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Lookup NU author(s): Dr Brian Moore,
Emeritus Professor Nicol Ferrier,
Professor Jim Edwardson
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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 (26)AI tracer and accelerator mass spectrometry (AMS). Following overnight fast, 13 AD patients (aged 63-76years) 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 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 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 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. Kaiger AG, Basel.
Author(s): Moore PB, Day JP, Taylor GA, Ferrier IN, Fifield LK, Edwardson JA
Publication type: Article
Publication status: Published
Journal: Dementia and Geriatric Cognitive Disorders
ISSN (print): 1420-8008
ISSN (electronic): 1421-9824
Publisher: S. Karger AG
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