There has been a strong link between human exposure to aluminium and the incidence of Alzheimers disease for half a century or more. However, without definite proof, there is still no consensus in the scientific community about the role of this known neurotoxin in this devastating brain disease.
The latest research from my group, published in the Journal of Trace Elements in Medicine and Biology, makes this link even more compelling. In my view, the findings are unequivocal in their confirmation of a role for aluminium in some if not all Alzheimers disease.
At the very least, these new results should encourage everyone and even those who have steadfastly maintained that aluminium has no role in the disease to think again.
I dont believe that is the only factor, but I think it is an important one which should be considered very seriously.
When our new results are put into the context of what is already known about aluminium and Alzheimers disease their significance becomes overwhelming and compelling.
We already know that the aluminium content of brain tissue in late-onset or sporadic Alzheimers disease is significantly higher than is found in age-matched controls. So, individuals who develop Alzheimers disease in their late sixties and older also accumulate more aluminium in their brain tissue than individuals of the same age without the disease.
Even higher levels of aluminium have been found in the brains of individuals, diagnosed with an early-onset form of sporadic (usually late onset) Alzheimers disease, who have experienced an unusually high exposure to aluminium through the environment (e.g. Camelford) or through their workplace. This means that Alzheimers disease has a much earlier age of onset, for example, fifties or early sixties, in individuals who have been exposed to unusually high levels of aluminium in their everyday lives.
We now show that some of the highest levels of aluminium ever measured in human brain tissue are found in individuals who have died with a diagnosis of familial Alzheimers disease.
The levels of aluminium in brain tissue from individuals with familial Alzheimers disease are similar to those recorded in individuals who died of an aluminium-induced encephalopathy while undergoing renal dialysis.
In support of our quantitative data, we have also used a recently developed and fully validated method of fluorescence microscopy to provide stunning and unequivocal images of aluminium in brain tissue from familial Alzheimers disease donors.
Familial Alzheimers disease is an early-onset form of the disease with first symptoms occurring as early as 30 or 40 years of age. It is extremely rare, perhaps 2-3% of all cases of Alzheimers disease. Its bases are genetic mutations associated with a protein called amyloid-beta, a protein which has been heavily linked with the cause of all forms of Alzheimers disease.
Individuals with familial Alzheimers disease produce more amyloid beta and the onset of the symptoms of Alzheimers disease are much earlier in life.
This new research may suggest that these genetic predispositions to early onset Alzheimers disease are linked in some way to the accumulation of aluminium (through normal everyday human exposure) in brain tissue.
Ageing is the main risk factor for Alzheimers disease and aluminium accumulates in human brain tissue with ageing. Environmental or occupational exposure to aluminium results in higher levels of aluminium in human brain tissue and an early onset form of sporadic Alzheimers disease. The genetic predispositions which are used to define familial or early-onset Alzheimers disease also predispose individuals to higher levels of brain aluminium at a much younger age.
Aluminium is accepted as a known neurotoxin, for example being the cause of dialysis encephalopathy, and its accumulation in human brain tissue at any age can only contribute to any ongoing disease state or toxicity.
We should take all possible precautions to reduce the accumulation of aluminium in our brain tissue through our everyday activities and we should start to do this as early in our lives as possible.
The new research, published in the Journal of Trace Elements in Medicine and Biology is available online and open access (http://www.sciencedirect.com/science/article/pii/S0946672X16303777)