Absorption of aluminium-26 in Alzheimer's disease, measured using accelerator mass spectrometry

Although chromosomal abnormalities underpin some early onset cases of familial Alzheimer's disease (AD), most cases are sporadic and not associated with such abnormalities. Aluminium (Al) is a significant but controversial risk factor for sporadic AD, and studies have reported associations between Al and the principal pathological features of AD, senile plaques and neurofibrillary tangles. The present study measured gastrointestinal (GI) absorption of Al under normal dietary conditions using ²⁶Al tracer and accelerator mass spectrometry (AMS). Following overnight fast, 13 AD patients (aged 63-76 years) and 13 age-matched controls (aged 62-76 years) ingested a fruit drink containing 27 ng ²⁶Al. Plasma samples were obtained before and 1 h after the drink and from these the fraction of ²⁶Al absorbed across the GI tract was estimated. The GI tract rigorously excludes Al with only 0.06-0.1% of the ingested Al being absorbed. The mean fraction absorbed by AD subjects exceeded controls by a factor of 1.64 (p ≤ 0.05, Anova). AMS is capable of determining < 10^-16 g of ²⁶Al with many orders of magnitude more sensitivity than other techniques. Using this sensitivity, we have shown, under normal physiological conditions, that the ability of the GI tract to exclude Al is reduced in AD, possibly leading to greater systemic exposure to Al. Public health measures to limit Al dietary uptake or bioavailability may decrease the prevalence of AD in the community and should be considered. Copyright (C) 2000 S. Karger AG, Basel.