Axonal damage is reduced following glatiramer acetate treatment in C57/bl mice with chronic-induced experimental autoimmune encephalomyelitis

Yossi Gilgun-Sherki, Hana Panet, Vered Holdengreber, Ronit Mosberg-Galili, Daniel Offen*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

73 Scopus citations

Abstract

Glatiramer acetate (GA) is efficacious in reducing demyelinating-associated exacerbations in patients with relapsing-remitting multiple sclerosis (RRMS) and in several experimental autoimmune encephalomyelitis (EAE) models. Here we report that GA reduced the clinical and pathological signs of mice in chronic EAE induced by myelin oligodendrocyte glycoprotein (MOG). GA-treated mice demonstrated only mild focal inflammation, and less demyelination, compared with controls. Moreover, we also found minimal axonal disruption, as assessed by silver staining, antibodies against amyloid precursor protein (APP) and non-phosphorylated neurofilaments (SMI-32), in the GA-treated group. In conclusion, our study demonstrated for the first time that axonal damage is reduced following GA treatment in C57/bl mice with chronic MOG-induced EAE.

Original languageEnglish
Pages (from-to)201-207
Number of pages7
JournalNeuroscience Research
Volume47
Issue number2
DOIs
StatePublished - 1 Oct 2003

Funding

FundersFunder number
National Parkinson Foundation
Ministry of Health, State of Israel

    Keywords

    • Axonal damage
    • Experimental autoimmune encephalomyelitis (EAE)
    • Glatiramer acetate
    • Multiple sclerosis (MS)
    • Myelin oligodendrocyte glycoprotein (MOG)

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