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Alzheimer’s disease: A Commentary on Biofilms, Beta Amyloid and their Locations

Jennifer R DiBiagio, Suresh G Joshi and Herbert B Allen

The pathological study of brains affected by Alzheimer’s disease (AD) has shown the presence of spirochetal infection. These bacteria produce a detectible biofilm as a defense mechanism, impenetrable by both the immune system and antibiotic medications. The failure of the innate immune system at the site of biofilm deposition ultimately leads to the pathognomonic beta-amyloid (Aβ) plaques of AD at the exact same location as visualized by immunological staining. Furthermore, recent studies show that senile plaques are partially composed of bacterial Aβ in addition to that of the host. The bacterial and neuropathology similarities continue with similar staining results using all of the following: silver impregnation techniques, green thioflavin S fluorescence, anti-AβPP, and anti-AβPP antibodies. TUNEL assay of senile plaques further support the DAPI visualization and in situ hybridization detection of bacterial DNA with extracellular DNA fragmentation that corresponds to spirochetal apoptosis in the plaque’s biofilms, confirming the plaques are composed of spirochetes, Aβ, and biofilm. These significant similarities of biofilms and Aβ substantiate our hypothesis that amyloid of AD is located in the extracellular space.