What is it about?
Alzheimer's disease (AD) has many hypotheses as to its etiology, and has now been found to have the same 16 MSIDS (Multiple Systemic Inflammatory Disease Sydrome) inflammatory factors also found in chronic Lyme disease/PTLDS and Long Covid. AD has also been found to be associated with spirochetes like Lyme disease (Borrelia burgdorferi) along with biofilm, amyloid and phosphorylated tau in the brain in multiple autopsy studies. This case study is the first time that it has been proven that Lyme disease has a direct causative relationship with AD in a live human being. I reversed p-tau 217, the most sensitive and specific biomarker for AD, using dapsone combination therapy, an 8-9 week oral, generic antibiotic protocol that hits the biofilm/persister forms of the bacteria.
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Photo by Robina Weermeijer on Unsplash
Why is it important?
There have been no effective therapies for AD to date. The anti-amyloid drugs like lecanemab and donanemab on the average, lower p-tau by 23% over 6+ years. I lowered p-tau by 63% and normalized it in 8-9 weeks. This implies that the amyloid production in the brain in some cases of AD when CLD/PTLDS is present is due to Lyme spirochetes, offering a potential solution to some, in a disease that has no cures.
Perspectives
We desperately need a multicenter, placebo-controlled, randomized clinical trial to evaluate dapsone combination therapy and the 16 point MSIDS model in the treatment of not only chronic Lyme disease/PTLDS but also those diagnosed with Alzheimer's dementia.
Richard Horowitz
Read the Original
This page is a summary of: Improving biomarkers of inflammation including phosphorylated tau in a patient with chronic Lyme disease/post-treatment Lyme disease syndrome using dapsone combination therapy: A case study and literature review, Journal of Alzheimer s Disease Reports, April 2026, SAGE Publications,
DOI: 10.1177/25424823261445434.
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