Abstract
INTRODUCTION
Dementia, notably Alzheimer’s disease (AD), presents a significant challenge for aging populations due to its progressive cognitive decline caused by neuronal degeneration. The hallmark attributes of AD include amyloid beta plaques and neurofibrillary tangles caused by hyperphosphorylation of tau. Multiple studies have explicitly investigated tau phosphorylation, revealing that phosphorylated tau is significantly elevated in the majority of AD brains. Current medications for AD offer limited palliative care, underscoring the urgent need for multifaceted therapies targeting various AD pathogenic pathways. Natural products have been vastly researched for their potential in AD drug development and, hence, in this study, the therapeutic potential of Ficus deltoidea (FD) is highlighted by determining its neuroprotective effects on hippocampal histology and AD-related protein expression in an AD-like rat model.
METHODS
This study induced AD-like conditions in male albino Wistar rats using D-galactose (D-gal) and aluminium chloride (AlCl3), known as senescence and neurotoxic agents, respectively. The AD-induced rats were orally administered with FD extract at varying dosages for 12 weeks. Subsequent investigations including Morris water maze (MWM) test, hippocampal tissue examination via Nissl staining and measurement of hyperphosphorylated tau (p-tau) expression were performed to assess the neuroprotective effects of FD.
RESULTS
MWM results demonstrated that AD-induced rats exhibited impaired spatial learning and memory, which were significantly improved with FD co-administration. The AD-induced rats showed a significant loss of pyramidal neurons in the cornu ammonis 1 (CA1) sub-region of the hippocampus. However, FD administration successfully reversed these morphological aberrations. Furthermore, FD-treated rats exhibited an apparent decrease in p-tau expression in their brains.
CONCLUSION
The administration of FD resulted in a lower p-tau level, which improved learning and memory, along with reduced neuronal loss. These findings indicate that early intervention with FD may serve as a preventive measure against AD and offer therapeutic benefits for AD medication development.