Background: To date it is proved that Alzheimer's disease (AD) is characterized by a multifactorial etiology which comprises mitochondrial dysfunction, energy depletion, inflammation, and oxidative stress associated with glutathione depletion. All these factors are known to be impacted by beta amyloid protein (Aβ), which is responsible for the activation of amyloidogenic cascade. In the present work a rat intracerebroventricular Aβ(1-40) infusion model of early AD was employed to investigate the effects of Ibuprofen-Glutathione (IBU-GSH) conjugate on morphological modifications, Aβ plaque formation, apoptosis, learning, and memory performance.