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As a classic acute phase marker, CRP induces monocyte-macrophage migration, expression of tissue factor with adhesion molecules and monocyte chemotactic protein-1 [15, 16, 17]
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This broad spectrum of manifestations reflects the complexity of its pathophysiology, which involves a combination of dopaminergic neuron loss, oxidative stress, alpha-synuclein aggregation into Lewy bodies, mitochondrial dysfunction, neuroinflammation, and disruptions in the gut-brain axis 5,6,7,8,9