Aluminium and the pathogenesis of senile plaques: studies in Alzheimer's disease and chronic renal failure

Abstract

Aluminium and silicon are co-localised as aluminosilicate at the centre of the senile plaque core. These focal deposits appear to be a consistent and specific feature associated with A4 amyloid fibrils in the plaque core and are not associated with other types of amyloidosis. A pathogenic role for AI and Si is suggested by the finding of A4 amyloid deposits, immature senile plaques and an abnormal content and distribution of these elements in the brains of patients (<55 years) with chronic renal failure. Evidence suggests that AI uptake and distribution within the brain is mediated by transferrin. The distribution of transferrin receptors may account for the vulnerability of regions such as the hippocampus and cortex which are selectively involved in Alzheimer's disease.