Assessing Caffeine's Neuroprotective Effects on Rotenone-Induced Parkinson's Disease: Unravelling the Neurological Dynamics of Striatal Impact

Abstract

The alarming prevalence of Parkinson's disease (PD) has prompted a search for standard therapeutic interventions capable of altering or halting its progression. Identifying a neuroprotective or disease-modifying therapy for PD is akin to pursuing the Holy Grail. Numerous studies have affirmed the therapeutic benefits of adenosine A2A receptor blockade in alleviating both motor and non-motor symptoms in PD. Furthermore, A2A receptors are selectively localized in the basal ganglia. This study aimed to evaluate the impact of caffeine on the striatum of rats with PD induced by rotenone. Fifty adult male Wistar rats, weighing between 150 and 200g, were utilised in this study. The rats were randomly assigned to five groups, each consisting of ten rats: Group A (vehicle group, alcohol, 3mL/kg), group B (rotenone-only treated with 3mg/kg, ip.), group C (caffeine 30mg/kg + rotenone 3mg/kg, ip.), group D (rotenone 3mg/kg + caffeine 30mg/kg, ip.), and group E (caffeine-only treated with 30mg/kg, ip.). The findings revealed a significant (p<0.05) reduction in body weight and relative brain weight in response to caffeine treatments. Rotenone administration induced histological changes akin to those observed in PD, encompassing neuronal structural derangement, degenerated striatal bundled fibre, and loss of myelinated neurons and Nissl substance. This study adds to the growing body of research supporting the therapeutic potential of caffeine in PD. The results highlight caffeine's neuroprotective properties and its ability to mitigate striatal lesions. The pursuit of effective interventions for PD remains crucial, and caffeine emerges as a promising therapeutic agent in this regard.