Since autophagy is a catabolic process for unnecessary or dysfunctional cytoplasmic contents mediated by lysosomal degradation pathways and autophagy mediates both TDP43 (59) and α-synuclein turnover (60), two of the major components of protein aggregates in degenerating neurons respectively in ALS and PD, we evaluated the effects of L-BMAA or LCS-MaCe on the protein levels of TDP-43 and α-synuclein. The gene discussed is TARDBP; the disease is Parkinson disease.