Recently, aluminium (Al) has been identified as one of the environmental factors responsible to cause certain neurodegenerative diseases, particularly Alzheimer`s Disease (AD). However, the relationship between Al and AD is controversial. We examined aluminium induced oxidative stress in the brain of mice when aluminium acetate was administered. Albino mice were divided into four groups containing 10 animals each. The first group of animals were treated as controls and administered distilled water, to the second group of animals single dose of aluminium acetate (3.5 mg kg-1 body weight) was given. To the third group of animals double doses (7 mg kg-1 body weight) were given with 72 h interval. To the 4th group of animals multiple doses (14 mg kg-1 body weight) with 72 h interval were given. Exposure to sublethal dose (3.5 mg kg-1) of aluminium acetate has revealed significant variations in detoxification enzymes like xanthine oxidase (XOD), superoxide dismutase (SOD), catalase (CAT) and Lipid Peroxidation (LP) in different regions of brain (cerebral cortex, cerebellum, striatum, medulla) of albino mice. Present results revealed that aluminium acetate exposure increased the activities of XOD, SOD, CAT and LP in all the brain regions in a dose dependent manner, so that it induced the oxidative stress in brain of albino mice.