Date: October 13, 2014
Source: Keele University
Summary:
A world authority on the link between human exposure to aluminum in everyday life and its likely contribution to Alzheimer’s disease says in a new report that it may be inevitable that aluminum plays some role in the disease.
world authority on the link between human exposure to aluminum in everyday life and its likely contribution to Alzheimer’s disease, Professor Christopher Exley of Keele University, UK, says in a new report that it may be inevitable that aluminum plays some role in the disease.
He says the human brain is both a target and a sink for aluminum on entry into the body – “the presence of aluminum in the human brain should be a red flag alerting us all to the potential dangers of the aluminum age. We are all accumulating a known neurotoxin in our brain from our conception to our death. Why do we treat this inevitability with almost total complacency?”
Exley, Professor in Bioinorganic Chemistry, aluminum and Silicon Research Group in The Birchall Centre, Lennard-Jones Laboratories at Keele University, writes in Frontiers in Neurology about the ‘aluminum Age’ and its role in the ‘contamination’ of humans by aluminum.
He says a burgeoning body burden of aluminum is an inevitable consequence of modern living and this can be thought of as ‘contamination’, as the aluminum in our bodies is of no benefit to us it can only be benign or toxic.
Professor Exley says: “The biological availability of aluminum or the ease with which aluminum reacts with human biochemistry means that aluminum in the body is unlikely to be benign, though it may appear as such due to the inherent robustness of human physiology. The question is raised as to ‘how do you know if you are suffering from chronic aluminum toxicity?’ How do we know that Alzheimer’s disease is not the manifestation of chronic aluminum toxicity in humans?
“At some point in time the accumulation of aluminum in the brain will achieve a toxic threshold and a specific neurone or area of the brain will stop coping with the presence of aluminum and will start reacting to its presence. If the same neurone or brain tissue is also suffering other insults, or another on-going degenerative condition, then the additional response to aluminum will exacerbate these effects. In this way aluminum may cause a particular condition to be more aggressive and perhaps to have an earlier onset - such occurrences have already been shown in Alzheimer’s disease related to environmental and occupational exposure to aluminum.”
Professor Exley argues that the accumulation of aluminum in the brain inevitably leads to it contributing negatively to brain physiology and therefore exacerbating on-going conditions such as Alzheimer’s disease. He suggests that this is a testable hypothesis and offers a non-invasive method of the removal of aluminum from the body and the brain. He says the aluminum hypothesis of Alzheimer’s disease will only be tested if we are able to lower the body and hence brain burden of aluminum and determine if such has any impact upon the incidence, onset or aggressiveness of Alzheimer’s disease.
Professor Exley adds: “There are neither cures nor effective treatments for Alzheimer’s disease. The role of aluminum in Alzheimer’s disease can be prevented by reducing human exposure to aluminum and by removing aluminum from the body by non-invasive means. Why are we choosing to miss out on this opportunity? Surely the time has come to test the aluminum hypothesis of Alzheimer’s disease once and for all?”
Story Source:
The above story is based on materials provided by Keele University. Note: Materials may be edited for content and length.
Journal Reference:
Chris Exley. Why industry propaganda and political interference cannot disguise the inevitable role played by human exposure to aluminium in neurodegenerative diseases, including Alzheimer’s disease. Front. Neurol., October 2014 DOI: 10.3389/fneur.2014.00212
Cite This Page:
Keele University. "Aluminum: Its likely contribution to Alzheimer's disease." ScienceDaily. ScienceDaily, 13 October 2014. <www.sciencedaily.com/releases/2014/10/141013090451.htm>.
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