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Neurodegenerative disorders such as Parkinson's disease, present a global health concern with limited therapeutic options. In this context, dietary interventions have emerged as a potential strategy to counteract the oxidative stress and inflammation underlying these conditions. Rice bran enzymatic extract (RBEE), rich in bioactive compounds, has shown ability in modulating neuroinflammatory responses and improving mitochondrial function. This study investigates the neuroprotective potential of RBEE in a murine model of PD induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The results reveal that RBEE supplementation effectively preserves the dopaminergic population and reduces MPTP-induced gliosis in the Substantia Nigra (SN). Moreover, RBEE enhances mitochondrial Complex I activity in mouse brains.These findings underscore the potential of RBEE as a dietary supplement to mitigate neuronal loss, neuroinflammation, and mitochondrial dysfunction associated with PD. RBEE is shown as a promising novel candidate in neuroprotective strategies, offering hope in the quest for effective preventive and therapeutic measures in PD.

[Display omitted] • RBEE contains bioactive compounds, including γ-oryzanol, tocopherols and tocotrienols. • RBEE exhibits neuroprotection and decreases GAL-3+ microglia cells. • RBEE enhances mitochondrial activity in vitro using mouse brain extracts. • Incorporating RBEE into the diet may prevent neurodegenerative processes. Neurodegenerative disorders such as Parkinson's disease, present a global health concern with limited therapeutic options. In this context, dietary interventions have emerged as a potential strategy to counteract the oxidative stress and inflammation underlying these conditions. Rice bran enzymatic extract (RBEE), rich in bioactive compounds, has shown ability in modulating neuroinflammatory responses and improving mitochondrial function. This study investigates the neuroprotective potential of RBEE in a murine model of PD induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The results reveal that RBEE supplementation effectively preserves the dopaminergic population and reduces MPTP-induced gliosis in the Substantia Nigra (SN). Moreover, RBEE enhances mitochondrial Complex I activity in mouse brains. These findings underscore the potential of RBEE as a dietary supplement to mitigate neuronal loss, neuroinflammation, and mitochondrial dysfunction associated with PD. RBEE is shown as a promising novel candidate in neuroprotective strategies, offering hope in the quest for effective preventive and therapeutic measures in PD. [ABSTRACT FROM AUTHOR]