Aluminum has been identified as a neurotoxin for over 100 years.' Its toxic impacts were demonstrated most dramatically when long-term hemodialysis patients (with chronic renal failure) were treated with aluminum-containing phosphate binders, and/or dialysate made using water with high dissolved aluminum levels.2 Many of these kidney patients developed dialysis dementia and other complications including osteomalacia and osteoporosis.

There are similarities between the brains ofAlzheimer's and dialysis dementia patients. Senile plaques have been observed in both, as have decreased levels of choline acetyltransferase activity and gamma-aminobutyric acid concentrations.3-6 Such similarities have provided further support for the hypothesis that aluminum toxicity is the key to Alzheimer's disease, although many researchers reject this suggestion. Opponents of this viewpoint argue that aluminum deposition in the brains of Alzheimer's patients only occurs late in the disorder, because the blood-brain barrier prevents aluminum entry until it is damaged by extensive nerve cell death or by other causes, such as amyloid deposition. Secondly, they claim that even when incorporated into the brain, aluminum is relatively benign. Thirdly, they point out that pathological changes caused experimentally in animals by aluminum are not identical to those seen in the brains of Alzheimers disease patients. This article provides evidence to refute such objections.