ArticleBiomolecules2023
Time- and Sex-Dependent Effects of Fingolimod Treatment in a Mouse Model of Alzheimer's Disease.
Article in Biomolecules, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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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.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- NPC1 deficiency engages a lysosome-genome-immune program linked to neurodegeneration and cellular aging signatures.bioRxiv : the preprint server for biology · 2026Article
- The Role of Sphingosine-1-Phosphate Signaling in Cerebral Ischemia/Reperfusion Injury and Alzheimer's Disease Pathology.International journal of molecular sciences · 2026Review
- Synergistic Neuroprotection in Tauopathic Mice via Green-Synthesized Silver Nanoparticles Co-delivering Methylene Blue and Moringa oleifera.Molecular neurobiology · 2025Article
- Dual Mechanisms of Cognitive Function and Pathological Improvements by the Selective S1PR1/5 Modulator Siponimod in 3xTg-AD Mice.Molecular neurobiology · 2025Article
- Drug repurposing for Alzheimer's disease: a Delphi consensus and stakeholder consultation.Alzheimer's research & therapy · 2025Review
- The sphingosine-1-phosphate signaling pathway (sphingosine-1-phosphate and its receptor, sphingosine kinase) and epilepsy.Epilepsia open · 2025Review
- The ABC transporter A7 modulates neuroinflammation via NLRP3 inflammasome in Alzheimer's disease mice.Alzheimer's research & therapy · 2025Article
- Apolar Extracts of St. John's Wort Alleviate the Effects of β-Amyloid Toxicity in Early Alzheimer's Disease.International journal of molecular sciences · 2024Article
- Repurposing drugs against Alzheimer's disease: can the anti-multiple sclerosis drug fingolimod (FTY720) effectively tackle inflammation processes in AD?Journal of neural transmission (Vienna, Austria : 1996) · 2023Review
- Article
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Authors and funding
8 authors at 2 institutions in 4 countries.
Funding
Abstract
Alzheimer's disease (AD) is the most common cause of dementia. Fingolimod has previously shown beneficial effects in different animal models of AD. However, it has shown contradictory effects when it has been applied at early disease stages. Our objective was to evaluate fingolimod in two different treatment paradigms. To address this aim, we treated male and female APP-transgenic mice for 50 days, starting either before plaque deposition at 50 days of age (early) or at 125 days of age (late). To evaluate the effects, we investigated the neuroinflammatory and glial markers, the Aβ load, and the concentration of the brain-derived neurotrophic factor (BDNF). We found a reduced Aβ load only in male animals in the late treatment paradigm. These animals also showed reduced microglia activation and reduced IL-1β. No other treatment group showed any difference in comparison to the controls. On the other hand, we detected a linear correlation between BDNF and the brain Aβ concentrations. The fingolimod treatment has shown beneficial effects in AD models, but the outcome depends on the neuroinflammatory state at the start of the treatment. Thus, according to our data, a fingolimod treatment would be effective after the onset of the first AD symptoms, mainly affecting the neuroinflammatory reaction to the ongoing Aβ deposition.
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Registered trials
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.