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Lastly, oxidative stress and mitochondrial dysfunction, prominently arising from dopamine autooxidation and impaired mitophagy pathways (e.g., mutations in PINK1, PRKN), are central to neuronal degeneration in PD, emphasizing their importance as therapeutic targets [22, 23]

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PD-1/PD-L1 immune checkpoint and p53 loss facilitate tumor progression in activated B-cell diffuse large B-cell lymphomas