An Association of Pathogens and Biofilms with Alzheimer’s Disease
A few notable points:
- Spirochetes were visualized in the neurofibrillary tangles and senile plaques in the brains of individuals with AD, and peptidoglycan was also located near Aβ deposits .
- Several studies show combined evidence that spirochetes are detectable in the brains of about 90% of AD patients, whereas they were often not present in non-AD brains, with periodontal spirochete presence being even higher at over 93%, showing a significant association of spirochetes with AD .
- Infections with spirochetes induce cytokine release, and spirochete lipoproteins, including lipopolysaccharide-binding protein (LBP), can activate TLR to stimulate TNF production .
- TNF production and cytokine release induce inflammation locally and systemically in infected individuals, but it is unclear whether or not the inflammation seen in AD brains is due to spirochete infections.
- After these early results, researchers hypothesized that two of the potential spirochetes could be Treponema pallidum or Borrelia burgdorferi, based on the neurological symptoms that the bacteria are known to cause, and these organisms have been highly studied in relation to AD.
- The article discusses the role of biofilm which frankly has been completely ignored by mainstream media and research.
- Biofilm formed by Bb exhibit similar pathology to one of the hallmarks of AD, and that is AB plaque deposition, which was present in brain samples.
- While the conclusion is directed toward oral treponemes, it states the next logical step would investigate brain tissue samples from AD patients to correlate spirochetes and other pathogens’ association with AD.
Just a few weeks prior to this paper, another paper found Bb co-localizing with amyloid markers in Alzheimer’s Disease brain tissues. Important excerpts:
The results showed the presence of B. burgdorferi antigen and DNA in patients with AD pathology and among those, one of them was previously diagnosed with Lyme disease. Interestingly, a significant number of Borrelia-positive aggregates with a known biofilm marker, alginate, were found along with the spirochetal structures. Our immunohistochemical data also showed that Borrelia-positive aggregates co-localized with amyloid and anti-phospho-tau markers. To further prove the potential relationship of B. burgdorferi and amyloids, we infected two mammalian cell lines with B. burgdorferi which resulted in a significant increase in the expression of amyloid-β and p-Tau proteins in both cells lines post-infection. These results indicate that B. burgdorferi can be found in AD brain tissues, not just in spirochete but a known antibiotics resistant biofilm form, and its co-localized amyloid markers. In summary, this study provides evidence for a likely association between B. burgdorferi infections and biofilm formation, AD pathology, and chronic neurodegenerative diseases.
But, just a month prior to this paper, infamous Lyme denialist Gary Wormser essentially states ‘Nothing to see here,’ regarding a connection between Lyme disease and Alzheimer’s and Lewy Body dementia: