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Dapsone is an anticatalysis for Alzheimer's disease exacerbation
Jong Hoon Lee1, Badar Kanwar2, Chul Joong Lee3
1Science and Research Center, Seoul National University College of Medicine, Seoul, Republic of Korea.
Iscience
|May 11, 2022
Summary
Dapsone (4,4'-diaminodiphenyl sulfone, DDS) significantly reduces Alzheimer's disease (AD) incidence and prevalence by inhibiting the cGAS/STING inflammatory pathway. This suggests DDS may be a preventive therapeutic option for AD.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Brain inflammation accelerates neurodegeneration.
- Alzheimer's disease (AD) involves activation of the cGAS/STING innate immune pathway.
- Leprosy patients offer a unique cohort for studying neuroinflammation and potential therapeutic interventions.
Purpose of the Study:
- To investigate the effect of dapsone (DDS) on Alzheimer's disease (AD) in patients with leprosy.
- To determine if DDS acts as a neuroinflammasome competitor and cGAS/STING pathway inhibitor in the context of AD.
- To evaluate DDS as a potential preventive therapeutic option for AD exacerbation.
Main Methods:
- Four patient groups were defined based on AD diagnosis and DDS prescription status: T1 (DDS/AD diagnosed), T2 (DDS/AD undiagnosed), T3 (No DDS/AD diagnosed), T4 (No DDS/AD undiagnosed).
- Comparative analysis of AD incidence and prevalence across the four defined treatment groups.
- Assessment of dapsone's impact on the cGAS/STING signaling pathway and neuroinflammation.
Main Results:
- Dapsone significantly reduced AD incidence (T1 vs. T3).
- AD prevalence was significantly higher in patients not taking dapsone (T2 vs. T3).
- Dapsone intake was associated with decreased AD prevalence (T1 vs. T4).
Conclusions:
- Dapsone (DDS) demonstrates a significant preventive effect on Alzheimer's disease (AD) exacerbation.
- Inhibition of the cGAS/STING pathway by DDS appears crucial for its therapeutic benefits in AD.
- Dapsone represents a potential preventive therapeutic strategy for managing exacerbated AD.
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