Discussion on the Bioethical Challenges Arising from the Microbiology and Pathology of Alzheimer’s Disease

We have presented evidence based on our work and the work of others that Alzheimer’s disease is
caused by spirochetes that make biofilms both inside and outside of neurons. The extracellular
biofilms have been shown to cause upregulation of the innate immune system molecule Toll-like
receptor 2 (TLR2). The TLR2, by known pathways, eventuates in nuclear factor kappa B (NFκB) and
tumor necrosis factor alpha (TNFα) and these molecules lead to beta amyloid and tissue destruction
respectively. This well-documented concept of microbial pathogenicity has been largely disregarded in
favor of the beta amyloid hypothesis which has been in place for the past twenty-five years. These
factors comprise the first ethical challenge. The second challenge is treatment and research efforts
are being utilized at, or near, the end of the pathogenic cascade and not at the beginning of the
process at which time the spirochetes are easily treatable. Last is the markedly expensive effort to
develop new therapeutic agents (none of which has been curative) which are not and have not been
aimed at the true pathogen. All these together could lead to a large ethical challenge in the new
millennium. Given all the above and considering that millions of patients have been/and are involved,
ignoring the likely microbial pathogenesis in AD could possibly become one of history’s greatest
ethical calamities.