Evidence map›Paper›PMID 31313064›Full record

ReviewNeuromolecular medicine2019

Beneficial Effects of Fingolimod in Alzheimer's Disease: Molecular Mechanisms and Therapeutic Potential.

Efthalia Angelopoulou, Christina Piperi

Abstract readReview
PubMed Publisher
In one paragraph

Review in Neuromolecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

24 citing papers in PubMed, 36 citations in OpenAlex.

  1. The Therapeutic Potential of Purmorphamine Across Disease Models.Journal of cellular and molecular medicine · 2026
    Review
  2. Review
  3. Review
  4. Review
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  6. Review
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  8. Glial Sphingosine-Mediated Epigenetic Regulation Stabilizes Synaptic Function inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  9. Review
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  12. Article
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  16. Review
  17. Article
  18. Long-Term Administration of Triterpenoids FromFrontiers in aging neuroscience · 2021
    Article
  19. Article
  20. Tianma Formula Alleviates Dementia via ACER2-Mediated Sphingolipid Signaling Pathway Involving AEvidence-based complementary and alternative medicine : eCAM · 2021
    Article
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

2 authors at 1 institution in 1 country.

Efthalia AngelopoulouDepartment of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, 75 M. Asias Street - Bldg 16, 11527, Athens, Greece.
Christina PiperiDepartment of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, 75 M. Asias Street - Bldg 16, 11527, Athens, Greece. cpiperi@med.uoa.gr.ORCID 0000-0002-2701-0618
National and Kapodistrian University of Athens · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD), the most common cause of dementia remains of unclear etiology with current pharmacological therapies failing to halt disease progression. Several pathophysiological mechanisms have been implicated in AD pathogenesis including amyloid-β protein (Aβ) accumulation, tau hyperphosphorylation, neuroinflammation and alterations in bioactive lipid metabolism. Sphingolipids, such as sphingosine-1-phosphate (S1P) and intracellular ceramide/S1P balance are highly implicated in central nervous system physiology as well as in AD pathogenesis. FTY720/Fingolimod, a structural sphingosine analog and S1P receptor (S1PR) modulator that is currently used in the treatment of relapsing-remitting multiple sclerosis (RRMS) has been shown to exert beneficial effects on AD progression. Recent in vitro and in vivo evidence indicate that fingolimod may suppress Aβ secretion and deposition, inhibit apoptosis and enhance brain-derived neurotrophic factor (BDNF) production. Furthermore, it regulates neuroinflammation, protects against N-methyl-D-aspartate (NMDA)-excitotoxicity and modulates receptor for advanced glycation end products signaling axis that is highly implicated in AD pathogenesis. This review discusses the underlying molecular mechanisms of the emerging neuroprotective role of fingolimod in AD and its therapeutic potential, aiming to shed more light on AD pathogenesis as well as direct future treatment strategies.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsAntigens, NeoplasmApoptosisBlood-Brain BarrierBrain-Derived Neurotrophic FactorDrug Evaluation, PreclinicalFingolimod HydrochlorideHumansImmunologic FactorsInflammationMiceMice, TransgenicMitogen-Activated Protein KinasesAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAntigens, NeoplasmBdnf protein, ratBrain-Derived Neurotrophic FactorFingolimod HydrochlorideImmunologic FactorsMitogen-Activated Protein KinasesMOK protein, humanNerve Tissue ProteinsNeuroprotective AgentsN-MethylaspartatePhosphotransferases (Alcohol Group Acceptor)SphingolipidsSphingosine-1-Phosphate ReceptorsSphingosine Kinasesphingosine kinase 2, humanAlzheimer’s diseaseAmyloid-betaFingolimodS1PSphingolipids

Identifiers

PMID31313064
OpenAlexW2960333761

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.