ArticleThe American journal of pathology2011
Anti-inflammatory effects of FTY720 do not prevent neuronal cell loss in a rat model of optic neuritis.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 32 citations in OpenAlex.
- The physiological and pathological effects of sphingolipid metabolism and signaling in the central nervous system.Brain pathology (Zurich, Switzerland) · 2026Review
- The functional antagonist of sphingosine-1-phosphate, FTY720, impairs gut barrier function.Frontiers in pharmacology · 2024Article
- Molecular Effects of FDA-Approved Multiple Sclerosis Drugs on Glial Cells and Neurons of the Central Nervous System.International journal of molecular sciences · 2020Review
- CatWalk gait analysis in a rat model of multiple sclerosis.BMC neuroscience · 2016Article
- Mitochondrial injury and cognitive function in HIV infection and methamphetamine use.AIDS (London, England) · 2016Article
- Systemic Escherichia coli infection does not influence clinical symptoms and neurodegeneration in experimental autoimmune encephalomyelitis.BMC neuroscience · 2015Article
- Beneficial effect of chronic Staphylococcus aureus infection in a model of multiple sclerosis is mediated through the secretion of extracellular adherence protein.Journal of neuroinflammation · 2015Article
- Neurodegeneration in Autoimmune Optic Neuritis Is Associated with Altered APP Cleavage in Neurons and Up-Regulation of p53.PloS one · 2015Article
- Article
- Sphingolipids in ocular inflammation.Advances in experimental medicine and biology · 2014Review
- Diffusion tensor imaging detects treatment effects of FTY720 in experimental autoimmune encephalomyelitis mice.NMR in biomedicine · 2013Article
- NADH-dehydrogenase type-2 suppresses irreversible visual loss and neurodegeneration in the EAE animal model of MS.Molecular therapy : the journal of the American Society of Gene Therapy · 2013Article
- Fingolimod: direct CNS effects of sphingosine 1-phosphate (S1P) receptor modulation and implications in multiple sclerosis therapy.Journal of the neurological sciences · 2013Review
- Lysophospholipids and their receptors in the central nervous system.Biochimica et biophysica acta · 2013Review
- Current options for the treatment of optic neuritis.Clinical ophthalmology (Auckland, N.Z.) · 2012Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In multiple sclerosis, long-term disability is caused by axonal and neuronal damage. Established therapies target primarily the inflammatory component of the disease, but fail to prevent neurodegeneration. Fingolimod (codenamed FTY720) is an oral sphingosine 1-phosphate (S1P) receptor modulator with promising results in phase II trials in multiple sclerosis patients and is under further development as a novel treatment for multiple sclerosis. To evaluate whether FTY720 has neuroprotective properties, we tested this drug in a rat model of myelin oligodendrocyte glycoprotein-induced optic neuritis. FTY720 exerted significant anti-inflammatory effects during optic neuritis and reduced inflammation, demyelination, and axonal damage; however, FTY720 treatment did not prevent apoptosis of retinal ganglion cells (RGCs), the neurons that form the axons of the optic nerve. Consistent with this lack of effect on RGC survival, FTY720 treatment did not improve visual function, nor did it prevent apoptosis of RGCs in vitro. We observed a persistent activation of apoptotic signaling pathways in RGCs under FTY720 treatment, a possible underlying mechanism for the lack of neuroprotection in the presence of strong anti-inflammatory effects, Furthermore, FTY720 shifted the remaining inflammation in the optic nerve toward neurotoxicity by modest up-regulation of potential neurotoxic cytokines. We conclude that FTY720-induced anti-inflammation and axon protection did not of itself protect neurons from apoptotic cell death.
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