This study is undertaken to characterize the effects of inhibition of NADPH oxidase by a widely used NADPH oxidase inhibitor apocynin on learning and memory deficits in paraquat and maneb-induced mouse PD model.
NADPH oxidase-derived H<sub>2</sub>O<sub>2</sub> mediates the regulatory effects of microglia on astrogliosis in experimental models of Parkinson's disease.
This study aimed to investigate associations between serum NOX1 (NADPH oxidase1), ferritin, selenium (Se), and uric acid (UA) levels and clinical parameters in patients with PD.
Thus, our findings revealed the critical role NADPH oxidase-mediated microglial activation in driving LC/NE neurodegeneration induced by PQ and Mb, providing new insights into the pathogenesis of environmental toxins-induced PD.
This study supports a critical role for NADPH-oxidase in the pathogenesis of PD and suggests that targeting this enzyme or enhancing extracellular antioxidants may provide novel therapies for PD.