Alzheimer's disease and aluminum toxicology.

A recent paper by C. N. Martyn and colleagues (1) appears to reinforce the environmental dismetabolic aluminum hypothesis of McLaclan (2), i.e., the involvement of abnormal aluminum (III) accumulation in the brain in the etiology of Alzheimer's disease (AD). Another recent review by Deary and Whelley (3) remarkably presents AD as a peculiar syndrome, which may represent the final result of diverse etiological factors. The essential, only postmortem determined features of AD are a) senile plaques (i.e, neuronal degeneration areas, mainly of the cortex and hippocampus); b) neurofibrillary degeneration (proliferation of regular helix-shaped pairs of neurofilaments 10 nm in diameter, helically wound around each other with periodic twists 80 nm apart); and c) reduction of neurotransmitter activity, especially in the cholinergic system. Literature data and work carried out in these laboratories lend credit to the possible involvement of aluminum (III) in all three hallmarks of AD.

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