One study found that aluminium concentration was far higher in several commercially available brands of fresh and reconstituted orange juice, and concluded that drinking most brands of so called fresh and pure orange juice might result in far greater exposure to aluminium than drinking a similar volume of tap water (The Lancet, May 16, 1992).
Silicic acid and fluoride are said to protect against excess accumulation of aluminium, although increased accumulation in lung, bone and brain does occur with age (The Lancet, March 21, 1992).
But the most damning new research points the finger at mercury, a substance rated among the most toxic known to man, particularly that present in amalgam fillings.
A medical research team at the University of Kentucky in Lexington, Kentucky, who have been investigating the possible link between mercury and AD, found high levels of the element in the brain tissue of AD victims (Neurotoxicology, 1986; 7: 197-206; Biol Trace Element Res, 1987; 13: 19-23), and WR Markesbery and his team found that the highest trace element in the brains of 10 autopsied AD patients was mercury (Brain Research, 1990; 533: 125-31).
As with aluminium, however, the Markesbery study noted that whether mercury was a possible cause of AD, or simply a deposit on a degenerating brain, remained to be determined. They concluded: "This and our previous studies suggest that mercury toxicity could play a role in neuronal degeneration in AD."
The link between mercury and AD was strengthened by Haley et al, who found that mercury fed rats developed a diminished tubulin level similar to people with AD. Tubulin is a protein needed for the healthy formation of nerve tissue in the brain, and a lack of tubulin will result in messages in the brain not connecting properly. When fed aluminium, the rats displayed no change in tubulin levels (Federation of American Societies for Experimental Biology, 75th Annual Meeting, 21-25 April 1991).
Markesbery and his team also found diminished levels of zinc and selenium in the 10 AD-affected brains they examined. This is significant in that zinc and selenium are known to have a protective role against heavy metal poisoning in tissue.
It has also been suggested that low levels of zinc, coupled with high levels of mercury, could make the brain more susceptible to aluminium deposits. Or that mercury and aluminium both contribute to AD.
The Markesbery team noted that "the source of brain mercury in AD is not known, although dental amalgams and environmental sources such as seafood are potential sources". However, even the World Health Organization concedes that the public's highest daily exposure to mercury comes from dental amalgam fillings. (For a more detailed analysis of the potential dangers associated with amalgam, see The WDDTY Dental Handbook).
To date, medicine has pooh-poohed the possible mercury connection, pouring all resources into the development of a magic bullet. Nevertheless, controversy rages over tacrine, the only drug licensed (in the US and France) for the treatment of AD. The drug is currently under consideration for licensing in other parts of Europe, including the UK.
Tacrine is a "cholinergic enhancer". The cholinergic system is involved in cognitive functions, ie, learning process, memory, perception, reasoning, etc, which are all affected by AD. People with AD suffer a significant loss of cholinergic neurons.