The Historical Development of the Pathological Changes in Alzheimer’s Disease Based on Microbiology, Anatomy, and Physiology
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Abstract
The major pathological changes in Alzheimer’s disease were found in hippocampal specimens from Alzheimer disease patients. We contend that spirochetal bacteria that make biofilms cause these changes. The spirochetal/biofilm complexes induce the changes of note including neurofibrillary tangles, senile plaques, beta amyloid, and atrophy. It has been shown previously that when spirochetes make biofilms, they create beta amyloid simultaneously. When the biofilm is made intracellularly (in the neuron), the beta amyloid that is also produced, interacts with tau protein and converts it to hyperphosphorylated tau. This leads directly to neurofibrillary tangles. Produced extracellularly (outside the neuron), the biofilms, which are coated by beta amyloid, form the senile plaques. The interaction of the biofilm in the senile plaques with the innate immune system molecule Toll-like receptor 2 produces beta amyloid by known pathways. The atrophy, both total and regional, is produced when the neurons disintegrate. All these pathological findings take considerable time that fits with the clinical course of the disease. For instance, it takes up to two years for spirochetes to make a single biofilm. This differs from other microbes such as Chlamydia pneumoniae, Porphyromonas gingivalis, and Herpes simplex that make biofilms in minutes. The long time for development therefore fits better with spirochetes compared to other organisms.
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