Aluminium is the most widely distributed metal in the environment and is extensively used in daily life that provides easy exposure to human beings. The exposure to this toxic metal occurs through air, food and water. However, there is no known physiological role for aluminium within the body and hence this metal may produce adverse physiological effects. Chronic exposure of animals to aluminium is associated with behavioural, neuropathological and neurochemical changes. Among them, deficits of learning and behavioural functions are most evident. Some epidemiological studies have shown poor performance in cognitive tests and a higher abundance of neurological symptoms for workers occupationally exposed to aluminium. However, in contrast to well established neurotoxic effects, neurobehavioural studies of aluminium in rodents have generally not produced consistent results. Current researches show that any impairment in mitochondrial functions may play a major role in many human disorders including neurodegenerative disorders. Being involved in the production of reactive oxygen species, aluminium may cause impairments in mitochondrial bioenergetics and may lead to the generation of oxidative stress which may lead to a gradual accumulation of oxidatively modified cellular proteins. In this review, the neuropathologies associated with aluminium exposure in terms of neurobehavioural changes have been discussed. In addition, the impact of aluminium on the mitochondrial functions has also been highlighted.