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Current research implicates several interrelated pathogenic mechanisms, including persistent neuroinflammation, mitochondrial dysfunction [27], excessive production of reactive oxygen species (ROS) [28], reduced dopamine synthesis [8], impaired cerebral glucose metabolism [8], and the accumulation of misfolded -synuclein in the form of Lewy bodies [29]
Notably, several factors reported may limit the clinical impact of such agents [62]
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