The common affected mechanisms for both mutations encompass impairment in neurite outgrowths, increased levels of oxidative stress and mitochondrial dysfunction, increased ER stress, imbalanced apoptosis and accumulation of α-synuclein aggregates, are shown in blue. The individual effects of the triplication of SNCA are impaired neuronal differentiation, DNA damage and increased levels of α-synuclein, whereas the ones of A53T mutation of SNCA are mitochondrial transport dysfunction, lysosomal activity impairment and accumulation of α-synuclein in fibrils, shown in red.