A possible explanation to account for these metabolic modifications could implicate the canonical WNT/β-catenin pathway, an apparently crucial factor in the progression and development of many neurodegenerative diseases.143 Previous research reported upregulation of WNT/β-catenin signaling in the motor neurons of SOD-1-ALS transgenic models,144 which, in return, may activate pyruvate dehydrogenase kinase-1 and consequently hinder the conversion of pyruvate into acetyl-CoA and hampers its entry into the tricarboxylic acid (TCA) cycle. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.