Chronic exposure to aluminium (Al) remains a controversial possible ca
use of sporadic forms of Alzheimer's disease (AD). This article review
s the evidence that once Al enters the brain and individual brain cell
s, it may be involved in three pathological processes: (1) the product
ion of abnormal forms of tau leading to the formation of cellular neur
ofibrillary tangles and neuropil threads; (2) the processing of the am
yloid precursor protein, resulting in the formation of beta-amyloid de
posits and senile plaques, and (3) that via the mutual histocompatibil
ity system, Al could be involved in the initiation of the immune respo
nse observed in AD patients. Despite recent evidence that Al could be
involved in these processes, a conclusive case that exposure to Al ini
tiates the primary pathological process in sporadic AD remains to be e
stablished.