Interestingly, comparable decreases in glycerophospholipids levels and matching alterations in PUFA concentrations had been formerly shown in a SOD1 transgenic model180 and ALS patients respectively.181 Moreover, lipidomics analysis on the ALS mouse model bearing the SOD1-G93A mutation distinguished altered phosphatidylcholine profiles in the cerebral cortex,182,183 possibly indicating a common pathogenic mechanism between TDP-43 and SOD1 toxicity. Here, SOD1 is linked to amyotrophic lateral sclerosis.