Alzheimers Disease: A Novel Hypothesis for the Development and the Subsequent Role of Beta Amyloid

Spirochetes, biofilms, and innate immune system activity have all been recently found in the brains of Alzheimer’s disease patients. The mechanism and actions of those factors in producing the disease were discussed in those studies. However, neither the production nor the role of beta amyloid was included in the discussion of those studies. In this commentary, we hypothesize how the development of beta amyloid occurs as a result of the activation of the innate immune system first responder Toll-like receptor 2 (TLR 2) and its major pathway (MyD88). This leads not only to TNFα, but also NFκB. Both of these molecules have been previously shown to induce the secretases necessary to cleave the amyloid precursor protein. This leads directly to beta amyloid. Further, the beta amyloid (Aβ) has been shown to be antimicrobial and its presence on and around the hippocampal plaques (the pathological hallmark of Alzheimer’s disease) has been demonstrated. It becomes apparent that the Aβ tries to kill the spirochetes but cannot penetrate the biofilm. Its build-up then interrupts and destroys the brain tissue.