SOD1 and amyotrophic lateral sclerosis: In addition, we demonstrated (a) that the cycad toxin L-BMAA, at this sub-toxic dose, improves survival rate and motor performances, delays paralysis onset and prevents body weight loss in SOD1 G93A mice during the development of the disease and that (b) the plasma membrane transporter Na+/Ca2+ exchanger 3, NCX3, contributes to the protection elicited by L-BMAA-PC thus representing a target for setting on new strategies in ALS intervention.