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Simultaneously, it downregulates genes associated with inflammation (IL-6, TNF-alpha), oxidative damage, fibrosis (TGF-beta in some contexts), and tissue destruction (certain metalloproteinases)

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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