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Updated: Apr 19, 2026
Author Spotlight: Creating a Versatile Experimental Autoimmune Encephalomyelitis Model Relevant for Both Male and Female Mice
Published on: October 13, 2023
Chronic exercise confers neuroprotection in experimental autoimmune encephalomyelitis
William M Pryor1, Kimberly G Freeman, Rebecca D Larson
1Department of Kinesiology, University of Georgia, Athens, Georgia; Department of Neuroscience, The Scripps Research Institute, Jupiter, Florida.
Abstract:
Multiple sclerosis (MS) is an autoimmune disease that affects the CNS, resulting in accumulated loss of cognitive, sensory, and motor function. This study evaluates the neuropathological effects of voluntary exercise in mice with experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Two groups of C57BL/6J mice were injected with an emulsion containing myelin oligodendrocyte glycoprotein and then randomized to housing with a running wheel or a locked wheel. Exercising EAE mice exhibited a less severe neurological disease score and later onset of disease compared with sedentary EAE animals. Immune cell infiltration and demyelination in the ventral white matter tracts of the lumbar spinal cord were significantly reduced in the EAE exercise group compared with sedentary EAE animals. Neurofilament immunolabeling in the ventral pyramidal and extrapyramidal motor tracts displayed a more random distribution of axons and an apparent loss of smaller diameter axons, with a greater loss of fluorescence immunolabeling in the sedentary EAE animals. In lamina IX gray matter regions of the lumbar spinal cord, sedentary animals with EAE displayed a greater loss of α-motor neurons compared with EAE animals exposed to exercise. These findings provide evidence that voluntary exercise results in reduced and attenuated disability, reductions in autoimmune cell infiltration, and preservation of axons and motor neurons in the lumbar spinal cord of mice with EAE.
Insights
Voluntary exercise in mice with experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), reduced disease severity. Exercise preserved motor neurons and axons, offering potential therapeutic benefits for MS.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Multiple sclerosis (MS) is a central nervous system (CNS) autoimmune disease causing progressive neurological deficits.
- Experimental autoimmune encephalomyelitis (EAE) serves as a key animal model for studying MS pathogenesis.
- Understanding factors that modulate EAE progression is crucial for developing MS therapies.
Purpose of the Study:
- To investigate the neuropathological impact of voluntary exercise on EAE in mice.
- To assess the effects of exercise on disease severity, immune cell infiltration, demyelination, and neuronal preservation in the spinal cord.
Main Methods:
- C57BL/6J mice were induced with EAE using myelin oligodendrocyte glycoprotein.
- Mice were divided into two groups: voluntary exercise (running wheel) and sedentary (locked wheel).
- Neurological scores, immune cell infiltration, demyelination, neurofilament integrity, and motor neuron loss were evaluated.
Main Results:
- Exercising EAE mice showed significantly reduced neurological disease scores and delayed onset compared to sedentary controls.
- Reduced immune cell infiltration and demyelination were observed in the spinal cord's white matter of exercising mice.
- Exercise group exhibited better preservation of axons and reduced loss of α-motor neurons in the spinal cord.
Conclusions:
- Voluntary exercise attenuates clinical disability in the EAE model.
- Exercise reduces autoimmune attack and neuroinflammation in the CNS.
- Physical activity promotes neuroprotection, preserving axons and motor neurons in EAE, suggesting therapeutic potential for MS.
