ArticleJournal of neuroscience research2017
Effects of fingolimod administration in a genetic model of cognitive deficits.
Article in Journal of neuroscience research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
The trial behind it
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Who cites it
9 citing papers in PubMed.
- Fingolimod Effects on Motor Function and BDNF-TrkB Signaling in a Huntington's Mouse Model Are Disease-Stage-Dependent.International journal of molecular sciences · 2026Article
- Drug repurposing for Alzheimer's disease: a Delphi consensus and stakeholder consultation.Alzheimer's research & therapy · 2025Review
- Drug protection against radiation-induced neurological injury: mechanisms and developments.Archives of toxicology · 2025Review
- Age-Related Transcriptional Deregulation of Genes Coding Synaptic Proteins in Alzheimer's Disease Murine Model: Potential Neuroprotective Effect of Fingolimod.Frontiers in molecular neuroscience · 2021Article
- Fingolimod Affects Transcription of Genes Encoding Enzymes of Ceramide Metabolism in Animal Model of Alzheimer's Disease.Molecular neurobiology · 2020Article
- Photobiomodulation (660 nm) therapy reduces oxidative stress and induces BDNF expression in the hippocampus.Scientific reports · 2019Article
- Modulatory Effects of Fingolimod (FTY720) on the Expression of Sphingolipid Metabolism-Related Genes in an Animal Model of Alzheimer's Disease.Molecular neurobiology · 2019Article
- Developmental Genes and Regulatory Proteins, Domains of Cognitive Impairment in Schizophrenia Spectrum Psychosis and Implications for Antipsychotic Drug Discovery: The Example of Dysbindin-1 Isoforms and Beyond.Frontiers in pharmacology · 2019Review
- Neuropsychiatric Systemic Lupus Erythematosus Is Dependent on Sphingosine-1-Phosphate Signaling.Frontiers in immunology · 2018Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Notwithstanding recent advances, cognitive impairments are among the most difficult-to-treat symptoms in neuropsychiatric disorders. Deficits in information processing contributing to memory and sociability impairments are found across neuropsychiatric-related disorders. Previously, we have shown that mutations in the DTNBP1 gene (encoding dystrobrevin-binding protein 1 [dysbindin-1]) lead to abnormalities in synaptic glutamate release in the prefrontal cortex (PFC) and hippocampus and to cognitive deficits; glutamatergic transmission is important for cortical recurrent excitation that allows information processing in the PFC. To investigate possible means of restoring glutamate release and improving cognitive impairments, we assess the effects of increasing endogenous levels of brain-derived neurotrophic factor (BDNF) in a dysbindin-1-deficient mouse model. Increasing endogenous levels of BDNF may aid in remediating cognitive deficits, given the roles of BDNF in synaptic transmission, plasticity, and neuroprotection. To increase BDNF, we use a novel strategy, repeated intraperitoneal injections of fingolimod (Gilenya). Sphingolipids have recently been shown to have therapeutic value in several neurology-related disorders. Both wild-type (WT) and mutant (MUT) genotypes were tested for sociability and recognition memory, followed by measuring endogenous BDNF levels and presynaptic [Ca
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