Prior Studies:·
In 2005 Andrasi, et al. measured aluminum levels in specific brain regions (e.g. hippocampus, entorhinal cortex, and two areas of the frontal cortex) of three AD patients and 3 non-demented controls. Compared to the controls there was a 2.6-fold to 6.8-fold higher aluminum levels in these regions of the AD brain1. In 2009 Fjell, et al., looking at 142 healthy controls and 122 people with AD, found that these same regions of the brain had the most atrophy in those with AD compared to controls2.·
In 2011 Russina, et al, measured both aluminum and mercury in the brains of 28 histologically-confirmed cases of AD and 27 healthy controls. There was a four-fold higher level of aluminum in the hippocampus of the AD patients compared to the controls. There was no difference in mercury levels3.·
In 2017 Exley, et al. measured aluminum in the brains of 12 people diagnosed with familial AD. Aluminum levels were in all cases higher than normal and in 5 of the 12 cases they were eight-fold higher than normal4.
These three studies involved measuring aluminum in a total of only 43 brains of people diagnosed with AD. Scientists who were still doubtful that the known neurotoxin aluminum is a causal factor of AD have called for a larger study measuring aluminum in more AD brains and controls and more studies demonstrating aluminum neurotoxicity at concentrations found at physiological conditions.
New Study: A new study was published in 2018 by McLachlan, et al., of 186 autopsied brains taken from those diagnosed with AD and 53 controls. The amount of aluminum in the temporal lobe (Brodmann areas A20-A22) was 6-fold greater in those with AD than the controls5. This study has increased the total number of autopsied brains with AD having significantly above normal levels of aluminum to 229. It can now be concluded based upon the study of these 229 brains that higher than normal levels of aluminum are both a hallmark of AD and a causal factor of AD. Particularly when coupled with Fjell’s work with 122 people with AD showing that the regions of the brain that are aluminum hot-spots also are same the regions with most atrophy in the brains of those with AD2.
What is perhaps most interesting about McLachlan’s paper is the author’s ambivalence toward aluminum chelation therapy for removing aluminum from the brains of those with AD. It is pointed out that “… once bound, aluminum is particularly refractory to chelation-based removal …”. But then the author goes on to describe some of his own work6, first reported in 1991, by saying “Interestingly, the only clinical trial specifically designed to remove aluminum from the brains of live control and 48 AD patients using the trivalent metal chelator desferrioxamine (DF) resulted in halving the rate of neuro-degeneration and cognitive decline in the DF-treated group”.
This ambivalence toward chelation therapy evidently is due to the authors being unaware of the work published in 2006 by Exley, et al., who stabilized and in some cases reversed the cognitive decline in 15 AD patients by using silica rich drinking water for 12 weeks to facilitate aluminum excretion7,8. The authors must also be unaware of the work published in 1998 by Belles, et al. showing that silica rich drinking water given to rats for just 5 weeks dramatically lowered aluminum levels in 6 regions of the brain (e.g. cortex, hippocampus, striatum, cerebellum, thalamus, and olfactory lobe)9. Even aluminum in bone was over 90% removed in just 5 weeks by silica rich drinking water9.
Here is a link to a study published in Jan 2020 after this write up. This study analyzed brains of people with Familial Alzheimer’s. Aluminum was associated with Tau Tangles in people with familial Alzheimer’s. https://content.iospress.com/articles/journal-of-alzheimers-disease/jad191140?fbclid=IwAR2rP1158kVi6W2wNHVvvGXoSY4qyfkudAjlg_N21B9_P_ToU3mwVPkfYIw
My wife Laurie Adamson has set up a facebook information group called Alzheimer’s: Late and Early Onset, APOE4https://www.facebook.com/groups/509038829797535
References
1. Andrasi, E., et al.; Brain Al, Mg, and P contents and Alzheimer-diseased patients; J. Alzheimer’s Dis.; 7:273-84 (2005)
2. Fjell, A.M., et al.; One-year brain atrophy evident in healthy aging; J. Neurosci.; Dec.; 29(48):15223-31 (2009)
3. Rusina, R., et al.; Higher aluminum concentrations in Alzheimer’s disease after Box-Cox data transformation; Neurotox. Res.; 20, 329-33 (2011)
4. Mirza, A., et al.; Aluminum in brain tissue in familial Alzheimer’s disease; J. Trace Elements in Medicine and Biology; Mar.; 40:30-36 (2017)
5. McLachlan, D.R.C., et al.; Aluminum in neurological disease – a 36 year multicenter study; J. Alzheimer’s Dis. Parkinsonism; 8: 457 (2018) https://www.omicsonline.org/open-access/aluminum-in-neurological-disease–a-36-year-multicenter-study-2161-0460-1000457.pdf
6. McLachlan, D.R.C.; et al.; Intramuscular desferrioxamine in patients with Alzheimer’s disease; The Lancet; 337(8753):1304-8 (1991)
7. Exley, C., et al.; Non-invasive therapy to reduce the body burden of aluminum in Alzheimer’s disease; J. Alzheimer’s Dis.; Sept., 10(1):17-24 (2006)
8. Davenward, S., et al.; Silicon-rich mineral water as a non-invasive test of the ‘aluminum hypothesis’ in Alzheimer’s disease; J. Alzheimer’s Dis.; 33(2):423-30 (2013)
9. Belles, M., et al.; Silicon reduces aluminum accumulation in rats: Relevance to the aluminum hypothesis of Alzheimer’s disease; Alzheimer’s Dis. Assoc. Disorders; 12(2):83-7 (1998)
Dennis N Crouse, PhD Harvard, Scientist and Author