Additional redox pathways involved in PD are androgen receptor-induced neurodegeneration [24], production of oxidatively modified forms of α-synuclein and increased α-synuclein aggregation [25, 26], degradation of antioxidant enzyme quinone oxidoreductase 1 (NQO1) [27], reduction of the deglycase activity of protein DJ-1 [28], activation of gene LRRK2 [29], and tetrahydrobiopterin (BH4) and tyrosine hydroxylase (TH) metabolism impairment [30]. This evidence concerns the gene TH and Parkinson disease.