Attenuation of age-related cognitive decline and memory deficits through apomorphine administration.

Abstract

Oxidative stress, stemming from heightened production of reactive oxygen species and free radicals, significantly contributes to the aging process. Apomorphine emerges as a pivotal medication for managing Alzheimer's, Parkinson's and other age-related conditions. This study aims to explore the memory-enhancing and neuroprotective properties of apomorphine, utilizing male Albino Wistar rats aged 4 and 24 months as subjects. Rats were intraperitoneally injected with apomorphine for 6 days. Decreased glutathione peroxidase, superoxide dismutase and catalase activities with increased lipid peroxidation were observed in the brain and plasma samples of aged rats, which were reversed upon apomorphine administration. Superoxide dismutase (SOD) and AChE activities were significantly decreased along with a decline in short-term- and long-term memory of aged rats, which was reverted by apomorphine. Furthermore, a notable reduction in biogenic amines and metabolite levels in the brains of aged rats was reversed in aged rats treated with apomorphine. The findings indicate a significant restoration of memory impairment and oxidative stress in aged rats by apomorphine. Overall, our data suggests that apomorphine, at a dosage of 1mg/kg, holds promise as a potential therapeutic intervention for dementia and associated disorders in elderly patients.