Neuroprotective Role of Formononetin in a Scopolamine-Induced Alzheimer’s Disease Mouse Model

The progressive neurodegenerative illness known as Alzheimer's disease (AD) is typified by memory loss, cognitive decline, and neural malfunction. A common tool for creating experimental models of cognitive impairments resembling AD is scopolamine, a muscarinic receptor antagonist. Because of flavonoids’ anti-inflammatory, antioxidant, and neuroprotective qualities, the hunt for natural neuroprotective drugs has accelerated in recent years. This study investigated the neuroprotective effects of formononetin (10, 20, and 30 mg/kg; p.o) in a scopolamine-induced AD model. It examined its impact on oxidative stress indicators and cognitive performance. Scopolamine (1 mg/kg; i.p), administered for 3 days, significantly impaired memory and locomotor activity. Memory and learning capacities were assessed using behavioral tests such as the Open Field Test and the Y-maze Test. The findings revealed that pretreatment with formononetin, at a dosage of 30 mg/kg, significantly mitigated the behavioral changes induced by scopolamine. Formononetin improved memory, as evidenced by a higher percentage of spontaneous alterations in the Y-maze test. Additionally, it enhanced locomotor activity, as indicated by a higher square-crossing count in the OFT. Biochemical analysis showed that scopolamine therapy elevated TBARS levels and reduced GSH levels in the brain. In contrast, formononetin restored approximately 95% of GSH levels and reduced TBARS levels by 95%. The present study aims to investigate the neuroprotective efficacy of formononetin against scopolamine-induced cognitive and biochemical impairments that mimic AD pathology.