Aluminium and Alzheimer's disease

A number of environmental factors have been put forward as possible contributory causes of Alzheimer's disease in some people. Among these is aluminium. There is circumstantial evidence linking this metal with Alzheimer's disease, but no causal relationship has yet been proved. As evidence for other causes continues to grow, a possible link with aluminium seems increasingly unlikely. This factsheet looks at the circumstantial evidence and current medical and scientific views.

Causes of Alzheimer's disease

Researchers believe that in the majority of those affected, Alzheimer's disease results from a combination of different risk factors rather than one single cause. Such factors, which vary from person to person, may include age, genetic predisposition, other diseases or environmental agents.

The chief symptoms of Alzheimer's disease are progressive decline of memory and other higher mental functions. These changes are associated with the loss of brain cells and the development of two kinds of microscopic damage in the brain known as 'plaques' and 'tangles'.

Plaques consist of an abnormal deposit of a particular protein called beta amyloid between the brain cells. Tangles occur within cells, and are formed from abnormal thread-like deposits of a protein called tau, which is normally part of the cell's 'skeleton'.

(For more information about causes of Alzheimer's disease see Factsheet 450, Am I at risk of developing Alzheimer's disease?, and Factsheet 405, Genetics and dementia.)

Evidence linking aluminium and Alzheimer's disease

The hypothesis that there is a link between aluminium and Alzheimer's disease was first put forward in the 1960s (Terry and Pena 1965, Klatzo et al 1965). Since then, researchers have claimed a number of other circumstantial links between aluminium and Alzheimer's disease, as follows:

Aluminium has been shown to be associated both with plaques and with tangles in the brains of people with Alzheimer's disease (Crapper et al 1976). However, the presence of aluminium does not mean that the aluminium was the causal factor − it is more likely to be a harmless secondary association.
Some have claimed that people with Alzheimer's disease have a higher than average level of aluminium in their brains. However, other studies find no difference between the overall amount of aluminium in the brains of people with Alzheimer's and the amount in normal brains (Trapp et al 1978).
Studies of other sources of aluminium, such as tea, antacid medications and antiperspirants have also failed to show a positive association with Alzheimer's disease (Flaten and Odegård 1988).
People with kidney failure are unable to excrete aluminium, and yet they frequently have to be treated with compounds that contain aluminium. Aluminium accumulates in nerve cells that are particularly vulnerable in Alzheimer's disease. However, even after years of high exposure to aluminium, patients with kidney failure are no more likely to develop dementia or the hallmark pathological changes of Alzheimer's disease (Netter et al 1990).
Treatment with desferrioxamine (DFO), a drug which binds aluminium and removes it from the body, also has a major effect on iron stores in the body. Therefore the effects of DFO may have nothing to do with aluminium (Gomez et al 1998).
There have been many experimental studies on animals and on isolated cells showing that aluminium has toxic effects on the nervous system, but in almost all cases the doses of aluminium used were much higher than those occurring naturally in tissues (Gitelman 1988).

Sources of aluminium

The main sources of aluminium in our diet include tea, beer, baked products, drinking water, toothpaste, aluminium-based antacids, aluminium cookware and some canned beverages (Rao and Rao 1995). Aluminium uptake from our diets is usually very low, with more than 99% passing through the digestive system unabsorbed. Absorption increases significantly in the presence of acidic foods such as orange juice. The small amount of aluminium that is absorbed into the body is rapidly excreted by the kidneys in urine, except in individuals with impaired kidney function, where aluminium retention within the body is responsible for dialysis dementia.

Aluminium is naturally present in some water, and aluminium sulphate is widely used in the treatment of public water supplies. However, intake of aluminium from water is very small in comparison with other sources.

Some aluminium from the air may enter the lungs as dust, but this form is highly insoluble, and hardly any reaches the rest of the body.

Only a minute proportion of the aluminium we ingest from these various sources is absorbed by the body, and even this small fraction is usually excreted in the urine or harmlessly deposited in bone, which acts as a 'sink' to remove aluminium.

The expert view on aluminium

Since the idea that the metal might be a risk factor for Alzheimer's disease was first proposed there have been numerous conferences on aluminium and health. The medical research community, international and government regulatory agencies and the aluminium industry all review the evidence at frequent intervals. The overwhelming medical and scientific opinion is that the findings outlined above do not convincingly demonstrate a causal relationship between aluminium and Alzheimer's disease, and that no useful medical or public health recommendations can be made − at least at present (Massey and Taylor 1989).

It has proved extremely difficult to devise studies to resolve this problem one way or another. Alzheimer's is a common disease with multiple causes, while aluminium is widespread in the environment, and there are no methods that allow us to measure an individual's 'body burden' or lifetime exposure to this element.

In the future, it is possible that suitable 'transgenic' animal models (which develop the pathological features of Alzheimer's disease in animals' brains) will enable scientists to determine if such changes are accelerated or exacerbated by aluminium at levels that correspond to normal human exposure.

For details of Alzheimer's Society services in your area, visit alzheimers.org.uk/localinfo
For information about a wide range of dementia-related topics, visit alzheimers.org.uk/factsheets

References

Crapper D R, Krishnan S S and Quittkat S (1976) 'Aluminium, neurofibrillary degeneration and Alzheimer's disease'. Brain 99: 67-80

Flaten T P and Odegård M (1988) 'Tea, aluminium and Alzheimer's disease'. Food and Chemical Toxicology 26 (11-12): 959-60

Gitelman H J ed (1988) Aluminium and health, a critical review, London: CRC Press

Gomez M, Esparza J L, Domingo J L, Singh PK and Jones M M (1998) 'Comparative aluminium mobilizing actions of deferoxamine and four 3-hydroxypyrid-4-ones in aluminium-loaded rats'. Toxicology 130 (2): 175-81 (7)

Klatzo I, Wisniewski H and Streicher E (1965) 'Experimental production of neurofibrillary pathology: 1. Light microscopic observations'. Journal of Neuropathology and Experimental Neurology 24: 187-99

Massey RC and Taylor D eds (1989) Aluminium in food and the environment. London: Royal Society of Chemistry Netter P, Kessler M, Gaucher A and Bannwarth B 'Does aluminium have a pathogenic role in dialysis associated arthropathy?' Annals of the Rheumatic Diseases 49 (8): 573-75

Rao J K S and Rao V G (1995) 'Aluminium leaching from utensils - a kinetic study'. International Journal of Food Science and Nutrition 46: 31-38

Terry R D and Pena C (1965) 'Experimental production of neurofibrillary pathology: electron microscopy, phosphate histochemistry and electron probe analysis'. Journal of Neuropathology and Experimental Neurology 24: 200-10

Trapp G A, Miner G D, Zimmerman R L, Mastri A R, Heston L L (1978) 'Aluminum levels in brain in Alzheimer's disease'. Biological Psychiatry 13 (6): 709-18