Mercury and Alzheimer's Disease: the Evidence

Last Summer, some fellow students in my doctoral program put together a presentation on Alzheimer's disease which stated that there was no proof that it was linked to heavy metals.


Being familiar the work of Boyd Haley, PhD, I decided to write a response to their presentation in order to inform them and the rest of class that, although there is surely more to still be uncovered about the connection between Alzheimer's and metals, there is significant evidence that implicates mercury as a causative factor.


Here's a summary of what I wrote, with a bit of editing and some elaboration:


Despite the predominant attitude in the mainstream that Alzheimer's is definitively not related to heavy metals, there is quite a bit of evidence to the contrary and I feel it's important to take this into account. 

 

Boyd Haley, PhD is a professor of chemistry who has done perhaps more work than anyone on establishing the biological plausibility of mercury causing Alzheimer's disease.


According to Dr. Haley, the biochemistry lines up quite neatly, especially with regard to NFTs and the APOE4 allele. 


Here are some of his most important findings:

 

1.  Hg destroys tubulin and is able to directly create the neurofibrillary tangles [NFTs] that are seen in Alzheimer's.  NFTs are a result of the inability to properly create microtubules. 

 

2.  Hg disables creatine kinase, which is known to be inhibited in Alz patients.  It's a sulfur-based molecule, meaning that it has a high affinity for mercury. 

 

3.  Hg disables glutamine synthetase, which is the enzyme that removes glutamate from the synapse.  Abnormally high levels of glutamate are a standard observation in Alz patients.  Being an excitatory neurotransmitter, abnormally high levels cause neuronal destruction via excitotoxicity. 

 

Here's Dr. Haley discussing his work, in which he experimentally induced Alzheimer's disease in rats using mercury:


And here are some critical data points about the APOE4 gene:

 

Dr. Haley has identified the precise mechanism by which the APOE4 allele is associated with a significantly higher risk of Alz Dz.  The APOE protein runs through the cerebrospinal fluid and is a "housekeeping protein", as he refers to it. 


In addition to being involved in cholesterol metabolism, the APOE protein is also an endogenous chelator.

 

Here's how the biochemistry breaks down: the APOE2, APOE3, and APOE4 molecules are all identical except for two amino acid regions. 

 

APOE2, which is highly protective against Alz, has two cysteine groups, which--cysteine being a sulfur-based amino acid--operate as binding sites for Hg, allowing it to carry Hg out of the brain, into the CSF, and out of the body.

 

APOE3, which is moderately protective, has only one cysteine group, so it can only carry out one molecule of Hg at a time [50% less than APOE2]. 

 

APOE4, which is the one we hear about that's considered dire in terms of Alz risk, especially if you have two copies, has NO cysteine groups and thus does not function whatsoever as a transporter of Hg out of the brain.


So, in essence, the APOE4 gene does not GIVE someone Alzheimer's. It merely impairs the body's neurochelation and thus leads to increased levels of mercury [and likely other heavy metals], allowing Alzheimer's to develop.

Here's Dr. Haley giving the breakdown I just described:


Is this is the reason that Sun, et. al. determined that people with mercury fillings were more likely to develop Alzheimer's disease than those without?


Of course, other studies have not shown this connection, so not all the research is in agreement.


More investigation is certainly necessary, but anyone who says that there is definitive proof that Alzheimer's disease is not linked to heavy metals has clearly not reviewed all of the evidence.

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© 2019 by Matt Dorsey, BSc, MAcOM, LAc