Neuroprotective Effect of Glatiramer Acetate on Neurofilament Light Chain Leakage and Glutamate Excess in an Animal Model of Multiple Sclerosis
| Autor: | Rina Aharoni, Raya Eilam, Shaul Lerner, Efrat Shavit-Stein, Amir Dori, Joab Chapman, Ruth Arnon |
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| Rok vydání: | 2021 |
| Předmět: |
Encephalomyelitis
Autoimmune Experimental Multiple Sclerosis QH301-705.5 glatiramer acetate (GA) Intermediate Filaments Glutamic Acid glutamate Article Catalysis Inorganic Chemistry Mice Animals Biology (General) Physical and Theoretical Chemistry QD1-999 Molecular Biology Spectroscopy Cerebrospinal Fluid Organic Chemistry neurodegeneration Glatiramer Acetate General Medicine multiple sclerosis (MS) experimental autoimmune encephalomyelitis (EAE) neurofilament light (NFL) neuroprotection Axons Computer Science Applications Mice Inbred C57BL Chemistry Disease Models Animal Neuroprotective Agents Female Myelin-Oligodendrocyte Glycoprotein Peptides |
| Zdroj: | International Journal of Molecular Sciences; Volume 22; Issue 24; Pages: 13419 International Journal of Molecular Sciences International Journal of Molecular Sciences, Vol 22, Iss 13419, p 13419 (2021) |
| ISSN: | 1422-0067 |
| DOI: | 10.3390/ijms222413419 |
| Popis: | Axonal and neuronal pathologies are a central constituent of multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), induced by the myelin oligodendrocyte glycoprotein (MOG) 35–55 peptide. In this study, we investigated neurodegenerative manifestations in chronic MOG 35–55 induced EAE and the effect of glatiramer acetate (GA) treatment on these manifestations. We report that the neuronal loss seen in this model is not attributed to apoptotic neuronal cell death. In EAE-affected mice, axonal damage prevails from the early disease phase, as revealed by analysis of neurofilament light (NFL) leakage into the sera along the disease duration, as well as by immunohistological examination. Elevation of interstitial glutamate concentrations measured in the cerebrospinal fluid (CSF) implies that glutamate excess plays a role in the damage processes inflicted by this disease. GA applied as a therapeutic regimen to mice with apparent clinical symptoms significantly reduces the pathological manifestations, namely apoptotic cell death, NFL leakage, histological tissue damage, and glutamate excess, thus corroborating the neuroprotective consequences of this treatment. |
| Databáze: | OpenAIRE |
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