Yi-Heng Tai, et al. – Ludwig-Maximilians Universität München and the Technical University of Munich
To better understand how mitochondria affect MS, this study found key metabolic enzymes are downregulated in axons crossing lesions. In vivo measurements found metabolic dysfunction in lesion-associated axons, even those with no visible degeneration. Contrary to previous assumptions, metabolic issues precede mitochondrial oxidation. Components of the citric acid cycle are downregulated in both mouse models and MS patient brain tissue. Since metabolic dysfunction precedes axonal degeneration, restoring metabolic activity could halt disease progression.
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