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Among these, the abnormal aggregation of -synuclein (-syn) to form Lewy bodies, mitochondrial dysfunction, oxidative stress, impaired protein homeostasis, and neuroinflammation (the activation of microglia and astrocytes leads to the release of various inflammatory factors, such as tumor necrosis factor- (TNF-) and interleukin-1 (IL-1), which exacerbate neuronal damage) constitute the key links in the pathophysiology of PD [6, 7]