The purpose of this paper is to show properties and activity of aluminium as a potential etiological factor in the pathophysiology of Alzheimer's disease, with a focus on the epidemiological studies on drinking water and biochemical and cellular parameters which are the result of animal and in vitro experiments. Aluminium is a content of food. In the processed foods it is used as an additive, while in the plant foods it is absorbed from soil, where it is naturally present. Aluminium is also a content of drinking water as a naturally dissolved element, or as an additive in water purification. The amount of aluminum in drinking water makes up to 5% of the total daily intake, so it is possible that in the water are other factors that hinder or even encourage increased absorption of aluminum. Water with dissolved silicates and fluoride reduces the absorption of aluminum in the digestive system. Some cosmetics contain aluminum, as well as vaccines. Antacids and buffered aspirin may contain aluminium. Although being enviromentally abundant, aluminium is not essential for life. It is a widely recognised neurotoxin that inhibits biological systems and causes various adverse effects. The relationship between aluminium exposure and Alzheimer's disease has been the subject of scientific debate for several decades. However, the complex characteristics of aluminium bioavailability make it difficult to evaluate and therefore, the relationship remains to be established. Mounting evidence has suggested that significance of oligomerization of beta-amyloid protein and neurotoxicity in the Alzheimer's disease pathophysiology.