Alzheimer's disease: a novel hypothesis for the development and the subsequent role of beta amyloid

Abstract

Spirochetes, biofilms, innate immune system activity have all been recently found in the brains of Alzheimer's disease patients. The mechanism and actions of those entities in producing the disease were postulated in those studies. The production and role of beta amyloid were not included in the discussion; we hypothesize herein how the development of that molecule occurs as a result of the Toll-like receptor 2 activation leading not only to TNFα, but also NFκB which themselves have been previously shown to induce the secretases necessary to cleave the amyloid precursor protein. This leads directly to beta amyloid. 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 buildup then interrupts and destroys the neurocircuitry of the brains.