2007: Alzheimer's neuroborreliosis with trans-synaptic spread of
infection  

Group: alt.support.alzheimers Date: Wed, Dec 5, 2007, 8:36am From:
CaliforniaLyme@cs.com (SarahO.)
1: Med Hypotheses. 2007;68(4):822-5. Epub 2006 Oct 20. Links
Alzheimer's neuroborreliosis with trans-synaptic spread of infection and
neurofibrillary tangles derived from intraneuronal spirochetes.
MacDonald AB.
Department of Pathology, St Catherine of Siena Medical Center, 50 Rte 25
A, Smithtown, NY 11787, United States. inmacdonald@yahoo.com
<inmacdonald@yahoo.com>
In the realm of dementia, it is astonishing to note that neurofibrillary
tangles (NFT) are microscopically identical in a childhood illness
(SSPE) and in a dementia of late adult life (Alzheimer's disease). The
words "Alzheimer-type" NFT in peer reviewed scientific articles written
by acknowledged experts underscore the striking similarities in
"tangles" in two different diseases. Subacute Sclerosing Panencephalitis
(SSPE) is caused by infection with atypical measles virus. Alzheimer's
disease has no known cause. There is little controversy in suggesting
that all of the Tangles in SSPE infected neurons are produced by slow
viral type variant of Measles infection. But the mere suggestion that
infection might be a cause of Alzheimer's disease confounds the
establishment. If a good case is to be made for infection in Alzheimer's
disease, an excellent nerve cell infection model is needed. Monkeys have
provided a very reasonable model. Recently, a primate neuroborreliosis
brain infection model demonstrated that Borrelia injected into the skin
of monkeys resulted in the appearance of Borrelia transcriptomes in
brain neurons. If Borrelia can travel from skin to brain in the monkey,
then why not look at human Alzheimer's tissues to see if the DNA of
Borrelia is present in the human brain? The molecular detection tools
perfected in animal neuroborreliosis studies have been applied to human
Alzheimer's disease brain tissues. Seven of ten cases of Alzheimer's
disease from McLean Hospital Brain Bank of Harvard University yielded
positive signals for infectious DNA in a small pilot study. Alzheimer's
diseased neurons analyzed with DNA probes, produced little "dots" of
positive staining. Granulovacuolar bodies in Alzheimer's diseased
neurons (little dots in a bubble), are one of the expected microscopic
profiles of Alzheimer's disease. "Little dots" inside nerve cells are
also signatures of viral infectious agents inside of nerve cells. So
with the assistance of the microscope and the tools of molecular
biology, a new model of infection emerges as a cause of "Alzheimer's-
type" neurofibrillary tangles. Here I hypothesize that it is chronic
infection of human neurons in Alzheimer's disease that produces
neurofibrillary tangles by a pathway similar to the chronic SSPE
infection tangle pathway. In addition, transmission of infection from
nerve to nerve is proposed to explain the evolution of Alzheimer's
disease. Herein is offered a new view for the origins and for the
progression of diseased nerves with tangle formations in Alzheimer's
disease based on infection.
PMID: 17055667
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Alzheimer Disease studies are forever stuck on amyloid plaques and
neurofibrillary tangles.  AD DOES have a known cause. The root cause
comes from a viral infection, discovered in the early 1900s by the late
great Dr. James R. Hunt. Throughout his entire career, his main interest
was in the motor and sensory function of the facial nerves. Thirty years
after his first paper on the sensory aspects of the facial nerves, he
brought together his entire clinical experience with geniculate
neuralgia including a masterful review of the anatomic literature
combined with spectacular illustrations published in the year of his
death. Dr. Hunt came from a family of doctors, educated in the United
States and abroad, named in the book  "Who's Who", yet  few doctors ever
heard of him or the disease he discovered.  A coverup!!!

EddyJean