University Institute of Pathology, Division of Neuropathology, University Medical School (CHUV), 1011, Lausanne, Switzerland. and University of British Columbia, Department of Psychiatry, Kinsmen Laboratory of Neurological Research, Vancouver, B.C. V6T 1Z3, Canada.
The cause, or causes, of the vast majority of Alzheimer's disease cases are unknown. A number of contributing factors have been postulated, including infection.
It has long been known that the spirochete Treponema pallidum, which is the infective agent for syphilis, can in its late stages cause dementia, chronic inflammation, cortical atrophy and amyloid deposition.
Spirochetes of unidentified types and strains have previously been observed in the blood, CSF and brain of 14 AD patients tested and absent in 13 controls.
In three of these AD cases spirochetes were grown in a medium selective for Borrelia burgdorferi. In the present study, the phylogenetic analysis of these spirochetes was made.
Positive identification of the agent as Borrelia burgdorferi sensu stricto was based on genetic and molecular analyses. Borrelia antigens and genes were co-localized with beta-amyloid deposits in these AD cases.
The data indicate that Borrelia burgdorferi may persist in the brain and be associated with amyloid plaques in AD.
They suggest that these spirochetes, perhaps in an analogous fashion to Treponema pallidum, may contribute to dementia, cortical atrophy and amyloid deposition.
Further in vitro and in vivo studies may bring more insight into the potential role of spirochetes in AD.
PMID: 15665404 [PubMed - as supplied by publisher]
Posted by david1097 (Member # 3662) on :
Has anybody ever used an Omiya Reservoir for direct treatment Lyme brain infections. This is a device that is inserted through a hole in the skull and covered by the scalp.
It is basically a pipe that gets filled with drugs that are delivered directly to the brain. Whne it gets empty a needle is inserted and the Reservoir is replenished. It is very similar to a chest port except it goes into the brian.
Since it contacts the brain and CFS directly there is no Blood brain barrier to attenuate the dose.
Posted by trevor (Member # 4353) on :
Hi, Lida Matman describes the causative influence, with excellent photos, of lyme spirochetes in Alzheimers and so many other neurodegenerative diseases in her book "Cell Wall Deficient Forms: Stealth Pathogens". She'll be speaking at the upcoming conference in SF.
-trevor/oliver
Posted by bg (Member # 46416) on :
My sister-in-law was 40 when she died from early on-set Alzheimer's disease.
She had this mind-robbing disease for 8-14 years and treated for severe depression the entire time.
Mayo Clinic removed her brain, and they did an autopsy taking about 5 months to determine that it was AD.
Her brain tissue was sent to the east coast as there was a former Iowa City MD who saw/tested her. As different developments in early onset AD have come, tissue has been tested.
They feel her teenage children then, 16 and 13, will NOT inherit her illness as some cases do.
If there is any tissue left, would it be to late to check for spirochetes since there is no blood to test? Just curious. She died in 93. Betty G.
Posted by lymemomtooo (Member # 5396) on :
Does anyone know if Ronald Reagan ever had a Western Blot? Just curious.
Posted by whatever (Member # 10234) on :
Medical Hypotheses. 2006 Oct 19.
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.
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 [PubMed - as supplied by publisher]
[ 19. November 2006, 11:08 AM: Message edited by: whatever ]
Posted by Tincup (Member # 5829) on :
Good info.. thank for posting, whatever.
Posted by GiGi (Member # 259) on :
It's long been known that heavy metals as well as parasites are found in the Alzheimer/dementia brain as well. That is why removing the heavy metals is so important. The microbes lose their anaerobe terrain.
Going by my own experience, the heavy metals had entered my brain straight from the teeth via nerve tubulin into the brain long before my tick bite. The picture is the same in Parkinsons and a number of other neuro diseases. The blood brain barrier was damaged already by the metals which made the entry for the microbes very easy.
A portion of Dr. K's publication of years ago:
".....the cells of the body are harmed by toxic metals whereas the invading microorganisms can often thrive in a heavy metal environment. Research by Ludwig, Voll and others in Germany, by Omura and myself here in the US, showed that microorganisms tend to set up their housekeeping in those body compartments, that have the highest pollution with toxic metals. The body's own immune cells are incapacitated in those areas whereas the microorganisms multiply and thrive in an undisturbed way. The teeth, jawbone, Peyers patches in the gutwall, the groundsystem (connective tissue) and the autonomic ganglia are common sites of metal storage - where microorganisms thrive. Furthermore, those body areas also are vasoconstricted and hypoperfused (by blood, nutrients and oxygen), which fosters the growth of anaerobic germs, fungi and viruses."
Take care.
[ 19. November 2006, 12:13 PM: Message edited by: GiGi ]
Posted by whatever (Member # 10234) on :
Thanks GiGi for the additional info on heavy metals. That really helps to build a coherent picture, since, having read a lot about AD, with this new theory it was looking to me like a wild grab bag of different causal hypotheses for AD. But to see two hypotheses working together (bacteria and heavy metals) like that makes for a stronger composite hypothesis.
![[Big Grin]](biggrin.gif)