Rivastigmine is known cholinesterase inhibitor and clinically being used drug for Alzheimer’s disease (AD) patients however, its effects on disease related other pathological mechanisms are not known. The present study was conducted to investigate the effect of rivastigmine on AD related pathological events involving nitrosative stress, endoplasmic reticulum stress and protein degradation machinery. Firstly, the effects of rivastigmine on cognitive impairment, acetylcholinesterase (AChE) activity, tau phosphorylation and amyloid aggregation were validated. Further, the assessment for effect of rivastigmine on the disease pathology related oxidative parameters (level of glutathione, malonaldihyde), nitrite level, intracellular calcium level and protein level of inducible nitric oxide synthase was done. Besides these, its effects on endoplasmic reticulum (ER) stress markers (GRP78, GADD153, caspase12), proteasome activity, neuronal apoptosis and astrocytes activation were estimated. Rivastigmine treatment significantly attenuates the disease related cognitive impairment, oxidative alterations and nitrosative stress along with inhibition of augmented intracellular calcium level. The increased calcium level may induct the ER stress, which was subsequently observed in both cortical and hippocampus regions and was significantly attenuated with rivastigmine treatment. Interestingly, rivastigmine mediated observed enhanced proteasome activity may facilitate the removal of amyloid deposits as found in study along with its inhibition on neuronal apoptosis. In conclusion, findings suggested that in addition to AChE inhibition rivastigmine also significantly contribute in AD related other pathological mechanisms, exhibiting its antioxidative, antinitrosative, antiapoptotic activities along with its role in removal of misfolded protein aggregates and inhibition of astrocytes activation.