{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["He S"],"funding":["University of Texas Health Science Center at San Antonio intramural institutional research funds","William and Ella Owens Medical Research Foundation","NIA NIH HHS","Cure Alzheimer's Fund","Cure Alzheimer's Fund","Methodist Hospital Foundation","National Institute on Aging"],"pagination":["e2410910"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11948024"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(12)"],"pubmed_abstract":["Innate immune activation plays a crucial role in the pathogenesis of Alzheimer's disease (AD) and related dementias (ADRD). The cytosolic DNA sensing pathway, involving cGAMP synthase (cGAS) and Stimulator of Interferon Genes (STING), has emerged as a key mediator of neurodegenerative diseases. However, the precise mechanisms through which cGAS activation influences AD progression remain poorly understood. In this study, we observed significant up-regulation of cGAS-STING signaling pathway in AD. Notably, this increase is primarily attributed to microglia, rather than non-microglial cell types. Using an inducible, microglia-specific cGAS knockout mouse model in the 5xFAD background, we demonstrated that deleting microglial cGAS at the onset of amyloid-β (Aβ) pathology profoundly restricts "],"journal":["Advanced science (Weinheim, Baden-Wurttemberg, Germany)"],"pubmed_title":["Microglial cGAS Deletion Preserves Intercellular Communication and Alleviates Amyloid-β-Induced Pathogenesis of Alzheimer's Disease."],"pmcid":["PMC11948024"],"funding_grant_id":["P30 AG013319","R01 AG061729","T32 AG021890","RF1 AG061729","P30 AG066546","T32AG021890","R01 AG085545","P30 AG044271"],"pubmed_authors":["Bhattacharjee A","Li X","He S","Zhao S","Song S","Han X","Mittra N","Wang H","Liu F"],"additional_accession":[]},"is_claimable":false,"name":"Microglial cGAS Deletion Preserves Intercellular Communication and Alleviates Amyloid-β-Induced Pathogenesis of Alzheimer's Disease.","description":"Innate immune activation plays a crucial role in the pathogenesis of Alzheimer's disease (AD) and related dementias (ADRD). The cytosolic DNA sensing pathway, involving cGAMP synthase (cGAS) and Stimulator of Interferon Genes (STING), has emerged as a key mediator of neurodegenerative diseases. However, the precise mechanisms through which cGAS activation influences AD progression remain poorly understood. In this study, we observed significant up-regulation of cGAS-STING signaling pathway in AD. Notably, this increase is primarily attributed to microglia, rather than non-microglial cell types. Using an inducible, microglia-specific cGAS knockout mouse model in the 5xFAD background, we demonstrated that deleting microglial cGAS at the onset of amyloid-β (Aβ) pathology profoundly restricts ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2025-07-04T03:05:39.791Z","creation":"2025-07-04T03:05:39.791Z"},"accession":"S-EPMC11948024","cross_references":{"pubmed":["39908354"],"doi":["10.1002/advs.202410910"]}}