643417 (JPco-fuND)Horizon 2020 Framework Programme 643417 (PROP-AD)Leibniz-Gemeinschaft (DE) SAW-2015-IPB-2Ministerium für Wissenschaft und Wirtschaft, Land Sachsen-Anhalt EFREMinisterium für Wissenschaft und Wirtschaft, Land Sachsen-Anhalt ZS/2016/05/78617Nasjonalforeningen for Folkehelsen 16154Norsk forskningsrådet 251290 FRIMEDIONorsk forskningsrådet 260786 PROP-AD
6 · The paper itself

Abstract

Fingolimod is an approved treatment for relapsing-remitting multiple sclerosis (MS), and its properties in different pathways have raised interest in therapy research for other neurodegenerative diseases. Fingolimod is an agonist of sphingosine-1-phosphate (S1P) receptors. Its main pharmacologic effect is immunomodulation by lymphocyte homing, thereby reducing the numbers of T and B cells in circulation. Because of the ubiquitous expression of S1P receptors, other effects have also been described. Here, we review preclinical experiments evaluating the effects of treatment with fingolimod in neurodegenerative diseases other than MS, such as Alzheimer's disease or epilepsy. Fingolimod has shown neuroprotective effects in different animal models of neurodegenerative diseases, summarized here, correlating with increased brain-derived neurotrophic factor and improved disease phenotype (cognition and/or motor abilities). As expected, treatment also induced reductions in different neuroinflammatory markers because of not only inhibition of lymphocytes but also direct effects on astrocytes and microglia. Furthermore, fingolimod treatment exhibited additional effects for specific neurodegenerative disorders, such as reduction of amyloid-β production, and antiepileptogenic properties. The neuroprotective effects exerted by fingolimod in these preclinical studies are reviewed and support the translation of fingolimod into clinical trials as treatment in neurodegenerative diseases beyond neuroinflammatory conditions (MS).

Indexed as

Alzheimer DiseaseAnimalsAnti-Inflammatory Agents, Non-SteroidalDisease Models, AnimalDrug Evaluation, PreclinicalEpilepsyFingolimod HydrochlorideHumansLymphocytesMiceMultiple SclerosisNervous System DiseasesNeuroprotective AgentsRatsSphingosine 1 Phosphate Receptor ModulatorsAnti-Inflammatory Agents, Non-SteroidalFingolimod HydrochlorideNeuroprotective AgentsSphingosine 1 Phosphate Receptor Modulators

Identifiers

PMID32696271
PMCPMC7419396
OpenAlexW3045327856

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.