AD Is No Joke

… but if you have it you will not appreciate nor be offended by anything written here.

Nancy and Ronnie go to a restaurant in California not too far from their ranch.


The waiter says, My name is Alfons and I will be your server… the special today is Lomito a la Pobre. Nancy says, I will have that. And what about the vegetable? replies the waiter. He will have the same, says Nancy.

Bacterial biofilms may play a role in lupus, research finds

Understanding how biofilms trigger autoimmunity may ultimately lead to changes in patient treatment, Dr. Gallucci said. “So understanding how the biofilms affect flares could lead to a different treatment approach. Now, they give immune suppressive drugs. Maybe you want to do something else, like treat the underlying infection.”


Alzheimer’s Disease: Assessing the Role of Spirochetes, Biofilms, the Immune System, and Amyloid-β with Regard to Potential Treatment and Prevention

Alzheimer’s disease (AD) is an infectious disease caused by spirochetes, and these spirochetes form biofilms, which attract the innate immune system.

Where spirochetes have been found in the brains of Alzheimer’s disease (AD), it may be considered an infectious disease; this is the first and most important consideration [1, 2]. It is also a chronic disease, a biofilm-associated disease, [3] and an autoimmune disease [4]. Further, it is a debilitating disease, a socially-destructive disease, an exceedingly expensive disease, and, lastly, a deadly disease [5]. This review will focus on the biofilm portion of the disorder as well as the autoimmune response. It will also touch on some rational therapeutic concepts for this most irrational of diseases.

The infectious nature of AD was revealed when spirochetes (both dental and Lyme) were shown to be present in the brains of affected patients [1]. The dental microbes travel from the oral cavity during times of disruption of the dental plaque and subsequent bacteremia following dental procedures; i.e., any time blood is seen. The hippocampus (which is the initial site of cerebral involvement in AD) is approximately 4 cm from the posterior pharynx. Lyme borrelia travel to the brain via the blood stream during the secondary stage of that disease following the erythema migrans lesion [6]. This secondary stage is characterized by fever, myalgias, arthralgias, and other systemic symptoms. The spirochetes have an affinity for neural tissue and pass through the blood-brain barrier easily [7].

Once the spirochetes are in the brain, they attach, divide (albeit very, very slowly) [8], and multiply. When they reach a quorum, they begin to spin out a biofilm (Fig. 1) [9]. This represents approximately 150 spirochetal cells which are 0.3 microns in diameter (10 cells are necessary on a two-dimensional culture plate for a quorum to begin). Because of the exceedingly slow division, it takes approximately 2 years to accumulate sufficient organisms to make one biofilm. The biofilm is protective and is a response of the organisms to ensure their survival, inasmuch as it encases them in “slime” (Fig. 2).

Quorum sensing is one triggering mechanism for the production of biofilms; other organisms in other diseases may form biofilms when subjected to different stimuli. These stimuli include salt and water, as seen in eczema and tinea versicolor [10, 11]. Low dose antibiotics and quorum sensing are seen in psoriasis [12] and arthritis [4]. Further, elevated temperatures and exposure to alcohol and other chemicals promote biofilms [13].

None of the commonly used antibiotics penetrate biofilms; and, none of the immunologic molecules from either arm of the immune system, whether innate or adaptive, are able to penetrate either.

…This is the very essence of autoimmunity, namely the body attacking itself; this occurs when the body’s own innate immune system produces TNF-α or Aβ and attacks the biofilm encasing the spirochetes. In the process of doing this, the surrounding tissue is destroyed instead. Such is the case with the biofilm produced by staphylococcus in eczema and streptococcus in psoriasis; these biofilms call forth the innate immune system and the whole process of tissue destruction is set in motion [4]. The consequences of AD are much more dire however, because they lead to total destruction of the mind.

Where the pathology is the same and where both diseases are caused by spirochetes, and where spirochetes are sensitive to penicillin, a reasonable approach would be to follow the same treatment schedule as syphilis [21]. With that treatment, penicillin administered at any time prior to the onset of tertiary syphilis is curative. The same can reasonably be said for AD; penicillin administered any time prior to the onset of tertiary disease would also be curative. Lyme disease is most closely aligned with syphilis with erythema migrans equivalent to the chancre. In most cases, it is one tick bite compared to one chancre, so the treatment could be reasonably the same [7].

None of this is codified; but, the current treatment is most likely harmful with the biofilms being dispersed without the spirochetes being killed. This would conceivably lead to many more biofilms, because all the spirochetes within the previous biofilm are capable of making new biofilms.

The story of AD is then one of spirochetes that make biofilms that activate the innate immune system. The first responder is TLR 2 and TLR 2 generates NF-kB and TNF-α that not only damage tissue in an attempt to kill the biofilm-encased spirochetes, but also lead to the production of Aβ. All of the foregoing leads to dementia. Treatment with a bactericidal antibiotic with a concomitant biofilm disperser seems most reasonable; but, as has been stated previously, any neurologic damage is irreversible. It is therefore of the utmost importance to treat early in the course of this disease.

Bacterial Amyloid and DNA are Important Constituents of Senile Plaques: Further Evidence of the Spirochetal and Biofilm Nature of Senile Plaques

The present results demonstrate that Aβ and bacterial DNA are important constituents of pure in vitro Borrelia biofilms and those formed in senile plaques in vivo. These results are additional evidence that senile plaques are formed by spirochetal colonies and correspond to bacterial biofilms. Biofilm formation in senile plaques further sustains chronic infection and inflammation and contributes to the development of slowly progressive dementia in AD.