A reduction in complex I activity and expression has been reported in the SN of patient's with PD and inhibitors of this complex (such as rotenone and mitochondrial permeability transition pore) induce a parkinsonian phenotype in animal models,30, 31, 32 change the expression of α-synuclein33 and effect the aggregation of α-synuclein even in the absence of mitochondrial complex I.34 Therefore, the inhibition of complex I by aggregating α-synuclein could be a key step in the pathogenesis of PD. Here, SNCA is linked to Parkinson disease.