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Initiation and progression of PD is dependent upon cellular events, including failures in the protein degradation machinery, oxidative stress, mitochondrial dysfunction, defects in mitochondrial autophagy (mitophagy) and the continuous accumulation of α-synuclein, driven through cell to cell interactions between glial cells and neurons that ultimately lead to apoptosis [7,10,18]

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Building on observations of α‑syn species and EVs originating from erythrocytes in PD patients, emerging evidence suggests a potential erythrocyte‑to‑brain transmission route