Dapsone is an anticatalysis for Alzheimer's disease exacerbation

Jong Hoon Lee*, Badar Kanwar, Chul Joong Lee, Consolato Sergi, Michael D. Coleman

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


Brain inflammation generally accelerates neurodegeneration. Alzheimer's disease (AD) triggers an innate immune response by activating a cytosolic DNA sensor cyclic-GMP-AMP synthase (cGAS)/stimulator of interferon genes (STING) signaling pathway. Our study investigated patients with leprosy and AD. They were treated with dapsone (4,4′-diaminodiphenyl sulfone, DDS) as a neuroinflammasome competitor and cGAS/STING pathway inhibitor. Four groups were defined: Treatment (T) 1: DDS prescribed AD diagnosed, T 2: DDS prescribed AD undiagnosed, T 3 DDS unprescribed AD diagnosed, and T 4: DDS unprescribed AD undiagnosed. Dapsone effects on AD can be clearly distinguished according to dapsone presence or absence. T1:T3 proved that the incidence of AD was significantly reduced by dapsone. T2:T3 proved that the prevalence of AD was significantly high without dapsone. T1:T4 proved that the prevalence decreased when taking dapsone. Our study demonstrates that dapsone can prevent AD exacerbation and may represent a preventive therapeutic option for exacerbated AD.

Original languageEnglish
Article number104274
Issue number5
Early online date20 Apr 2022
Publication statusPublished - 20 May 2022

Bibliographical note

© 2022 The Authors. This is an open access article under the CC BY-NC-ND license 4.0


  • Biological sciences
  • Clinical neuroscience
  • Health sciences
  • Neuroscience


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