Neuroprotective effect of ropinirole against Aβ1-42-induced neurochemical perturbations and cognitive impairments in a rodent model

The primary objective of this study was to investigate the protective effects of ropinirole (ROP) medication given for an extended period following the induction of cognitive decline, oxidative stress, and deterioration of mitochondria in a Wistar rat model by A beta(1-42) . This study aimed to examine the neuroprotective efficacy of ROP in a stereotaxis model of AD. The Wistar rats were randomly assigned into four groups. Group I was considered as a sham, group II served as A beta-infusion alone, Group III was A beta(1-42) + ROP (5 mg/kg/i.p.), and Group IV was A beta(1-42) + ROP (10 mg/kg/i.p.). Our research revealed that ROP (10 mg/kg, b.wt.) attenuates the cognitive deficits caused by A beta(1-42) -infused, which also correlates with the barnes maze, where (10 mg/kg, b.w.t.) shows significant improvement in spatial learning and memory. At the same time, ROP was rescued from oxidative damage, decreased lipid peroxidation rates, and inhibited acetylcholinesterase activity caused, demonstrating antioxidant benefits. In addition, a higher dose of ROP restored mitochondrial membrane potential in A beta(1-42) rats. Furthermore, histopathological examination showed that ROP treatment reduced neuronal loss, especially in the hippocampus. We conclude that ROP's protective effects in reducing oxidative stress and modulating mitochondrial function might have a propensity in AD pathogenesis.