The Cause and Cure of Alzheimer’s

A Detective Story

Alzheimer’s is a devastating and terrifying illness. My grandmother (pictured above on her wedding day) had it.  We watched her lose herself piece by piece. She was not alone – currently around 850,000 people in the UK are living with dementia. In 1907 when the disease was identified by Alois Alzheimer it was rare, but it is now so ubiquitous that it has come to be accepted as a hazard of aging. Like lumbago.

Knowing and not knowing

I am a trained academic and I have grown increasingly incredulous at the mountain of evidence about the cause of Alzheimer’s that has been ignored. It’s a story of knowing and yet not knowing.

Although modern medical science officially does not know what causes Alzheimer’s there has been much speculation. We’ve had oxidative stress (Pratico 2000), or dysregulation of calcium (Leferla 2002) or iron (Yokel 2006), problems with micro-tubules (Matsuyama 1989), problems with neurotransmission and G-protein-coupled receptor (GPCR) signalling (Cowburn 2001), and problems with upregulation of neuroinflammatory signalling (Pratico 2000). But none of these explanations properly fit. They are not able to fully explain why neurones degenerate in the particular pattern and regions characteristic of Alzheimer’s. Nor account for the gradual changes over time which results in progressive deterioration of neurons.

Since the mid 1980s research into the aetiology of Alzheimer’s has been focused on genetics. This has only been helpful in the sense of proving that genes are definitely not the cause. Twin studies show that in 60-70% of cases only one identical twin is affected by Alzheimer’s (Nee LE et al 1987; Pedersen 2004). If it’s not genes then there must surely be some environmental cause.

The Environment

So, we are looking for an element in the environment, something with neurotoxic properties; something that has increased in the last century.

Over a hundred years ago in a 1911 issue of JAMA, there was a paper by William Gies entitled ‘Some objections to the use of alum baking-powder’. Mr Gies had discovered via experimentation that aluminium was toxic to humans and animals and recommended it be removed from the food supply.

Looking back over the past century we can see that Mr Gies was not a lone voice. The weight of accumulated evidence demonstrating the neurotoxicity of aluminium is staggering. And aluminium is in everything: food, water, packaging, medications, utensils, and cosmetics. No experiments are necessary as the effects can be easily observed in the natural environment. In occupational health, for example, it is widely acknowledged that the ingestion of aluminium causes neurological disorders and cognitive impairment (Sinczuk-Walczak 2003). Rifat (2006) found that thousands of miners who had inhaled aluminium powder later suffered neurodegenerative diseases correlated with their length of exposure.

Animal models have also shown that chronic ingestion of aluminium at human dietary levels triggers neurodegenerative disease in rats (Walton 2007). In his aged rats study Walton (2009) showed that small doses of aluminium can accumulate over a lifetime and trigger neurodegenerative disease in otherwise healthy animals with no genetic predisposition. Biopsies showed neuropathology characteristic of Alzheimer’s, including cognitive deterioration, and deposits of aluminium in the hippocampus and pyramidal cells.

More than forty years ago Perl and Brody (1980) presented evidence from X-ray spectrometric that aluminium accumulates in neurofibrillary tangle-bearing neurons. Aluminium is widely bio-available to humans and is known to accumulate at higher concentrations in brain regions that are selectively affected in Alzheimer’s, including the entorhinal cortex (an area that shows the earliest pathological changes in Alzheimer’s), hippocampus, and the amygdala (Walton 2006).

So, observational, in-vitro and in-vivo studies show that aluminium is neurotoxic. Medical science knows it too. It must know or it would not have been able to identify the cause and cure of a new disease called Dialysis Encephalopathy in 1972.

Dialysis Encephalopathy

Dialysis encephalopathy was a complication of dialysis and the symptoms were characterized by dementia and speech alterations, progressing to psychosis and death.  In 1976 Alan Alfrey discovered that dialysis patients had ten times more aluminium in their brains than controls. In muscle and bone the levels were a hundred times higher (Alfrey 1976).  Epidemiological evidence about aluminium toxicity mounted. The higher the concentrations of aluminium in the water supply, the worse the outbreaks at dialysis clinics. Once the dialysis clinics started using reverse-osmosis water, the outbreaks ceased. Fortunately, treatments with aluminium-chelating agents, usually desferrioxamine, successfully removed the aluminium and prevented many deaths (Akrill 1993).

Following the experience with dialysis encephalopathy, intramuscular injections of desferrioxamine were later tested in a small two year long study published in the Lancet, as a treatment for Alzheimers (McLachlan 1991). McLachlan writes,

 “The mean rate of decline was twice as rapid for the no-treatment group. We conclude that sustained administration of desferrioxamine may slow the clinical progression of the dementia associated with AD.”

This study was presented in The New Scientist in 1991 (https://www.newscientist.com/article/mg12917520-400-aluminium-mop-slows-alzheimers-disease/) and the research team were hopeful that a breakthrough had been made.

The New Scientist asks the obvious question,

‘Would a slightly higher dose [of desferrioxamine] retard the development of Alzheimer’s even more? And would continued use of the drug hold back the course of the disease?’ But then answers it, ‘These questions and others will have to wait to be answered. Lack of funding has delayed follow-up studies.’

However, the postscript is telling,

“McLachlan, leader of the study and director of the University of Toronto’s centre for research in neurodegenerative diseases, has for years refused to comment on the possible link between aluminium in the environment and Alzheimer’s disease. This latest study, and a growing body of epidemiological evidence, has convinced him that there is now enough evidence to call for
governments to investigate the amount of aluminium people are exposed to in food, the air, water supplies and even in cosmetics.”

Here the lead goes cold. We almost knew but then we didn’t. A follow-up study never was published. And governments never did investigate the amount of aluminium people were exposed to.   

Fast forward forty years and we now understand even more about the mechanisms by which aluminium wreaks havoc in the body.  Aluminium replaces iron, calcium and magnesium in many enzyme reactions. It has been suggested that it binds transferrin and in this way is transported across the blood brain barrier.  Basically, it is a rogue metal ion, which is able to compete with and replace other bio-metals in essential processes. It causes damage in four ways; it antagonises magnesium biochemistry including that of ATP and DNA; it disrupts iron homeostasis; it is a pro-oxidant and it is an antigen, which has serious implications for auto-immune conditions.

In 2017, world renowned expert in aluminium toxicity, Professor Chris Exley made the first ever measurements of aluminium in brain tissue from 12 donors diagnosed with familial Alzheimer’s disease (Mirza et al 2017). The concentrations of aluminium were extremely high; higher than all previous measurements of brain aluminium except cases of known aluminium-induced encephalopathy.

Chris Exley concluded that,

“There are clearly many potential contributory factors in the aetiology of Alzheimer’s disease but what is now being suggested is that without concomitant pathologically-significant deposits of aluminium there would not be any Alzheimer’s disease.”(Exley 2017)

Chris Exley goes on the say that there may be mutations associated with metabolism and enzymatic processing that “predispose individuals to a more rapid accumulation and/or longer retention of aluminium in brain tissue. For example, one or more of these mutations may result in the enhanced absorption of aluminium across the gastrointestinal tract in individuals with familial Alzheimer’s disease.”

Although of course one does not need to absorb aluminium across the gastrointestinal tract when one is injected with it via the adjuvant in annual influenza vaccines.

To conclude this tale of knowing and not knowing, I share the following statement by Alzheimer’s UK, who resolutely do not know.

“As yet no study or group of studies has been able to confirm that aluminium is involved in the development of Alzheimer's disease. No convincing relationship between amount of exposure or aluminium in the body and the development of Alzheimer's disease has been established.”

Ackrill P, Day JP (1993) The use of desferrioxamine in dialysis-associated aluminium disease. Contrib Nephrol 102, 125-134.

Alfrey AC 1976, LeGendre GR, Kachney MD. The dialysis encephalopathy syndrome: possible aluminium intoxication. N Engl J Med 1976:294:184–188.

Cowburn RF, O’Neill C, Bonkale WL, Ohm TG, Fastbom J (2001) Receptor-G-protein signalling in Alzheimer’s disease. Biochem Soc Symp 67, 163-175.

Exley, C., 2017. Aluminum should now be considered a primary etiological factor in Alzheimer’s disease. Journal of Alzheimer's disease reports, 1(1), pp.23-25.

Gies WJ (1911) Some objections to the use of alum bakingpowder. JAMA 57, 816-821.

LaFerla FM (2002) Calcium dyshomeostasis and intracellular signalling in Alzheimer’s disease. Nat Rev Neurosci 3, 862-872.

Matsuyama SS, Jarvik LF (1989) Hypothesis: microtubules, a key to Alzheimer disease. Proc Natl Acad Sci U S A 86, 8152-8156.

Mirza, A., King, A., Troakes, C. and Exley, C., 2017. Aluminium in brain tissue in familial Alzheimer’s disease. Journal of Trace Elements in Medicine and Biology, 40, pp.30-36.

Nee LE, Eldridge R, Sunderland T, Thomas CB, Katz D, Thompson KE, Weingartner H, Weiss H, Julian C, Cohen R (1987) Dementia of the Alzheimer type: clinical and family study of 22 twin pairs. Neurology 37, 359-363.

Pedersen NL, Gatz M, Berg S, Johansson B (2004) How heritable is Alzheimer’s disease late in Life? Findings from Swedish twins. Ann Neurol 55, 180-185.

Perl DP and Brody AR (1980) Alzheimer’s disease: X-ray spectrometric evidence of aluminum accumulation in neurofibrillary tangle-bearing neurons. Science 208, 297-299.

Pratico D, Delanty N (2000) Oxidative injury in diseases of the central nervous system: focus on Alzheimer’s disease. Am J Med 109, 577-585.

Rifat SL, Eastwood MR, McLachlan DR, Corey PN (1990) Effect of exposure of miners to aluminium powder. Lancet 336, 1162-1165.

Sinczuk-Walczak H, Szymczak M, Razniewska G, Matczak W, Szymczak W (2003) Effects of occupational exposure to aluminum on nervous system: clinical and electroencephalographic

findings. Int J Occup Med Environ Health 16, 301-310.

Walton JR (2006) Aluminum in hippocampal neurons from humans with Alzheimer’s disease. Neurotoxicology 27, 385-394.

Walton JR (2007) A longitudinal study of rats chronically exposed to aluminum at human dietary levels. Neurosci Lett 412, 29-33.

Walton JR (2009) Functional impairment in aged rats chronically exposed to human range dietary aluminium equivalents. Neurotoxicology 30, 182-193.

Yokel RA (2006) Blood-brain barrier flux of aluminum, manganese, iron and other metals suspected to contribute to metal-induced neurodegeneration. J Alzheimers Dis 10,223-253.

---