SOD1 and amyotrophic lateral sclerosis: In particular, many studies, accomplished in different ALS models (mutant SOD1, TDP-43, or FUS/TLS), demonstrated that an impairment of the ER–mitochondria communication [188,193,194] causes an altered mitochondrial Ca2+ capacity, inducing a significant decrease in the mitochondrial membrane potential and an increase in the rate of the production of mitochondrial ROS [153].