SOD1 and amyotrophic lateral sclerosis: Here, we attempted to formulate a model shown in Fig. 8 based on: 1) elevated ROS and dysfunctional neuronal mitochondria in ALS (supported by the data showing decreased cardiolipin content in spinal cords of SOD1-G93A 120d group); 2) upregulation of cholesterol synthesis due to altered lactate metabolism in neuronal mitochondria; 3) accumulation of cholesteryl esters composed of PUFAs as a protective mechanism against lipid peroxidation.