Because of an increasing therapeutic need to understand the underlying mechanism of myelin damage and repair in pathologies such as multiple sclerosis (MS), we used 1H-MRS to longitudinally characterize the metabolic changes in the cerebellum associated with de- and re-myelination in the cuprizone mouse model. Our results, in line with similar findings in the corpus callosum, suggest that a group of metabolites provide a unique neurochemical signature of cuprizone induced de- and re-myelination. Additionally, we observe a reversible and robust increase of GABA levels upon cuprizone feeding that goes in contradiction with current trends in clinical studies of MS patients.
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