Study: Association of Pathogens & Biofilms With Alzheimer’s Disease – But Wormser Repeats ‘No Evidence’ Mantra

Study: Association of Pathogens & Biofilms With Alzheimer’s Disease – But Wormser Repeats ‘No Evidence’ Mantra

January 5, 2022

https://www.mdpi.com/2076-2607/10/1/56/htm

An Association of Pathogens and Biofilms with Alzheimer’s Disease

by Sandhya T. Chakravarthi¹ and Suresh G. Joshi^1,2,*

^*Author to whom correspondence should be addressed.

Academic Editor: Giuseppantonio Maisetta

Microorganisms 2022, 10(1), 56; https://doi.org/10.3390/microorganisms10010056

Received: 16 December 2021 / Revised: 23 December 2021 / Accepted: 24 December 2021 / Published: 28 December 2021

(This article belongs to the Special Issue Antimicrobial Testing (AMT))

Abstract

As one of the leading causes of dementia, Alzheimer’s disease (AD) is a condition in which individuals experience progressive cognitive decline. Although it is known that beta-amyloid (Aβ) deposits and neurofibrillary tangles (NFT) of tau fibrils are hallmark characteristics of AD, the exact causes of these pathologies are still mostly unknown. Evidence that infectious diseases may cause AD pathology has been accumulating for decades. The association between microbial pathogens and AD is widely studied, and there are noticeable correlations between some bacterial species and AD pathologies, especially spirochetes and some of the oral microbes. Borrelia burgdorferi has been seen to correlate with Aβ plaques and NFTs in infected cells. Because of the evidence of spirochetes in AD patients, Treponema pallidum and other oral treponemes are speculated to be a potential cause of AD. T. pallidum has been seen to form aggregates in the brain when the disease disseminates to the brain that closely resemble the Aβ plaques of AD patients. This review examines the evidence as to whether pathogens could be the cause of AD and its pathology. It offers novel speculations that treponemes may be able to induce or correlate with Alzheimer’s disease.

(Please see link for full article)

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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 [27].
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 [27].
Infections with spirochetes induce cytokine release, and spirochete lipoproteins, including lipopolysaccharide-binding protein (LBP), can activate TLR to stimulate TNF production [30].
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:

https://academic.oup.com/cid/advance-article-abstract/doi/10.1093/cid/ciab993/6446212?redirectedFrom=fulltext

Abstract

The role that microorganisms might have in the development of Alzheimer’s disease is a topic of considerable interest. In this article we discuss whether there is credible evidence that Lyme disease is a cause of Alzheimer’s disease and critically review a recent publication claiming that Borrelia burgdorferi sensu stricto infection, the primary cause of Lyme disease in the United States, may cause Lewy body dementia.

We conclude that no convincing evidence exists that Lyme disease is a cause of either Alzheimer’s disease or Lewy body dementia.

Somethings never change.

For more:

https://www.change.org/p/the-us-senate-calling-for-a-congressional-investigation-of-the-cdc-idsa-and-aldf Lyme advocate Carl Tuttle sent a letter to the Editor-in-Chief of Clinical Infectious Diseases regarding the Wormser publication. Excerpt:

Any threat to the established narrative is met with staunch opposition as we see in the case of B. burgdorferi infection and possible connection to Alzheimer’s disease. Establishing this connection turns Lyme disease into something far more sinister proving that our public health officials have been asleep at the wheel while the disabled patient population and advocacy groups have been shouting from the rooftops for decades. [4]

Category:

Alzheimer's, Lyme, research

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