Abstract
Aluminum (Al) is a recognized neurotoxin causally linked to several neurodegenerative diseases with a dementia component. Al has long had a GRAS (Generally Recognized As Safe) rating by the US FDA, that allows Al salts to be used in food manufacture and clarification of urban drinking water supplies. Routine ingestion of Al salts throughout life causes bioavailable Al to accumulate in the brain where it specifically deposits in regions most vulnerable in Alzheimers disease (AD). AD has an insidious onset, developing slowly and progressively, producing cognitive deterioration in old age. The main source of Al exposure for humans is their total dietary Al intake from foods, water, other beverages, and Al additives. Prospective data collection from epidemiological studies attempting to quantify total dietary Al intake, to probe for AD causality, is virtually impossible to obtain in a human population where all its members are routinely exposed to abundant Al amounts from many sources. Longitudinal animal studies provide a parallel in that their feed and water intakes can be rigorously controlled throughout the life span. Such a study revealed that a significant proportion of rats, particularly those that consumed Al in an equivalent amount to the high end of the human total dietary Al range, progressively accumulated Al in their brain, accompanied by AD-related neuropathology and cognitive deterioration in old age. This article describes evidence for the close involvement of Al with the major AD hallmarks and provides suggestions that may help to remediate the current AD epidemic in westernized countries.
Keywords: Aluminum, Alzheimer's disease, food additives, water treatment, animal model, cognitive deterioration, Westernized Diet, Al additives, Aqueous Solutions, POST-INGESTION DISPOSITION
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