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PD is pathologically characterized by insolubilized α-synuclein accumulation in neurons and dopaminergic neurodegeneration in the substantia nigra of the midbrain
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The oxidative damage mediated by ROS resulting in the defect in control of apoptosis or programmed cell death and delayed clearance of apoptotic cells may prolong interaction between ROS and apoptotic cell macromolecules generating neoepitopes that subsequently broad spectrum of autoantibody formation leading to the tissue damage in SLE [6,7]
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