There is no doubt that the brain of a sufferer from Alzheimer’s disease contains an unusual quantity of aluminium. It now also seems fairly clear that the aluminium is especially concentrated in those structures that are most affected in Alzheimer’s disease and that it is found in association with the senile plaques and the neurofibrillary tangles. This of course has led to considerable speculation that aluminium could be the cause of, or a contributory factor to, the development of this type of dementia in at least some sufferers, if not most.
This theory is further strengthened by the results of experiments on animals that have shown neurofibrillary-tangle-like structures developing in brain cells exposed to large quantities of aluminium. Further, people with kidney failure who have to undergo renal dialysis run the risk of developing a confusional state if the dialysis procedure allows too much aluminium to enter their body. Although this is now rigorously controlled, in earlier days before the relationship between aluminium and brain damage in kidney patients was established, some people with kidney failure died of a condition known as dialysis encephalopathy. Excess levels of aluminium were implicated in this process.
Although this all makes for a good prima facie case for aluminium as a potential cause of Alzheimer’s disease, one has to remember that aluminium might be accumulating in the brain as a result of the condition rather than as an agent which is causing it. It is possible that damaged tissue may accumulate aluminium in greater quantities than undamaged tissue. Most people working in this field believe that aluminium accumulates passively as a consequence of ageing or damage to brain cells. Moreover, accumulation of aluminium is known to occur in other brain disorders, in which the characteristic changes of Alzheimer’s disease do not occur. The people dying of dialysis encephalopathy did not develop the same changes in the brain as are found in Alzheimer’s disease or if they did, to only a very minor and possibly insignificant extent. In addition, aluminium does not accumulate in all places where plaques and tangles occur and in at least one study it was found not to have accumulated in that part of the brain that is usually most severely affected by the abnormal changes. If aluminium really were important, one would have expected the highest levels in this area – the hippocampus.
A lot of prominence has recently been given to the level of aluminium in drinking water. Aluminium is added to the water supply as part of the purification process and in many parts of the country water has a naturally high level of aluminium dissolved in it. Although a recent study claims that Alzheimer’s disease appeared to be more common in parts of the country with higher than average levels of aluminium in the water, even this evidence is not strong enough to implicate aluminium as the cause of Alzheimer’s disease.
The study is a difficult one to interpret for a number of reasons; although in general it was reported that there were more cases of Alzheimer’s disease in areas where the water was high in aluminium, some areas with the highest levels were not associated with the greatest number of cases. Besides, we take in a lot more aluminium with our food than in our drinking water. The latter is responsible for only a small proportion of the 5-6 mg of aluminium that most adults ingest each day.
If aluminium is one day shown to be an important contributory factor and the scepticism of many of us shown to be inappropriate, it will prove very difficult to minimize our intake of the substance. Aluminium is one of the most common elements in the earth’s crust and is present all around us. Not only does it occur in our water and naturally in our food, it is a common component of some food additives. It is present in cosmetics and talcum powder and in the dust that we breathe.
In any case the link, if one exists, between aluminium and Alzheimer’s disease is unlikely to be a simple matter of cause and effect. Two people can live side by side for sixty years, having got married in their late teens or early twenties, consuming a very similar amount of aluminium throughout their life. Only one of them develops Alzheimer’s disease and their neighbours who probably have a not dissimilar lifestyle, are also spared. Why this selectivity? It is possible that some subjects with Alzheimer’s disease inherit a tendency to be particularly sensitive to aluminium or process it within their nervous systems in an abnormal manner. Although this possibility does exist, there is as yet no firm evidence in its favour.
Finally, an alternative and totally speculative hypothesis involves the suggestion that the aluminium that we consume during our adult lives is irrelevant and that if this element plays any part at all in causing Alzheimer’s disease, it is aluminium intake in early life, perhaps even before birth, that is important, causing damage to nerve cells in the brain which does not become apparent until much later in life. There is, however, no evidence at all at the moment to support this possibility and I only mention it for the sake of interest.
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