In particular, given that neurodegenerative diseases are often associated with abnormal protein accumulation25, 26, the mechanism by which ALS may take place is by the overexpression of human SOD1 in the motoneurons in agreement with Stathopulos et al. 27 that could be regarded as a destabilizing solution condition resulting as a consequence in loss of mitochondrial functionality and also in altered vescicle trafficking. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.