Neuroprotective effect of ropinirole against Aβ(1-42) -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 Aβ(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 Aβ-infusion alone, Group III was Aβ(1-42) + ROP (5 mg/kg/i.p.), and Group IV was Aβ(1-42) + ROP (10 mg/kg/i.p.). Our research revealed that ROP (10 mg/kg, b.wt.) attenuates the cognitive deficits caused by Aβ(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 Aβ(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.