ArticleCNS drugs2019
Fingolimod Increases Brain-Derived Neurotrophic Factor Level Secretion from Circulating T Cells of Patients with Multiple Sclerosis.
Article in CNS drugs, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Fingolimod Acutely Facilitates the Activation of TRKB in a BDNF-dependent Manner.Cellular and molecular neurobiology · 2026Article
- Sphingosine 1-phosphate receptor 1 modulators exert neuroprotective effects in central nervous system disorders.Frontiers in pharmacology · 2025Review
- Neurotrophic factors in multiple sclerosis.Frontiers in immunology · 2025Review
- The Compelling Role of Brain-Derived Neurotrophic Factor Signaling in Multiple Sclerosis: Role of BDNF Activators.CNS neuroscience & therapeutics · 2024Review
- Role of T cell-induced autoimmune response in the pathogenesis of glaucoma.International ophthalmology · 2024Review
- The relevance of BDNF for neuroprotection and neuroplasticity in multiple sclerosis.Frontiers in neurology · 2024Review
- The impact of disease modifying therapies on cognitive functions typically impaired in multiple sclerosis patients: a clinician's review.Frontiers in neurology · 2023Review
- Magnetic resonance imaging and ultrasound elastography in the context of preclinical pharmacological research: significance for the 3R principles.Frontiers in pharmacology · 2023Review
- Molecular Pharmacology and Novel Potential Therapeutic Applications of Fingolimod.Frontiers in pharmacology · 2022Review
- Transcriptomic Analysis of Peripheral Monocytes upon Fingolimod Treatment in Relapsing Remitting Multiple Sclerosis Patients.Molecular neurobiology · 2021Article
- The pattern of thyroiditis in multiple sclerosis: a cross-sectional study in a tertiary care hospital in Egypt.The Egyptian journal of internal medicine · 2020Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe pathophysiology of multiple sclerosis involves an autoimmune and a neurodegenerative mechanism. Central nervous system-infiltrating immune cells in multiple sclerosis also possess a neuroprotective activity through secretion of neurotrophins, such as brain-derived neurotrophic factor. Fingolimod was shown to slow the progression of disability and loss of brain volume.
objectiveThe objective of this study was to explore whether fingolimod induces secretion of neurotrophins by immune cells.
methodsBlood was drawn from 21 patients before the initiation of treatment with fingolimod and at 6 and 12 months of follow-up. The levels of the neurotrophic factors brain-derived neurotrophic factor, glial cell-derived neurotrophic factor, β-nerve growth factor, neurotrophin-3, neurotrophin-4, basic fibroblast growth factor, epidermal growth factor, and vascular endothelial growth factor were screened in the supernatants of separated T cells and monocyte cultures using a customized, multiplex enzyme-linked immunosorbent assay. Brain-derived neurotrophic factor levels were further validated by a specific enzyme-linked immunosorbent assay.
resultsTreatment with fingolimod significantly increased brain-derived neurotrophic factor secretion from T cells. A specific enzyme-linked immunosorbent assay confirmed these results in the supernatant of T cells after 6 and 12 months of therapy.
conclusionsT cells that reach the bloodstream of fingolimod-treated patients with multiple sclerosis may contribute to the neuroprotective effect of this therapy by increased secretion of brain-derived neurotrophic factor. This mechanism of action of fingolimod in patients with multiple sclerosis has not been previously reported.
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