The present study investigated the effect of madasiatic acid on VD(vascular dementia)-mediated memory loss and autophagy of neurons in mice model. The study demonstrated that VD-induced a significant increase (p < 0.05) in escape latency from day 2nd compared to the normal group. However, no significant change in escape latency was observed in VD-mice treated with 2 mg/kg doses of madasiatic acid compared to the normal mice. Rapamycin administration also caused a significant (p < 0.05) increase in escape latency in mice in comparison to the normal mice. But, increase in escape latency by rapamycin administration to mice couldn't be reversed on treatment with madasiatic acid. Madasiatic acid treatment of the VD-mice at 2 mg/kg doses prevented reduction in swimming time, decrease in distance travelled and lowering of platform crossing count. In madasiatic acid treated VD-mice spontaneous behavioral changes were efficiently prevented compared to the model group. Madasiatic acid treatment of the mice at 2 mg/kg dose reversed VD-induced promotion of Beclin-1 and LC3II level in the hippocampus tissues. VD-mediated inhibition of p-mTOR expression in mice hippocampus tissues was prevented on treatment with madasiatic acid. Treatment of the mice with 2 mg/kg madasiatic acid prevented VD-induced pathological changes in hippocampus tissues. Madasiatic acid treatment didn't prevent the VD-mediated reduction in mice neuronal viability in hippocampus tissues. Thus, madasiatic acid treatment prevented cerebral ischemia induced cognitive damage and neuronal loss in the mice model. It prevents over-activation of autophagy as well as promotes mTOR pathway activation in VD mice model. Thus, madasiatic acid can be of therapeutic significance for treatment of dementia however, further studies need to be performed to investigate it further.