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

Abstract

Background: Borrelia burgdorferi, the agent of Lyme disease, has been found to co-localize in Alzheimer's disease autopsy brain tissues with biofilm, amyloid, and phosphorylated tau. Objective: To determine whether dapsone combination therapy (DCT), a biofilm/persister antibiotic regimen with good central nervous system penetration can improve p-tau and peripheral inflammatory markers in a patient with chronic Lyme disease (CLD)/post-treatment Lyme disease syndrome (PTLDs). Methods: A 67-year-old female with CLD/PTLDs, and Ehrlichia, Babesia, Bartonella, and Coxiella burnetii had a 15-year history of joint pain with inflammation and mild cognitive impairment despite prior treatment with doxycycline. She was checked for changes in peripheral inflammation, i.e., rheumatoid factors (RFs) and changes in serum p-tau181, p-tau 217, and amyloid-β (Aβ) 42:40 ratios before and after treatment with DCT. Results: Elevated RFs at 20 IU/mL decreased into normal range three months post treatment accompanied by a decrease in pain with improved flexibility. An initially elevated serum p-tau 217 level in the blood at 0.33 pg/mL (normal range <0.15 pg/mL) prior to using DCT normalized, decreasing to 0.12 pg/mL three months post therapy, while p-tau 181 levels remained within normal limits. Aβ ratios simultaneously improved post DCT increasing from 0.185 pg/mL to 0.216 (normal range >0.170) accompanied by subjective improvements in concentration and recall. Conclusions: This is the first case study proving that a short term, biofilm/persister drug regimen, i.e., DCT, can potentially improve peripheral autoantibodies (RFs) and pathological triggers of neuroinflammation (p-tau, Aβ) in a patient with CLD/PTLDs.