APOE3-R136S Mutation Confers Resilience Against Tau Pathology via cGAS-STING-IFN Inhibition
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In mice homozygous for the Christchurch variant, microglial activation states are suppressed in PS19 mice (tau-associated pathology), promoting a homeostatic or "disease protective" response, whereas they are enhanced in APP/PS1 mice (amyloid-associated pathology), promoting a "disease-associated" state.
“In mice homozygous for the Christchurch variant, these studies indicate that microglial activation states are suppressed in PS19 mice (tau-associated pathology), promoting a homeostatic or “disease protective” response, whereas they are enhanced in APP/PS1 mice (amyloid-associated pathology), promoting a “disease-associated” state.”
From APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathology (2025) · cites this paper as [77]
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Experimental — accuracy not yet measuredThe impact of the Christchurch variant on microglial activation appears to be dependent on the stimulus, i.e., plaques or tau-laden neurons.
“Thus, the impact of the Christchurch variant appears to be dependent on the stimulus – i.e., plaques or tau-laden neurons.”
From APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathology (2025) · cites this paper as [77]
The Supplementary material (page unavailable) reports that the Christchurch variant altered microglial activation induced by tau pathology. It mentions high amyloid-beta pathology in a carrier but does not compare microglial responses to plaques and tau-laden neurons, so the proposed stimulus dependence is not established by our copy. (LLM, conf=0.82)
Experimental — accuracy not yet measuredMultiple studies have demonstrated that APOECh mutation broadly suppresses gliosis, dampens inflammatory gene expression, and modulates DAM phenotypes in an amyloid and tau-context dependent manner.
“Multiple studies have demonstrated that APOECh mutation broadly suppresses gliosis, dampens inflammatory gene expression, and modulates disease-associated microglial (DAM) phenotypes in an amyloid and tau-context dependent manner [4, 5, 7, 42, 50].”
From Astrocytic APOE3-Christchurch expression ameliorates brain amyloid-β pathology in 5xFAD mice (2026) · cites this paper as [42]
The Supplementary material (page not specified) reports that APOE3-R136S reduced the interferon response to tau pathology and rescued tau-induced microglial activation states. It does not establish broad suppression of gliosis or modulation of disease-associated microglial phenotypes across amyloid and tau contexts. (LLM, conf=0.84)
Experimental — accuracy not yet measuredWhile this report was being prepared, independent studies reported similar findings.
“While this report was being prepared, independent studies reported similar findings [41, 76, 77].”
From APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathology (2025) · cites this paper as [77]
Mounting evidence from human-based, in vitro, and in vivo studies has linked APOE3Ch to reduction in tau pathology.
“Mounting evidence from human-based, in vitro, and in vivo studies has linked APOE3Ch to reduction in tau pathology [3–7, 24, 26, 41, 42].”
From Astrocytic APOE3-Christchurch expression ameliorates brain amyloid-β pathology in 5xFAD mice (2026) · cites this paper as [42]
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Cites
APOE4 impairs myelination via cholesterol dysregulation in oligodendrocytes
Blanchard, J. W., Akay, L. A., Davila-Velderrain, J., von Maydell, D., Mathys, H., Davidson, S. M., Effenberger, A., Chen, C.-Y., Maner-Smith, K., Hajjar, I., et al. (2022) · Nature · doi:10.1038/s41586-022-05439-w · Cited by 493 · see citing works
Sepulveda-Falla, D., Sanchez, J. S., Almeida, M. C., Boassa, D., Acosta-Uribe, J., Vila-Castelar, C., Ramirez-Gomez, L., Baena, A., Aguillon, D., Villalba-Moreno, N. D., et al. (2022) · Acta Neuropathologica · doi:10.1007/s00401-022-02467-8 · Cited by 92 · see citing works
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Tran, K. M., Kwang, N. E., Butler, C. A., Gomez-Arboledas, A., Kawauchi, S., Mar, C., Chao, D., Barahona, R. A., Da Cunha, C., Tsourmas, K. I., et al. (2025) · Molecular Neurodegeneration · doi:10.1186/s13024-024-00793-x · Cited by 28 · see citing works
Astrocytic APOE3-Christchurch expression ameliorates brain amyloid-β pathology in 5xFAD mice
Raulin, A.-C., Alnobani, A., Rodriguez-Martinez, P., Lee, E., Linares, C., Yslas, A. R., Li, M., Ren, Y., Doss, S. V., Roy, B., et al. (2026) · Translational Psychiatry · doi:10.1038/s41398-026-04002-9
- Authors
- Naguib, S., Torres, E. R., Lopez-Lee, C., Fan, L., Bhagwat, M., Norman, K., Lee, S.-I., Zhu, J., Ye, P., Wong, M. Y., Patel, T., Mok, S.-A., Luo, W., Sinha, S., Zhao, M., Gong, S., & Gan, L.
- Affiliations
- Weill Cornell Medicine (US)
- University of Alberta (CA)
- Corresponding author
- Gan, Li
- ORCID
- Venue
- bioRxiv (Cold Spring Harbor Laboratory)
- Publisher
- Elsevier BV
- Published
- 2024
- PMC
- PMC11071490
- OpenAlex
- W4395961521
- Cited by
- 25
- References
- 2
- Citations by year
- 2026: 2 · 2025: 8 · 2024: 15
- Type
- posted content
- Language
- en
- Open access
- green
- doi.org
- Licence
- cc-by-nd
- Locations
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion, cc-by-nd)
- SSRN Electronic Journal (acceptedVersion)
- PubMed (publishedVersion)
- PubMed Central (submittedVersion, cc-by-nd)
- Funders
- National Institutes of Health (1f32ag085960-01)
- National Institute on Aging (R01AG072758, RF1AG079557, R01AG074541, R01AG079291)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Keywords
- tauopathy, microglia, interferon response, synaptic loss, demyelination, neuroprotection, PSEN1 mutations, amyloid-beta
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