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Further, NOX activation has been shown to be a sufficient trigger of seizure activity, while NOX inhibition reduced hyperactivity in multiple animal models of epilepsy (Malkov et al., 2019)
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Although alterations in metabolites associated with purine metabolism in PD are still debated due to inconsistent reports associated with disease progression, dysfunction of purine metabolism may play a significant role in the pathogenesis of PD by enhancing the oxidative stress and inflammatory processes that drive neurodegeneration
however, they are localized to distinct neuronal populations [30, 35]
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