Neuroprotective effect of glatiramer acetate on neurofilament light chain leakage and glutamate excess in an animal model of multiple sclerosis

Rina Aharoni, Raya Eilam, Shaul Lerner, Efrat Shavit-Stein, Amir Dori, Joab Chapman, Ruth Arnon

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish
Article number13419
JournalInternational Journal of Molecular Sciences
Volume22
Issue number24
DOIs
StatePublished - 1 Dec 2021

Keywords

  • Experimental autoimmune encephalomyelitis (EAE)
  • Glatiramer acetate (GA)
  • Glutamate
  • Multiple sclerosis (MS)
  • Neurodegeneration
  • Neurofilament light (NFL)
  • Neuroprotection

Fingerprint

Dive into the research topics of 'Neuroprotective effect of glatiramer acetate on neurofilament light chain leakage and glutamate excess in an animal model of multiple sclerosis'. Together they form a unique fingerprint.

Cite this