Aluminum Exposure and Alzheimer's Disease

The enclosed article from the Journal of Alzheimer's Disease is reprinted with the permission of the publisher, IOS Press. For a subscription to the journal, contact: http://www.iospress.nl The journal is a leading international publication of research on Alzheimer's, with a regular subscription price of US $450 annually, including postage and handling.

Journal of Alzheimer’s Disease 3 (2001) 541–549
ISSN 1387-2877 / $8.00 © 2001, IOS Press. All rights reserved

541 Aluminum exposure and Alzheimer’s disease Erik T. Jansson Department of the Planet Earth, Inc.,¹ 701 E Street, SE, Suite 200, Washington, DC 20003, USA Tel.: +1 202 543 5450; Fax: +1 202 543 4791; E-mail: planetearth@erols.com The regulatory agencies of the United States and Canada have placed aluminum on priority lists for research designed to fill data gaps relating to neurotoxicity. This is to create a factual basis for the establishment of health standards for drinking water. In this review, we consider evidence for a significant role for aluminum in AD. Aluminum has been implicated as a potential risk factor in Alzheimer’s Disease (AD) and for elderly cognitive impairment by epidemiology studies of drinking water and a food study. Most people experience aluminum brain overload in the aging process. Aluminum levels over 20 times higher than those of a middle- aged group were found in a brain autopsy study of elderly persons, roughly correlating over the age period with densities of senile plaques and neurofibrillary tangles. Persons with AD have been found to experience increased absorption of aluminum and higher blood levels. More controversially, the majority of brain studies also show elevated aluminum levels, though there is disagreement over location of metal buildup. Clinical intervention to lower brain aluminum by chelation has slowed the progression of AD. 1. Introduction Aluminum represents about eight percent of the Earth’s crust and has no known biological function. It was first recognized as a human neurotoxin in 1886, in a Prussian army study of amputees whose wounds had been treated with alum to staunch bleeding [72]. The first laboratory animal study linking aluminum to brain damage was published in 1937 [52]. Since that time, an extensive literature has accumulated, exploring the metal’s role in kidney dialysis encephalopathy [1], cog- nitive impairment [3,11], childhood learning disabili- ties [47], damage to the brain function of babies [10], ¹An US-Canadian group that specializes in bringing medical in- formation about toxins to the attention of governmental regulatory and research agencies. damage to brain function of workers (eg. welding and smelting) [43,53,67],AD [30,54,70] and elderly mental impairment short of dementia [26,40,41]. In the face of abundant aluminum exposure and its demonstrated toxicity, living organisms have both ac- tive and passive mechanisms to exclude aluminum. In the human, this includes gut design that reduces absorp- tion, internal chelation and excretion primarily through the kidney, sequestration in bone and binding by trans- ferrin, the blood based metal shuttle protein, which reduces blood levels. The brain has lower aluminum levels than many other tissues due to partial exclusion by the blood-brain barrier [83], an active efflux mech- anism for aluminum from the brain, probably as Al- citrate [83,84], as well as removal by other mechanisms such as by the gastrointestinal peptide YY [6]. While a complete understanding of the mechanism of aluminum toxicity would be ideal before regulatory actions are taken to limit human exposure to aluminum in drinking water, food, drugs and cosmetics, standards of proof in the regulatory area focus generally on the weight of the evidence rather than a complete under- standing of a disease process. For example, lead in gasoline, drinking water, and paint was regulated with relatively little information about the biology of action, which while still poorly characterized today have thor- oughly lowered lead levels, providing important public health benefits. The essential question is the degree to which the present epidemiology studies linking alu- minum to AD and elderly cognitive impairment can be buttressed by the biological literature. The US Environmental Protection Agency, Health Canada and the US National Institute of Environmental Health Sciences plan to undertake laboratory animal studies of the effects of drinking water aluminum on brain function [36]. In both nations, aluminum has been put on a priority list of drinking water contaminants that need the filling of data gaps to allow establishment of health regulatory standards. Here we review the epidemiology studies of AD in relation to aluminum exposure; look at studies of blood, bone and brain aluminum and review the capacity of chelation as an AD therapy. Journal of Alzheimer’s Disease 3 (2001) 541–549 ISSN 1387-2877 / $8.00Ó2001, IOS Press. All rights reserved

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