"Give with a free hand, but give only your own."
 -- J.R.R. Tolkien The Children of Hurin
- Aluminum -

General Information:

Wikipedia entry:
Dr. Ray Shahelien entry: 



I found this paper on the effects of aluminum and tau formation in a rat study.

Do aluminium and/or glutamate induce Alz-50 reactivity?

"...These results suggest: (1) aluminium enters neurons and (2) aluminium alone induces possible conformational changes in tau as detected by the Alz-50 antibody, while aluminium combined with glutamate, or glutamate alone, do not."
PMID: 9530999 [PubMed] and,

I wonder if it possible to have "aluminum poisoning"? I mean, if you somehow ingest too much aluminum, does it stick around like lead and mercury? I wonder if there is a way to flush it out. Also, I wonder if the presence of some other metal, such as mercury or lead or copper, could interfere with normal aluminum elimination processes, leading to excess aluminum, and therefore tau problems.

Known sources:

Natural sources:


Would decreased aluminum ingestion reduce the incidence of Alzheimer's disease?

D. R. McLachlan, T. P. Kruck, W. J. Lukiw and S. S. Krishnan
Department of Medicine, University of Toronto, Ont.
Canadian Medical Association Journal, Vol 145, Issue 7 793-804

Alzheimer's Disease: A Treatment Strategy
"I wrote this paper for my dad, who may have Alzheimer's Disease. It is the result of about 100 hrs work on medline and at the biomedical library."

2.4.  Aluminum chelation therapy

"The  potential  therapeutic  capacity  of  chelation  of aluminum  for  AD  was  demonstrated  [50].     A  low dose of the injectable desferrioxamine was used to re- move about a third of the aluminum (from 4.09 ug/g to 2.69 ug/g) from the brains of elderly AD patients over two years.   The trial slowed the disease process for the entire group by an average of 50 percent. Some good responder patients were benefited for up to five years [51].  Deaths mostly from pneumonia were dra- matically reduced from 9 in the untreated group to only 1 in the treatment group."

[Discusses oral chelation therapy]



"The Aluminum Hypothesis of Alzheimer’s disease began in 1965 with the demonstration that aluminum salts injected into the rabbit brain induced neurofibrillary tangles.  Since this initial report, there has been considerable basic, clinical and epidemiological research conducted to evaluate the biological plausibility of aluminum’s purported etiological role in Alzheimer’s disease.  Presently there is a widespread belief among the general public that aluminum plays some role in Alzheimer’s while, in contrast, a dwindling number of scientists continue to explore the link between this metal and the development of this disease.  The present paper reviews the scientific literature concerning the Aluminum Hypothesis and discusses the possible reason for the general lack of interest in the Aluminum Hypothesis among mainstream scientists."

Aluminosilicate Precipitation and Alzheimer's Disease

"The epidemiological features of both diseases can be explained using the hypothesis that the initiating factor is the precipitation of aluminosilicates in the brain. The combination of solubilized aluminum and the only water-soluble form of silicon, silicic acid, to form insoluble aluminosilicates is a peculiar and unique reaction in inorganic chemistry. An evaluation of the uptake and distribution of these compounds provides an explanation for the development of plaques and tangles and a rationale for the findings of the collective epidemiological studies."

Aluminium and the pathogenesis of senile plaques: studies in Alzheimer's disease and chronic renal failure
J. A. Edwardson1 and J. M. Candy1

(1)  MRC Neurochemical Pathology Unit, Newcastle General Hospital, NE4 6BE Newcastle upon Tyne, UK

"Abstract  Aluminium and silicon are co-localised as aluminosilicate at the centre of the senile plaque core. These focal deposits appear to be a consistent and specific feature associated with A4 amyloid fibrils in the plaque core and are not associated with other types of amyloidosis. A pathogenic role for AI and Si is suggested by the finding of A4 amyloid deposits, immature senile plaques and an abnormal content and distribution of these elements in the brains of patients (<55 years) with chronic renal failure. Evidence suggests that AI uptake and distribution within the brain is mediated by transferrin. The distribution of transferrin receptors may account for the vulnerability of regions such as the hippocampus and cortex which are selectively involved in Alzheimer's disease."

Aluminum neurotoxicity in mammals
H. M. Wisniewski1, R. C. Moretz1, J. A. Sturman2, 1, G. Y. Wen1 and J. W.

(1)  Institute for Basic Research in Developmental Disabilities, Departments of Pathological Neurobiology, New York State Office of Mental Retardation and Developmental Disabilities, USA
(2)  Developmental Biochemistry, 1050 Forest Hill Road, 10314 Staten Island, New York, USA

"Although aluminum comprises a large percentage of the Earth's crust, it is excluded from body tissues, and especially from the central nervous system. When aluminum is experimentally introduced to the central nervous system, several neurotoxic effects are observed:i.e. neurofibrillary changes, behavioral and cognitive deficits and enzymatic and neurotransmitter changes, as well as certain types of epileptic seizures."
"The localization of relatively high levels of aluminum in Alzheimer disease, Guamanian amyotrophic lateral sclerosis and Parkinsonism-dementia has led to the implication of aluminum as a pathogenic factor in these diseases. Recent studies have shown that microtubule-associated proteins are part of the paired helical filaments which make up the intraneuronal neurofibrillary tangle. Other studies have identified the protein making the vascular and neuritic (senile) plaque amyloid and located the gene responsible for this protein to chromosome 21."
"Our electron microprobe analysis studies have not found the levels of aluminum or silicon in either the neurofibrillary tangles or amyloid cores reported elsewhere, nor have the levels of aluminum been elevated in approximately one half of the tangles and plaque cores examined to date."

Precipitation and characterization of an aluminosilicate from
AlCl3-Na2SiO3-HCl in serum, of interest for Alzheimer disease.

Bilinski H, Horvath L, Trbojevic-Cepe M.

Ruder Boskovic Institute, Zagreb, Croatia.

"A precipitation experiment was performed with human serum to model aluminosilicate formation in brains of patients with Alzheimer disease. Aluminum and (or) silicate ions were added to serum in a 1:2 molar ratio at pH 7.4. Precipitates formed immediately and were left for 24 h at 37 degrees C before filtration. Silicate and aluminosilicate formed
precipitates with human serum proteins albumin, transferrin, and IgG. In untreated samples, the IgG/albumin ratio increased slightly compared with the ratio in dried serum. Diethylbarbiturate-washed precipitates had a
significantly lower protein content than did untreated ones. The IgG/albumin ratio increased considerably in the sample containing aluminosilicate. We conclude that IgG is the sodium dodecyl sulfate-soluble human protein most firmly bound to the aluminosilicate matrix. From 27Al magic-angle-spinning nuclear magnetic resonance (MAS NMR), a pronounced peak was found at 52.79 ppm and a minor peak at 0.53 ppm, suggesting that 4-coordinated aluminum predominates and that
6-coordinated aluminum is present in a smaller proportion. The 29Si MAS NMR spectrum shows a poorly ordered structure. The aluminosilicate formed also contains the cations Na+ > K+ > Ca2+ > Mg2+ and anions Cl- > PO4(3-). Rather than looking for aluminum toxicity to explain the effects of Alzheimer disease, one should consider that by precipitating such a composite phase, the balance of cations, anions, and proteins in human serum is changing."

PMID: 1394986 [PubMed - indexed for MEDLINE]




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Updated: July 2, 2012
Inception: July 2, 2012