Neurospirochetosis

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"Give with a free hand, but give only your own."
-- J.R.R. Tolkien The Children of Hurin
- Neurospirochetosis -

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Observations:
See also, Gum Disease

Neurospirochetosis (Spirochetes)

Wikipedia entry for spirochetes

http://en.wikipedia.org/wiki/Spirochetes

I don't even know where to begin with this one. I first read the abstract, and thought, hmmm... this is interesting. Then I waded through the "provisional full text .pdf". The author links together so many clues to this mystery that she has me me thinking, *this* might be the cause to not only Alzheimer's disease and its relatives, but maybe several other diseases such as CBD. For example, she points out that these bacteria have been found IN THE BRAINS of over 90% of those with AD symptoms that were tested, while NONE of the control samples had them. They may travel along the olfactory nerve, or other nerves or the lymphatic system and reach the brain. In the case of traveling long the olfactory nerve, that is consistent with the initial involvement of the olfactory lobe of the brain in the early symptoms of AD. Also, the presence of the bacteria have been shown to produce "neurofibrilary tangles" of tau proteins and "senile plaques" of amyloid beta protein. Exposure to Borrelia burgdorferi (Lyme disease) bacteria may lead to "hyperphosphorylation" of tau proteins.

Further searching leads me to possible treatments with antibiotics such as doxycycline, tetracycline, etc.

Anyway... read the papers. I think you will find them interesting.

Alzheimer's disease - a neurospirochetosis. Analysis of the evidence following Koch's and Hill's criteria.

Judith Miklossy

Correspondence: Judith Miklossy
Journal of Neuroinflammation 2011, 8:90 doi:10.1186/1742-2094-8-90

Published: 4 August 2011

Abstract (provisional)

It is established that chronic spirochetal infection can cause slowly progressive dementia, brain atrophy and amyloid deposition in late neurosyphilis.

Recently it has been suggested that various types of spirochetes, in an analogous way to Treponema pallidum, could cause dementia and may be involved in the pathogenesis of Alzheimer's disease (AD).

Here, we review all data available in the literature on the detection of spirochetes in AD and critically analyze the association and causal relationship between spirochetes and AD following established criteria of Koch and Hill.

The results show a statistically significant association between spirochetes and AD (P = 1.5 x 10-17, OR = 20, 95% CI = 8-60, N = 247).
When neutral techniques recognizing all types of spirochetes were used, or the highly prevalent periodontal pathogen Treponemas were analyzed, spirochetes were observed in the brain in more than 90% of AD cases.

Borrelia burgdorferi was detected in the brain in 25.3% of AD cases analyzed and was 13 times more frequent in AD compared to controls.

Periodontal pathogen Treponemas (T. pectinovorum, T. amylovorum, T. lecithinolyticum, T. maltophilum, T. medium, T. socranskii) and Borrelia burgdorferi were detected using species specific PCR and antibodies.

Importantly, co-infection with several spirochetes occurs in AD.

The pathological and biological hallmarks of AD were reproduced in vitro.

The analysis of reviewed data following Koch's and Hill's postulates shows a probable causal relationship between neurospirochetosis and AD.

Persisting inflammation and amyloid deposition initiated and sustained by chronic spirochetal infection form together with the various hypotheses suggested to play a role in the pathogenesis of AD a comprehensive entity.

As suggested by Hill, once the probability of a causal relationship is established prompt action is needed.

Support and attention should be given to this field of AD research.

Spirochetal infection occurs years or decades before the manifestation of dementia.

As adequate antibiotic and anti-inflammatory therapies are available, as in syphilis, one might prevent and eradicate dementia.

...

Conclusion

Various types of spirochetes, including B. burgdorferi, and six periodontal pathogen spirochetes ((T. socranskii, T. pectinovorum, T. denticola, T. medium, T. amylovorum and T. maltophilum) were detected in the brains of AD patients.

The pathological and biological hallmarks of AD, including increased AβPP level, Aβ deposition and tau phosphorylation were induced by spirochetes in vitro.

The statistical analysis showed a significant association between spirochetes and AD. The strongly significant association, the high risk factor and the analysis of data following Koch’s and Hill’s criteria, are indicative of a causal relationship between neurospirochetoses and AD.

Spirochetes are able to escape destruction by the host immune reactions and establish chronic infection and sustained inflammation.

In vivo studies with long exposure times will be necessary to efficiently study the sequence of events and the cellular mechanisms involved in spirochete induced AD-type host reactions and Aβ-plaque, “tangle” and “granulovacuolar” formation.

The characterization of all types of spirochetes and co-infecting bacteria and viruses is needed, in order to develop serological tests for the early detection of infection.

The pathological process is thought to begin long before the diagnosis of dementia is made therefore, an appropriate targeted treatment should start early in order to prevent dementia.

Persisting spirochetal infection and their persisting toxic components can initiate and sustain chronic inflammatory processes through the activation of the innate and adaptive immune system involving various signaling pathways.

In the affected brain the pathogens and their toxic components can be observed, along with host immunological responses.

The response itself is characteristic of chronic inflammatory processes associated with the site of tissue damage.

The outcome of infection is determined by the genetic predisposition of the patient, by the virulence and biology of the infecting agent
and by various environmental factors, such as exercise, stress and nutrition.

The accumulated knowledge, the various views, and hypotheses proposed to explain the pathogenesis of AD form together a comprehensive entity when observed in the light of a persisting chronic inflammation and amyloid deposition initiated and sustained by chronic spirochetal infection.

As suggested by Hill, once the probability of a causal relationship is established prompt action is needed. Similarly to syphilis, one may prevent and eradicate dementia in AD.

The impact on healthcare costs and on the suffering of the patients would be substantial.
http://www.jneuroinflammation.com/content/8/1/90/abstract
http://www.jneuroinflammation.com/content/pdf/1742-2094-8-90.pdf

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Natural sources:

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References:

Alzheimer's disease - a neurospirochetosis.
Posted on Friday, August 26, 2011 4:12:38 PM by Swordmaker
"The protocol is to take a heaping teaspoon of Baking Soda—I do it when I am in the shower—and load your toothbrush with the Soda. Then holding the toothbrush at a 45º angle to the tooth, brush into the gums, working the baking soda into the gums. Use all of the Baking soda and hit all off the gums line. Brush your tongue and the back of your tongue with a tongue brush. Leave the residue. Do not rinse. You will get to like the taste.

The second part of the protocol (this is not so palatable... but you can do it) is once or twice a week take a cap full of Clorox™ brand BLUE CAP bleach—do not use an off brand as we do not know the purity of any other brand—and put it in a glass. Add TWENTY caps fulls of water to make a 20 to 1 dilute mixture of water to bleach... and swish that around in your mouth like mouthwash. It is merely very strong "swimming pool water", called Dakin's Solution, but it will KILL any remaining bacteria in your mouth. It is also the only known substance that will dissolve plaque! Don't worry if you swallow any of it. It will convert to ordinary table salt in your stomach!"
http://www.freerepublic.com/focus/chat/2769347/posts

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