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

Although chromosomal abnormalities underpin some early onset cases of famil ial Alzheimer's disease (AD), most cases are sporadic and not associated wi th such abnormalities. Aluminium (Al) is a significant but controversial ri sk factor for sporadic AD, and studies have reported associations between A l and the principal pathological features of AD, senile plaques and neurofi brillary tangles. The present study measured gastrointestinal (GI) absorpti on of Al under normal dietary conditions using (26)AI tracer and accelerato r mass spectrometry (AMS). Following overnight fast, 13 AD patients (aged 6 3-76years) and 13 age-matched controls (aged 62-76 years) ingested a fruit drink containing 27 ng (26)AI. Plasma samples were obtained before and 1 h after the drink and from these the fraction of (26)AI absorbed across the G I 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 sub jects exceeded controls by a factor of 1.64 (p less than or equal to 0.05, Anova). AMS is capable of determining <10(-16)g of (26)AI 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 s ystemic exposure to Al. Public health measures to limit Al dietary uptake o r bioavailability may decrease the prevalence of AD in the community and sh ould be considered. Copyright (C) 2000 S. Kaiger AG, Basel.