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Although oxidative stress, mitochondrial dysfunction, and aberrant protein aggregation have been associated with Parkinsons disease, the exact origins of the disease remain unclear

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This process is morphologically marked by small mitochondria with condensed membrane densities, and biochemically by iron overload and GSH depletion, leading to loss of antioxidant defense and irreversible oxidative damage ( 3.2 Key molecular drivers of ferroptosis Iron Overload: Excess intracellular ferrous iron (Fe 2+ ) catalyzes the Fenton reaction, producing hydroxyl radicals (OH) that initiate lipid peroxidation cascades