PRKN and Parkinson disease: EAS also inhibited oxidative stress and restored the normal expression of PD-related proteins [Parkin, PINK1, DJ1, α-syn, and leucine-rich repeat kinase 2 (LRRK2)], demonstrating that EAS exerts its neuroprotective effects in PD by ameliorating mitochondrial dysfunction and structural damage (Liu et al., 2018).