ArticleJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2013
Glatiramer acetate protects against inflammatory synaptopathy in experimental autoimmune encephalomyelitis.
Article in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- A narrative review on the safety of glatiramer acetate in multiple sclerosis: focus on Europe.Therapeutic advances in chronic disease · 2025Review
- Interleukin-9 protects from microglia- and TNF-mediated synaptotoxicity in experimental multiple sclerosis.Journal of neuroinflammation · 2024Article
- Interferon-gamma ameliorates experimental autoimmune encephalomyelitis by inducing homeostatic adaptation of microglia.Frontiers in immunology · 2023Article
- Focus on the Role of the NLRP3 Inflammasome in Multiple Sclerosis: Pathogenesis, Diagnosis, and Therapeutics.Frontiers in molecular neuroscience · 2022Review
- Neuroprotective Effect of Glatiramer Acetate on Neurofilament Light Chain Leakage and Glutamate Excess in an Animal Model of Multiple Sclerosis.International journal of molecular sciences · 2021Article
- Molecular Effects of FDA-Approved Multiple Sclerosis Drugs on Glial Cells and Neurons of the Central Nervous System.International journal of molecular sciences · 2020Review
- Mechanisms of neurobehavioral abnormalities in multiple sclerosis: Contributions from neural and immune components.Clinical neurophysiology practice · 2019Review
- A Comprehensive Review on CopemylNeurology and therapy · 2017Review
- Glutamate, T cells and multiple sclerosis.Journal of neural transmission (Vienna, Austria : 1996) · 2017Review
- CCL5-Glutamate Cross-Talk in Astrocyte-Neuron Communication in Multiple Sclerosis.Frontiers in immunology · 2017Review
- Siponimod (BAF312) prevents synaptic neurodegeneration in experimental multiple sclerosis.Journal of neuroinflammation · 2016Article
- Glatiramer acetate guards against rapid memory decline during relapsing-remitting experimental autoimmune encephalomyelitis.Neurochemical research · 2015Article
- Exploring the role of microglia in mood disorders associated with experimental multiple sclerosis.Frontiers in cellular neuroscience · 2015Article
- Can we switch microglia's phenotype to foster neuroprotection? Focus on multiple sclerosis.Immunology · 2014Review
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glutamate-mediated excitotoxicity is supposed to induce neurodegeneration in multiple sclerosis (MS). Glatiramer acetate (GA) is an immunomodulatory agent used in MS treatment with potential neuroprotective action. Aim of the present study was to investigate whether GA has effects on glutamate transmission alterations occurring in experimental autoimmune encephalomyelitis (EAE), to disclose a possible mechanism of GA-induced neuroprotection in this mouse model of MS. Single neuron electrophysiological recordings and immunofluorescence analysis of microglia activation were performed in the striatum of EAE mice, treated or not with GA, at different stages of the disease. GA treatment was able to reverse the tumor necrosis factor-α (TNF-α)-induced alterations of striatal glutamate-mediated excitatory postsynaptic currents (EPSCs) of EAE mice. Incubation of striatal slices of control animals with lymphocytes taken from EAE mice treated with GA failed to replicate such an anti-glutamatergic effect, while activated microglial cells stimulated with GA in vitro mimicked the effect of GA treatment of EAE mice. Consistently, EAE mice treated with GA had less microglial activation and less TNF-α expression than untreated EAE animals. Furthermore, direct application of GA to EAE slices replicated the in vivo protective activity of GA. Our results show that GA is neuroprotective against glutamate toxicity independently of its peripheral immunodulatory action, and through direct modulation of microglial activation and TNF-α release in the grey matter of EAE and possibly of MS brains.
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