The occurrence of abnormal levels of AI(III) connected with human pathologies and with encephalopathies experimentally induced in experimental animals is reviewed and critically evaluated in molecular terms. It is assumed that phosphate-bearing biomolecules are elected targets for the biochemical action of Al(III) and the reactivity of the metal centre towards both inorganic phosphates and nucleotides, diphosphoglycerate, phosphorylated proteins, phospholipids and myo-inositol-phosphates is thoroughly reviewed. All these data are evaluated in the light of the potential relevance of higher Al(III) levels to the etiopathology of dialysis dementia and of Alzheimer's disease.