I assure you that after five years of researching this issue, we are quite familiar with this literature, Fred. The research you claim was "trashed" was done 18 years ago and the science has moved on from these papers!
The first you linked to apparently did a search for the DNA of just one specific spirochete, borellea burgdorferi, the spirochete that causes Lyme Disease, in the bodies of AD victims. . . plus the other Borellea members that share that gene sequence that causes Lyme disease. This test is capable of recognizing only the fourteen species of spirochetes that cause Lyme disease, out of more than two hundred so far identified and named species of spirochetes! None of those happen to be oral spirochetes. The borellea family is not really implicated in this set of hypotheses, although I believe some suggested it, along with the one that causes Syphilis, as a candidate back then. It is merely a spirochete, among hundreds, if not thousands, of other species of yet to be identified and classified spirochetes..
The second 1999 paper refers to a study that attempted to find spirochetes by looking with a microscope at the blood of living patients, and a few autopsied brain samples (n=7). I could not read the entire report, but I am aware of the extreme difficulty most microscopy studies have of even SEEING spirochetes because spirochetes are transparent!
We continually run into doctors who buy an inexpensive, standard microscope, thinking they are being economical, who then look and fail to see the spirochetes in the mouths' of their patients. You have to use a Phase Contrast Microscope or you simply won't see them unless you properly prepare the slide by staining! That's a time consuming task. We know of microscopic studies that were reported negative, that when duplicated with PCMicroscopes were found to be positive, with thousands of spirochetes that were literally invisible under the normal light of a regular microscope. Monday, I will look to see if we have a copy of this paper and see what their microscope protocol was. I know that some work was critcized for what I described. I don't know if this was one of those. But, again, the science has moved on since 1999, 12 years ago.
Adding exclamations points does not change the fact that the reason that this refutation is significant is that Miklossy's best data, both in the original 1993 paper and in the 2011 preprint, claim the strongest correlation (both positive and negative) for exactly this family of pathogens. The test is determinative, and has no subjectivity, and it finds NO no incidence of Lyme spirochetes in any AD victim.
The authors of the paper do not equivocate: It is a complete ass-kicking.
None of those happen to be oral spirochetes. The borellea family is not really implicated in this set of hypotheses,
Not in your set of hypotheses, but certainly it is in Miklossy's paper.
In fact, in addressing the fact that at least three other researchers failed to verify her claims in a 2004 paper, Miklossy makes the following extraordinarily bizarre claim:
In order to study the particular involvement of Borrelia burgdorferi in AD, it is important to analyze AD patients with a positive serology for Borrelia burgdorferi. Different types of spirochetes may be similarly involved in other AD cases [29,44].
This says nothing more or less than that Borrelia burgdorferi isn't likely to be present in AD cases except in areas where Borrelia burgdorferi is common. That's really NOT even convincing evidence of correlation, forget about causation.
The second 1999 paper refers to a study that attempted to find spirochetes by looking with a microscope at the blood of living patients, and a few autopsied brain samples (n=7). I could not read the entire report, but I am aware of the extreme difficulty most microscopy studies have of even SEEING spirochetes because spirochetes are transparent!
This claim is laughable.
You are suggesting that a peer-reviewed paper challenging a published result got past referees with specialization in this field because of poor experimental technique. Whatever experimental technique and apparatus were available to Miklossy when she started making these claims in 1993 were certainly available to any number of researchers who have been unable to reproduce her findings, especially in 2000 when this paper was written.
As for your notes on transmissibility in another post, you appear determined to miss the point about this. It is immaterial how long the progression of plaques produced by spirochetes to AD takes, or even if the patients keep reinfecting themselves. People are initially infected with these spirochetes somehow, and spirochetes are transmitted orally. That means epidemiologists should be seeing a significant correlation between AD patients and family members. We do not see this correlation when we correct for heritability according to the critical letter in the first citation.
Finally, your claims that you see elevated cholesterol, Type II diabetes and heart disease in patients with oral spirochetosis, is, quite frankly, not a scientific claim.
It might be interesting and it might be worth investigating, but, like the claim that walking under a ladder leads to BAD THINGS, it is essentially superstition on your part, and nothing more. Some superstitions have a basis in fact; some don't.
Metaboloic Syndrome is common, and is an accepted underlying explanation for these conditions in a large number of adults. The simultaneous presence of pathogens (of any kind) isn't dispositive of anything if those pathogens are as common in the oral microecology as you claim, because Metabolic Syndrome is also so common.
These people also all drink water. Or to take a more pertinent correlation, they all apparently go to the same dentist.
Can I therefore conclude that dentistry is the cause of Metabolic Syndrome? AD? Oral spirochetosis? [Hint: NO]