Tau Activation of Microglial cGAS–IFN Reduces MEF2C‐mediated Cognitive Resilience
Open accessAbstract
Pathological hallmarks of Alzheimer’s disease (AD) precede clinical symptoms by years, indicating a period of cognitive resilience before the onset of dementia. Here, we report that activation of cyclic GMP–AMP synthase (cGAS) diminishes cognitive resilience by decreasing the neuronal transcriptional network of myocyte enhancer factor 2c (MEF2C) through type I interferon (IFN-I) signaling. Pathogenic tau activates cGAS and IFN-I responses in microglia, in part mediated by cytosolic leakage of mitochondrial DNA. Genetic ablation of Cgas in mice with tauopathy diminished the microglial IFN-I response, preserved synapse integrity and plasticity and protected against cognitive impairment without affecting the pathogenic tau load. cGAS ablation increased, while activation of IFN-I decreased, the neuronal MEF2C expression network linked to cognitive resilience in AD. Pharmacological inhibition of cGAS in mice with tauopathy enhanced the neuronal MEF2C transcriptional network and restored synaptic integrity, plasticity and memory, supporting the therapeutic potential of targeting the cGAS–IFN–MEF2C axis to improve resilience against AD-related pathological insults.
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There is a window of opportunity for cGAS inhibition to reduce tau spread.
“Genetic deletion of cGAS did not reduce tau inclusions in 9-month-old P301S mice41, suggesting a ‘window of opportunity’ for cGAS inhibition to reduce tau spread.”
From The R136S mutation in the APOE3 gene confers resilience against tau pathology via inhibition of the cGAS-STING-IFN pathway (2025) · cites this paper as [41]
The Results section (‘cGAS loss rescues memory, synapse loss and plasticity’; page unavailable) reports no difference in tau aggregates in the hippocampi or entorhinal cortices of P301S mice after Cgas deletion. That supports the sentence’s finding about tau inclusions, but the paper does not establish a window in which cGAS inhibition reduces tau spread; its reported benefits concern memory, synapses and cognitive resilience. (LLM, conf=0.86)
Experimental — accuracy not yet measuredA brain permeable cGAS inhibitor (TDI6570/G097) formulated in chow protects against tau-induced deficits in P301S mice.
“Our previous work established the efficacy of a brain permeable cGAS inhibitor (TDI6570, also known as G097, hereafter referred to as cGASi) formulated in chow in protecting against tau-induced deficits in P301S mice41,44.”
From The R136S mutation in the APOE3 gene confers resilience against tau pathology via inhibition of the cGAS-STING-IFN pathway (2025) · cites this paper as [41]
The Results section (“Inhibiting cGAS protects synapses and cognition in tauopathy”) reports that brain-permeable TDI-6570 was given in chow to P301S mice and protected against synapse loss and cognitive deficits. Our copy does not identify TDI-6570 as “G097” (searched: G097 and the proposed alias), so that part of the attribution is unverified. (LLM, conf=0.87)
Experimental — accuracy not yet measuredPrevious work established the efficacy of a brain permeable cGAS inhibitor (TDI6570/G097) in protecting against tau-induced deficits in P301S mice.
“Our previous work established the efficacy of a brain permeable cGAS inhibitor (TDI6570, also known as G097, hereafter referred to as cGASi) formulated in chow in protecting against tau-induced deficits in P301S mice41,44.”
From <i>APOE3</i> - <i>R136S</i> mutation confers resilience against tau pathology via cGAS-STING-IFN inhibition (2024) · cites this paper as [41]
The Results section, “Inhibiting cGAS protects synapses and cognition in tauopathy” (page not provided), reports that chow-formulated TDI-6570 entered the brain and protected P301S mice against synapse loss and cognitive deficits. The cited passages support the efficacy claim, but our copy does not establish that TDI-6570 is also known as G097. (LLM, conf=0.87)
Experimental — accuracy not yet measuredIn a mouse model of tauopathy, pathological tau activates the cGAS-STING-IFN-I pathway in microglia, leading to suppression of MEF2C.
“In this axis, pathological tau activates the cyclic GMP‐AMP synthase (cGAS)‐stimulator of interferon genes (STING)‐IFN‐Ι pathway in microglia, leading to the suppression of MEF2C, a critical transcription factor for cognitive resilience [47].”
From Targeting Microglial Transcriptional Reprogramming as a Therapy Strategy for Alzheimer's Disease (2026) · cites this paper as [47]
Stimulation of the cGAS-STING pathway induces microglial dysfunction and sterile inflammation, which exacerbates AD.
“Stimulation of the cGAS-STING pathway induces microglial dysfunction and sterile inflammation, which exacerbates AD.”
From Blockade of STING Activation Alleviates Microglial Dysfunction and a Broad Spectrum of Alzheimer's Disease Pathologies (2024) · cites this paper as [20]
Recent work from Gan's group suggests that the cGAS-STING pathway is robustly activated in brains of tau transgenic mice, consistent with previous work in primary microglia treated with tau aggregates.
“While it is currently unknown whether tau-induced retrotransposons form eccDNA, recent work from Gan's group (Udeochu et al. 2023) suggests that the cGAS-STING pathway is robustly activated in brains of tau transgenic mice, consistent with previous work in primary microglia treated with tau aggregates (Jin et al. 2021).”
From The Role of Retrotransposons and Endogenous Retroviruses in Age-Dependent Neurodegenerative Disorders (2024) · cites this paper as Udeochu et al. 2023
Genetic deletion of cGAS did not reduce tau inclusions in 9-month-old P301S mice.
“Genetic deletion of cGAS did not reduce tau inclusions in 9-month-old P301S mice41, suggesting a ‘window of opportunity’ for cGAS inhibition to reduce tau spread.”
From The R136S mutation in the APOE3 gene confers resilience against tau pathology via inhibition of the cGAS-STING-IFN pathway (2025) · cites this paper as [41]
The cGAS-STING pathway plays a role in tau-induced neurodegeneration.
“The cGAS-STING pathway was previously shown to play a role in tau-induced neurodegeneration41.”
From The R136S mutation in the APOE3 gene confers resilience against tau pathology via inhibition of the cGAS-STING-IFN pathway (2025) · cites this paper as [41]
The source of IFN signaling could be partially attributed to hyperactive cGAS-STING in tauopathy mice and human AD brains.
“Our previous studies suggest that the source of IFN signaling could be partially attributed to hyperactive cGAS-STING in tauopathy mice and human AD brains41.”
From The R136S mutation in the APOE3 gene confers resilience against tau pathology via inhibition of the cGAS-STING-IFN pathway (2025) · cites this paper as [41]
cGAS inhibition mitigated tau-induced synaptic loss.
“Consistent with previous studies in tauopathy mice expressing mouse Apoe, cGAS inhibition mitigated tau-induced synaptic loss41.”
From The R136S mutation in the APOE3 gene confers resilience against tau pathology via inhibition of the cGAS-STING-IFN pathway (2025) · cites this paper as [41]
Cgas deletion mitigated tau-induced microglial IFN-I and protected against synapse loss, decreased synaptic plasticity, and cognitive deficits.
“Cgas deletion mitigated tau-induced microglial IFN-I and protected against synapse loss, decreased synaptic plasticity, and cognitive deficits41.”
From The R136S mutation in the APOE3 gene confers resilience against tau pathology via inhibition of the cGAS-STING-IFN pathway (2025) · cites this paper as [41]
The cGAS-STING pathway was previously shown to play a role in tau-induced neurodegeneration.
“The cGAS-STING pathway was previously shown to play a role in tau-induced neurodegeneration41.”
From <i>APOE3</i> - <i>R136S</i> mutation confers resilience against tau pathology via cGAS-STING-IFN inhibition (2024) · cites this paper as [41]
In tauopathy mouse models, the source of IFN signaling could be partially attributed to hyperactive cGAS-STING in tauopathy mice and the human AD brain.
“In tauopathy mouse models, our previous studies suggest that the source of IFN signaling could be partially attributed to hyperactive cGAS-STING in tauopathy mice and the human AD brain41.”
From <i>APOE3</i> - <i>R136S</i> mutation confers resilience against tau pathology via cGAS-STING-IFN inhibition (2024) · cites this paper as [41]
Cgas deletion mitigated tauopathy-induced microglial IFN-I and protected against synapse loss, synaptic plasticity, and cognitive deficits.
“Cgas deletion mitigated tauopathy-induced microglial IFN-I and protected against synapse loss, synaptic plasticity, and cognitive deficits41.”
From <i>APOE3</i> - <i>R136S</i> mutation confers resilience against tau pathology via cGAS-STING-IFN inhibition (2024) · cites this paper as [41]
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Expansion of highly interferon‐responsive T cells in early‐onset Alzheimer's disease
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Identification and development of cGAS inhibitors and their uses to treat Alzheimer's disease
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- Authors
- Udeochu, J. C., Amin, S., Huang, Y., Fan, L., Torres, E. R. S., Carling, G. K., Liu, B., McGurran, H., Coronas-Samano, G., Kauwe, G., Mousa, G. A., Wong, M. Y., Ye, P., Nagiri, R. K., Lo, I., Holtzman, J., Corona, C., Yarahmady, A., Gill, M. T., Raju, R. M., Mok, S.-A., Gong, S., Luo, W., Zhao, M., Tracy, T. E., Ratan, R. R., Tsai, L.-H., Sinha, S. C., & Gan, L.
- Affiliations
- Weill Cornell Medicine (US)
- Gladstone Institutes (US)
- Buck Institute for Research on Aging (US)
- University of Alberta (CA)
- Boston Children's Hospital (US)
- Massachusetts Institute of Technology (US)
- Corresponding author
- Amin, Sadaf
- Gan, Li
- ORCID
- Udeochu, Joe C.
- Amin, Sadaf
- Huang, Yige
- Fan, Li
- Torres, Eileen Ruth S.
- Carling, Gillian K.
- McGurran, Hugo
- Coronas-Samano, Guillermo
- Mousa, Gergey Alzaem
- Wong, Man Ying
- Nagiri, Ravi Kumar
- Lo, Iris
- Corona, Carlo
- Yarahmady, Allan
- Raju, Ravikiran M.
- Mok, Sue-Ann
- Gong, Shiaoching
- Luo, Wenjie
- Zhao, Mingrui
- Tracy, Tara E.
- Ratan, Rajiv R.
- Tsai, Li-Huei
- Sinha, Subhash C.
- Gan, Li
- Venue
- Nature Neuroscience
- Published
- 2023-04-24
- Volume
- 26
- Issue
- 5
- Pages
- 737-750
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- PMC
- PMC10166855
- OpenAlex
- W4366824412
- Cited by
- 289
- References
- 68
- Citations by year
- 2026: 71 · 2025: 108 · 2024: 86 · 2023: 24
- FWCI
- 51.86
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Nature Neuroscience (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- BrightFocus Foundation (A20201312F)
- JumpStart Research Career Development Program, Weill Cornell Medicine
- Boston Children’s Hospital (5K12HD052896)
- U.S. Department of Health & Human Services | National Institutes of Health (R01AG064239, R01AG072758)
- U.S. Department of Health & Human Services | NIH | National Institute on Aging (R01AG074541, R01AG054214)
- CureAD Fund Daedalus Fund
- JPB Foundation
- Tau Consortium CureAD Fund Daedalus Fund
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Developmental Neuroscience › Anesthesia and Neurotoxicity Research
- Keywords
- Alzheimer's disease, tauopathy, cGAS, type I interferon, MEF2C, microglia, cognitive resilience, mitochondrial DNA release, synaptic integrity, synaptic plasticity, memory, neuroinflammation
- MeSH terms
- Animals, Cognition, Immunity, Innate, Interferons, Nucleotidyltransferases, tau Proteins, Microglia, Mice, MEF2 Transcription Factors
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