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In the late stages of PD, the key molecular pathogenic mechanisms include the misfolding and aggregation of -synuclein, mitochondrial dysfunction, impaired protein clearance (related to inefficient ubiquitin-proteasome and autophagy-lysosomal systems), neuroinflammation and oxidative stress (57)

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Zinc efflux from mitochondria is mediated by ZnT9, a proton-coupled antiporter embedded in the inner membrane

The emergence of the nicotinamide riboside kinases in the regulation of NAD+ metabolism

Presented for research literature review only Stradaioli G et al