The hypothesis that aluminium (Al) is a cause of (or a risk factor in) the development of beta-amyloid plaques and neurofibrillary tangles (NFT) and dementia in Alzheimer's disease (AD) is based on studies by Wisniewski et al, Klatzo et al and Terry & Peña in 1965 that showed that injection of experimental animals with Al compounds induces the formation of NFT. Other publications revealed that Al affects cognitive functions in experimental animals and humans undergoing dialysis for renal failure. Electron probe and laser microprobe mass analysis (LAMMA) studies have demonstrated the presence of Al in NFT and cores of amyloid stars and nuclei of neurons in AD patients. Other studies have indicated the association between amyotrophic lateral sclerosis/Guam parkinsonism-dementia complex and Al in the environment. A recent report suggests that the chelating agent desferrioxamine slows the rate of cognitive decline in AD patients. Extensive studies of the pathology of AD and Al-induced encephalopathy by our group and others indicate that Al does not cause Alzheimer's disease neuropathology. However, under certain conditions, cognition can be affected when Al enters the brain. Therefore, for individuals with renal failure or undergoing dialysis or individuals with a damaged blood-brain barrier, the intake of Al should be controlled.