Similarly, transgenic models of Parkinson’s disease carrying human SNCA (α-synuclein) or mutations in PINK1, Parkin, or LRRK2 reproduce the selective loss of dopaminergic neuron, mitochondrial dysfunction, and behavioral deficits, offering valuable platforms for drug discovery and mechanistic studies [54,143,145,179]. This evidence concerns the gene PINK1 and Parkinson disease.