N-acetylaspartate (NAA), a neuronal metabolite, increases in blood during neurodegenerative diseases like amyotrophic lateral sclerosis (ALS). This study shows that NAA treatment in C2C12 myotubes increases lipid turnover, mitochondrial biogenesis, and oxidative metabolism, reducing glycolysis. This effect depends on NAA catabolism via aspartoacylase (ASPA), as CRISPR/Cas9 ASPA knockout cells are unresponsive. NAA treatment also increases resistance to atrophic stimuli. ALS mice show increased ASPA in muscles undergoing a glycolytic-to-oxidative switch, supporting NAA's role in skeletal muscle adaptation in neuromuscular disorders.
Publisher
Cell Death and Disease
Published On
Sep 19, 2024
Authors
Serena Castelli, Enrico Desideri, Leonardo Laureti, Federica Felice, Angela De Cristofaro, Silvia Scaricamazza, Giacomo Lazzarino, Maria Rosa Ciriolo, Fabio Ciccarone
Tags
N-acetylaspartate
neurodegenerative diseases
amyotrophic lateral sclerosis
muscle metabolism
mitochondrial biogenesis
lipid turnover
atrophy resistance
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