Rotenone-Induced Changes in Hippocampus Structures: Caffeine Emergence as a Potential Bedrock Remedy of Parkinson’s Disease

Introduction: The prevalence surrounding Parkinson’s disease (PD) is quite alarming, over 12 million of people are projected to be living with PD globally by 2040 and there is no definitive gold standard therapy to date. The major challenge in PD research is effective therapy without side effect, as the administrations of available therapy are accompany by severe complications. Aim: In response to this challenge, we assessed the effect of caffeine on CA2 region of hippocampus of rat model of PD induced by rotenone. Methods: The total of fifty (40) rats weighing 190-220g were used for this study, and the rats were randomly divided into 5 groups, each containing of 8 rats: Control group (non-pelletized feed and clean water), Rotenone treated group (3 mg/kg body weight of rotenone intraperitoneally [ip]), Pre-treated group (30 mg/kg body weight of caffeine for 10 days, then 3 mg/kg body weight of rotenone for 20 days, both ip), Post-treated group (3 mg/kg body weight of rotenone for 10 days, then 30 mg/kg body weight of caffeine for 20 days both ip), Caffeine treated group (caffeine-only treated with 30mg/kg, ip for 30 days). Results: The findings revealed a significant (p<0.05) as caffeine reversed the pathological features associated with rotenone induced PD such as reduction in body weight and relative brain weight, deficit in neurobehavioral assay coupled with neurohistopathological features homologous to those observed in PD, involving neuronal degeneration, demyelination, degeneration of Nissl corpuscles and cell body likewise significant loss of astrocytes in CA2 hippocampal region in rotenone treated groups.  Conclusion: In summary, caffeine mitigate the rotenone-induced neurotoxicity in hippocampus by modifying weight changes, degeneration of neuronal nuclei, myelinated nerve fibers, Nissl corpuscles and cell body, likewise modulating the degeneration and density of astrocytes, subsequently mounting caffeine’s neurotherapeutic potential in PD studies.