Discussion on the Leading Role of Spirochetes in Alzheimer’s Disease

For 25 years, the beta amyloid (Aβ) theory has been dominant as the cause of Alzheimer’s disease
(AD); and, recently, hyperphosphorylated tau (p-tau) has assumed a larger role. In consideration of
the recent pathological and microbiological findings, it seems appropriate and important to elevate the
pathogenic microbe theory and highlight the spirochete as the etiologic agent of this dreaded disease.
The evidence for spirochetes causing AD is considerable and cogent. Foremost in the discussion is
the microscopic pathology of general paresis (GP), a known spirochetal disease, and AD. The
pathology is identical; in both, there are senile plaques, p-tau, neurofibrillary tangles, a massive
amount of AB, and the presence of spirochetes. Spirochetes have been cultivated from AD brains;
this has never been demonstrated in GP or any other stage of syphilis. Further, polymerase chain
reaction (PCR) has identified the presence of the spirochetes (25% Lyme, and 75% dental). The
debility of AD urges the beginning of therapeutic interventions against these spirochetes before they
arrive in the brain or before they begin to make biofilms.