SOD1 and amyotrophic lateral sclerosis: Moreover, Szelechowski (2018) suggest that both glycolysis and FAO are decreased in fibroblasts from SOD1-ALS patients, whereas SOD1G93A motor neurons report increased activity in these two energy-producing pathways, with a larger preference for FAO.150 The study supports the existence of tissue-specific alterations in ALS pathophysiology and suggests that changes in mitochondrial morphology and mitochondrial bioenergetics accommodate a metabolic switch from glucose toward FAO and ketogenesis.