The differences between our results and those described by von Coelln et al may indicate that Parkin deficiency affects A53T and A30P α-synucleinopathies differently; Parkin deficiency may have a smaller effect on A53T α-synuclein-induced neurodegeneration due to the higher intrinsic aggregation potential [52] and toxicity of A53T α-synuclein than A30P α-synuclein, leading to a more rapidly progressive neurodegenerative phenotype in mice [15], [51]. The gene discussed is PRKN; the disease is synucleinopathy.