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Carnosine and skeletal muscle dysfunction in a rodent multiple sclerosis model.
Jan Spaas1,2,3, Pieter Van Noten4,5, Charly Keytsman6,7,4
1University MS Center (UMSC) Hasselt-Pelt, Hasselt, Belgium. jan.spaas@uhasselt.be.
Amino Acids
|October 13, 2021
Summary
Multiple sclerosis (MS) causes muscle weakness. While carnosine supplementation increased muscle carnosine levels in experimental autoimmune encephalomyelitis (EAE) mice, it did not improve muscle function or combat muscle atrophy in this MS model.
Area of Science:
- Neuroscience
- Muscle Physiology
- Nutritional Science
Background:
- Muscle weakness and fatigue are key symptoms in multiple sclerosis (MS).
- Reduced muscle carnosine levels were previously observed in MS patients and a rodent MS model.
- Carnosine is an endogenous dipeptide crucial for muscle contractile function and fatigue resistance.
Purpose of the Study:
- Confirm carnosine reduction in a chronic experimental autoimmune encephalomyelitis (EAE) model.
- Characterize structural and functional muscle alterations in EAE.
- Investigate carnosine supplementation's effect on muscle carnosine levels and function in EAE.
Main Methods:
- Immunohistochemistry to assess muscle fiber structure.
- Ex vivo contractility measurements to evaluate muscle function.
- Oral carnosine supplementation in EAE rodent models at varying doses.
Main Results:
- EAE mice exhibited progressive muscle fiber atrophy and a shift to a fast-twitch phenotype.
- Muscle strength and contraction speed were reduced in EAE mice.
- Carnosine supplementation increased muscle carnosine levels but did not improve muscle strength, speed, or fatigability.
Conclusions:
- EAE mice develop significant, time-dependent muscular alterations.
- Carnosine intervention, despite increasing muscle carnosine levels, failed to enhance muscle function in the EAE model.
- Further research is needed to understand and address muscle dysfunction in MS.

