Abstract: Alzheimer’s disease is a primary degenerative disease of the central nervous system. The progression of Alzheimer’s disease will ultimately lead to dementia, behavioral and cognitive impairments. Alzheimer’s is the commonest cause of dementia, a group of progressive condition which involves especially short-term memory loss, poor concentration, poor sense of time and space, difficulty in finding words or understanding other people, difficulty in perceiving and interpreting surroundings, mood changes and emotional upsets. The present study was designed to determine the ameliorating effect of ethanolic leaf extract of Ficus hispida Linn. (EEFH) on (amyloid beta) Aβ 25-35-induced cognitive deficits and oxidative stress in mice. Animals were treated with EEFH for periods of 4 weeks dose-dependently (200 and 400 mg kg-1) then received a single intracerebroventricular (i.c.v.) injection of Aβ 25-35 (10 μg mouse-1). Behavioral changes in the mice were evaluated using passive avoidance, Y-maze, Hole board and water-maze tests. Anti-oxidant enzymes and neuro-transmitter levels were also been estimated. EEFH at the dose of 400 mg kg-1 significantly ameliorated the cognitive and memory deficits caused by i.c.v. injection of Aβ 25-35. EEFH attenuated the Aβ-induced increase in brain levels of thiobarbituric acid reactive substances. There was an increase in glutathione peroxidase, glutathione reductase and super oxide dismutase activity in EEFH treated groups. The acetyl cholinesterase activity in the brain was lower in EEFH supplemented groups than the Aβ-injected group. EEFH treated group showed a significant alteration in behavior when compare to negative control in Y maze, Plus-maze and also in water maze tests. These findings suggest EEFH exerts a protective effect against cognitive deficits induced by Aβ 25-35 accumulation in Alzheimer’s disease, because of its potential antioxidant property.