Although PPARγ stimulation can play a role in modulating cellular redox balance by controlling the expression of NRF2 [38] as well as the anti-oxidant enzymes superoxide dismutase 1 (SOD1) and catalase [39, 40], it is not clear whether PPARγ-mediated protection against oxidative stress in the MPP+ model of PD involves SOD1 and catalase as one group demonstrated increased activity and expression of the enzymes [2] in response to rosiglitazone treatment whilst another found that SOD1 activity and expression remained unchanged [41]. Here, SOD1 is linked to Parkinson disease.