Ficus deltoidea attenuates tau hyperphosphorylation and neurodegeneration in a D-galactose and aluminum-induced Alzheimer's disease-like rat model.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder marked by cognitive decline, neuronal loss and abnormal tau phosphorylation. Although aluminum exposure has been suggested as a risk factor, no causal link to AD has been confirmed. The combination of D-galactose and aluminum chloride (AlCl₃) is widely used to model aging-related neurotoxicity, including oxidative stress, cognitive impairment and tau hyperphosphorylation. Ficus deltoidea (FD), a Southeast Asian plant rich in flavonoids like vitexin, exhibits antioxidant and anti-inflammatory properties, but its role in tau pathology remains unclear. In this study, male Wistar rats received D-galactose/AlCl₃ to induce AD-like pathology and were co-treated with FD extract (50, 100, or 200 mg/kg) and donepezil. The results showed that FD significantly improved spatial memory, reduced hippocampal neuronal loss and attenuated p-tau T181 levels. The apparent decrease in p-tau levels may have led to reduced neurodegeneration and improved learning and memory. These findings support FD's neuroprotective potential against aluminum-induced tauopathy and warrant further studies in translational AD-like models.