The selective loss of dopaminergic neurons of the SNpc results in dopamine depletion in the striatum [18], hence the mainstay of PD pharmacological treatment is dopaminergic drugs that replace the action of dopamine by activating dopamine receptors, the provision of a precursor that is metabolized to dopamine (e.g., levodopa), or the prevention of the breakdown of endogenous dopamine (e.g., monoamine oxidase-B (MAO-B) inhibitors and catechol-O-methyl transferase inhibitors (COMT) [19,20]. This evidence concerns the gene MAOB and Parkinson disease.