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After the model was expanded to include GS-H 2 Q adduct formation as a function of its reduction potential, it was then combined with the Reed glutathione model 21 in order to simulate how the quinone redox-metabolism of doxorubicin influenced the glutathione metabolism

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the failure of these treatments to restore function and slow functional disease progression can be traced to their inability to correct the underlying cause of the dysfunction- diminished synaptic connectivity among neurons in the striatum and neuronal loss in the substantia nigra (SN)

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