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Updated: Jul 4, 2026

Myelin Oligodendrocyte Glycoprotein (MOG35-55) Induced Experimental Autoimmune Encephalomyelitis (EAE) in C57BL/6 Mice
Published on: April 15, 2014
Behavioral and pathological outcomes in MOG 35-55 experimental autoimmune encephalomyelitis
M V Jones1, T T Nguyen, C A Deboy
1Johns Hopkins University, Department of Neurology, 600 N. Wolfe Street, Pathology Bldg Room 6-27, Baltimore, Maryland 21287, USA.
Abstract:
We measured inflammatory and neural markers of disease from 7 days to one year after induction of experimental autoimmune encephalomyelitis (EAE) by immunization with myelin oligodendrocyte glycoprotein (MOG) peptide. Axon loss began before behavioral signs when T cell infiltration and microglial activation were very subtle. Remyelination was only detectable ultrastructurally. Axon numbers in the dorsal column plateau around day 30 p.i. while behavioral measures (EAE scores, rotarod, grip strength) partially recover. These results provide a starting point for testing potential neuroprotective treatments for multiple sclerosis (MS).
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