* Now, until deeper studies are conducted, there are at least 3 choices related to Apoe's etc.

* From: Ray S. <mercure@PRIMENET.COM>

1. Depletion of GSH due to overload of mercury in relation to the particular liver capacity. I guess the size of the liver and it's capacity is not yet considered a genetic inherited defect ? This depletion causes that there are not enough cysteines/thiols available to be incorporated to the Apoe's, so they are replaced with arginines, and a strong supported of this theory is the apprearance of Apoe3's, as the middle-of-the-road condition before most thiols are extinct, leaving eventually only Apoe4's due to very limited availability of thiols.

2. Overload of the mercury with liver/gall detox capacity faltering under the sheer amount of mercury versus the personal capacity, causing also genetic damage to the cells synthezising Apoe2's, producing the emergence of the Apoe4's, still not an inhetired genetic condition, but direct effect of mercury damaging the DNA coding the Apoe's. Less logic but still possibly within the picture.

3. Inborn genetic damage causing the Apoe4's to appear. Probably causing some people to get Alzheimeristic, but is this the only explanation, is to be proven, propably not the only reason, but in proportion with 1. & 2. Why don't these people get Alzheimeristic already at VERY YOUNG age, as the mercury fillings are often placed into people before their teens, at least in Europe. Do people wait 'till their 60's or 70's in US before they get their mercury fillings ? Why is there no more, or even less Alzheimers in Europe compared to US, which leads me to :

4. Maybe there is an additional, not listed reason why mercury contributes to the Alzheimers like KIP suggested, as those 25 % don't have any trace of Apoe4's yet. Maybe disappearance of Apoe4's is rather an indication that the brains are "gotten" by mercury, but maybe the Apoe4 itself is a MINOR metal carrier in the brains ...

See, to my knowledge Glutathione, GSHpX and other glutathione related enzymes, other metalloproteins etc. are main mercury carriers compared to Apoe's. Of course I could be SEVERELY wrong here, but then obviously people would use Apoe2's as their Alzheimer-reversers in their studies instead of DMSA.

Maybe it is just so that even though Apoe4 may not be the main carrier to have enough meaning as the transporter, maybe it is a very sensitive indicator that the liver/gall detox capacity has become poor compared to the load (in agreeance with MR. Huggins whom I have found to be one of the most solid practical mercury biochemists regardless his dental theater that was closed, I DO RESPECT him as a practical mercury researcher, coming to the very same conclusions as he has after studying 5 or more years.) and telling that brains are gonna get mercurized, as there is no more thiols left.

Maybe these people also have other pointers, like HAIRLOSS, as the same thiols are incorporated to human hair, and if one starts loosing hair, there is no more thiols left to build hair, and the WEAK nails just people even further from the GENERAL LACK OF THIOLS like in Cysteines rather than Apo2 genetic damage.

Also, I swear that the weak nails can be IMPROVED WITH NAC/GSH supplementation, proving the Apoe less important, but that the general thiol supply and the general sulfur metabolism and overall liver/gall/gut/kidney mercury load is propably after all the MOST IMPORTANT single thing.

* From: <kiprs@IX.NETCOM.COM>

Where do you find data that says only "one-fifth of AD patients are victims of long-term, low-level exposure to HG vapor?" If we consider only mercury from amalgams, 80-90% of us are exposed. If we consider mercury from all sources, 100% of us are exposed. Why would AD victims have a much much lower exposure rate?

* From: <BULLOCK@UANSV3.VANDERBILT.EDU>

First, Alzheimer's is an adjective used to describe symptoms, not necessarily pathology. There are four genes known associated with AD like symptoms. About 1/5 of AD patients have a "defect" on chromosome 19--they inherit ApoE 4. "Normal" apolipoprotein E is ApoE 2. Apolipoprotein is somewhat of the garbage-collection device for the brain. ApoE 2 has two sulfhydrals (strong affinity for mercury). On ApoE 4, the sulfhydrals are replaced by arginines (no affinity for Hg). So, In My Humble Opinion (IMHO), about one-fifth of AD victims simply have no means of cleaning Hg from the brain--it's a transport problem. This is conjecture. It will take many many years of research to demonstrate if the arginines vs sulfhydrals results in an Hg load to the brain...just as it took many many years to demonstrate a high correlation between smoking and cancer. There are other familial diseases that are known inabilities to metabolize certain metals....like Wilson's and Cu.

Also make sure to read these books: Poison in Your Teeth: Mercury Amalgam (Silver) Fillings...Hazardous to Your Health! and Mercury Detoxification by Tom McGuire