SNCA and Parkinson disease: Despite the lack of a functional orthologue for human αSyn in the C. elegans genome, the overexpression of disease-associated mutant SNCA (A53T/A56P/A30P) proteins in C. elegans dopamine neurons leads to αSyn accumulation and locomotory defects, therefore phenocopying the cellular and physiological defects described in mammalian PD models [123,124,125,126,127].