The contribution of oxidation in PD pathogenesis has also been supported through clinical studies reporting alterations in serum glutathione peroxidase and superoxide dismutase activities, together with high malondialdehyde (MDA) levels in PD patients 23,24
In human studies, Nrf2 suppression has been linked to cataract formation in lenses collected from diabetic and older patients, with the upregulation of Keap1 (an Nrf2 suppressor) found in these individuals
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