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Updated: Jul 11, 2025

Determining Immune System Suppression versus CNS Protection for Pharmacological Interventions in Autoimmune Demyelination

Determining Immune System Suppression versus CNS Protection for Pharmacological Interventions in Autoimmune Demyelination

Published on: September 12, 2016

Novel therapeutic for multiple sclerosis protects white matter function in EAE mouse model.

Sarah Zerimech¹, Hung Nguyen¹, Arthur A Vandenbark^2,3,4

¹Anesthesiology and Perioperative Medicine (APOM), Oregon Health and Science University, Portland, OR, United States.

Frontiers in Molecular Medicine

|November 7, 2023

Summary

A novel therapeutic construct, DRhQ, was tested in a mouse model of multiple sclerosis (MS). DRhQ improved axon integrity and reduced inflammation, offering potential for progressive MS treatment.

Keywords:

CAP DRHQ astrocyte axon function microglia myelin

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Last Updated: Jul 11, 2025

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Myelin Oligodendrocyte Glycoprotein MOG35-55 Induced Experimental Autoimmune Encephalomyelitis EAE in C57BL/6 Mice

Myelin Oligodendrocyte Glycoprotein MOG35-55 Induced Experimental Autoimmune Encephalomyelitis EAE in C57BL/6 Mice

Published on: April 15, 2014

Simple and Efficient Production and Purification of Mouse Myelin Oligodendrocyte Glycoprotein for Experimental Autoimmune Encephalomyelitis Studies

Simple and Efficient Production and Purification of Mouse Myelin Oligodendrocyte Glycoprotein for Experimental Autoimmune Encephalomyelitis Studies

Published on: October 27, 2016

Area of Science:

Neuroscience
Immunology
Pathology

Background:

Multiple sclerosis (MS) is a chronic demyelinating disease characterized by significant axon dysfunction.
Previous research showed major histocompatibility complex Class II constructs could reverse experimental autoimmune encephalomyelitis (EAE) symptoms by inhibiting macrophage migration inhibitory factors (MIF) and extracellular signal-regulated kinase (ERK) activation.
These constructs also promoted remyelination and reduced inflammation.

Purpose of the Study:

To evaluate the effects of a novel third-generation construct, DRhQ, on axon integrity in the EAE mouse model.
To assess DRhQ's impact on both myelinated and unmyelinated axons in distinct white matter tracts.
To determine DRhQ's therapeutic potential for progressive MS, including its effect on ischemic vulnerability.

Main Methods:

Electrophysiology was used to compare axon conduction properties in corpus callosum slices and optic nerves of EAE mice.
The study examined the effects of EAE and DRhQ treatment on axon excitability, conduction velocity, and spatiotemporal summation.
Investigated the increased vulnerability of white matter to ischemia in the EAE model and the protective effects of DRhQ.

Main Results:

EAE induced alterations in axon excitability, delayed conduction, and slowed summation, correlating with astrocyte and microglia activation.
DRhQ treatment post-EAE onset significantly inhibited microglial and astrocyte activation.
DRhQ administration improved the functional integrity of myelinated axons and enhanced recovery from white matter ischemia.

Conclusions:

DRhQ treatment administered after EAE onset promotes white matter integrity and function.
DRhQ reduces the increased vulnerability to ischemic injury observed in the EAE MS model.
These findings suggest DRhQ has significant therapeutic potential for progressive multiple sclerosis.