Mitochonic acid 5 attenuates age-related neuromuscular dysfunction associated with mitochondrial Ca2+ overload in Caenorhabditis elegans.

Abstract

Mitochonic acid-5 ameliorates the pathophysiology of human mitochondrial-disease fibroblasts and Caenorhabditis elegans Duchenne muscular dystrophy and Parkinson's disease models. Here, we found that 10 μM MA-5 attenuates the age-related decline in motor performance, loss of muscle mitochondria, and degeneration of dopaminergic neurons associated with mitochondrial Ca²⁺ overload in C. elegans. These findings suggest that MA-5 may act as an anti-aging agent against a wide range of neuromuscular dysfunctions in metazoans.