<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>25(5)</volume><submitter>Lee JH</submitter><funding>Center for Preparedness and Response</funding><funding>Sorokdo National Hospital</funding><funding>Ministry of Health and Welfare</funding><pubmed_abstract>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.</pubmed_abstract><journal>iScience</journal><pagination>104274</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9079171</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Dapsone is an anticatalysis for Alzheimer's disease exacerbation.</pubmed_title><pmcid>PMC9079171</pmcid><pubmed_authors>Sergi C</pubmed_authors><pubmed_authors>Coleman MD</pubmed_authors><pubmed_authors>Kanwar B</pubmed_authors><pubmed_authors>Lee CJ</pubmed_authors><pubmed_authors>Lee JH</pubmed_authors></additional><is_claimable>false</is_claimable><name>Dapsone is an anticatalysis for Alzheimer's disease exacerbation.</name><description>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.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 May</publication><modification>2026-05-31T01:10:37.684Z</modification><creation>2024-10-16T14:46:24.191Z</creation></dates><accession>S-EPMC9079171</accession><cross_references><pubmed>35542045</pubmed><doi>10.1016/j.isci.2022.104274</doi></cross_references></HashMap>