MCOLN1 and amyotrophic lateral sclerosis: Furthermore, ML-SA1-induced lysosomal Ca2+ release by TRPML1 is able to promote a sort of autophagy reprogramming, leading to a long-lasting effect on motor neurons exposed to β-methylamino-L-alanine (L-BMAA), a neurotoxin reproducing Amyotrophic Lateral Sclerosis and Parkinsonism-Dementia Complex (ALS-PDC), a disease’s type of apparent environmental origin [54].