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Alzheimer's disease: a novel hypothesis for the development and the subsequent role of beta amyloid
Herbert B Allen*, Diego Morales, Krister Jones and Suresh G Joshi
Drexel University College of Medicine, Philadelphia, USA
- *Corresponding Author:
- Herbert B Allen
Drexel University College of Medicine, Philadelphia, USA
Tel: 2157625550
Fax: 2157625570
E-mail: Herbert.Allen@drexelmed.edu
Received date: March 23, 2016; Accepted date: April 23, 2016; Published date: April 25, 2016
Citation: Allen HB, Morales D, Jones K, Joshi SG (2016) Alzheimers Disease: A Novel Hypothesis for the Development and the Subsequent Role of Beta Amyloid. J Neuroinfect Dis 7:211. doi:10.4172/2314-7326.1000211
Copyright: © 2016 Allen HB, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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.
