Microglial cGAS Deletion Preserves Intercellular Communication and Alleviates Amyloid‐β‐Induced Pathogenesis of Alzheimer's Disease
Open accessAbstract
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 plaque accumulation and protects mice from Aβ‐induced cognitive impairment. Mechanistically, our study revealed cGAS promotes plaque‐associated microglia accumulation and is essential for inflammasome activation. Moreover, we showed that restricting cGAS‐mediated innate immunity is crucial for preserving inter‐cellular communication in the brain and induces pleiotrophin, a neuroprotective factor. These findings offer novel insights into the specific roles of the innate immune system in AD employing a cell‐type‐specific approach. The conclusions provide a foundation for targeted interventions to modulate the microglial cGAS‐STING signaling pathway, offering promising therapeutic strategy for AD treatment.
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STING interacts with cGAS and plays a significant role in Alzheimer's disease by promoting microglial dysfunction and neuroinflammation.
“The STING interacts with cGAS and plays a significant role in Alzheimer's disease by promoting microglial dysfunction and neuroinflammation [66, 67].”
From Targeting Microglial Transcriptional Reprogramming as a Therapy Strategy for Alzheimer's Disease (2026) · cites this paper as [66]
The Introduction describes cGAS activating STING through cGAMP, and the Discussion reports that microglial cGAS deletion alleviated neuroinflammation in an Alzheimer’s mouse model. This supports a role for the cGAS–STING pathway, but the study does not establish that STING itself promotes microglial dysfunction or that STING directly interacts with cGAS. (LLM, conf=0.82)
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Self-citation
- Authors
- He, S., Li, X., Mittra, N., Bhattacharjee, A., Wang, H., Song, S., Zhao, S., Liu, F., & Han, X.
- Affiliations
- The University of Texas at San Antonio Health Science Center (US)
- Second Xiangya Hospital of Central South University (CN)
- Corresponding author
- Liu, Feng
- Han, Xianlin
- Venue
- Advanced Science
- Publisher
- Wiley
- Published
- 2025-02-05
- Volume
- 12
- Issue
- 12
- Pages
- e2410910-e2410910
- ISSN
- 2198-3844 (ISSN-L)
- PMC
- PMC11948024
- OpenAlex
- W4407168988
- Cited by
- 34
- References
- 100
- Citations by year
- 2026: 20 · 2025: 14
- FWCI
- 12.27
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Advanced Science (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institute on Aging (R01 AG061729, R01 AG085545, T32AG021890, P30 AG066546, P30 AG013319, P30 AG044271)
- Methodist Hospital Foundation
- William and Ella Owens Medical Research Foundation
- Cure Alzheimer's Fund
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- Alzheimer's disease, microglia, cGAS, STING, cytosolic DNA sensing, amyloid plaques, innate immunity, intercellular communication, inflammasome, pleiotrophin, cognitive impairment, 5xFAD mice
- MeSH terms
- Cyclic Guanosine Monophosphate-Adenosine Monophosphate Synthase, Alzheimer Disease, Animals, Cell Communication, Disease Models, Animal, Humans, Immunity, Innate, Membrane Proteins, Mice, Inbred C57BL, Nucleotidyltransferases, Signal Transduction, Amyloid beta-Peptides, Microglia, Mice, Knockout, Mice
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