Microglia TREM2R47H Alzheimer-linked variant enhances excitatory transmission and reduces LTP via increased TNF-α levels
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To study the mechanisms by which the p.R47H variant of the microglia gene and Alzheimer’s disease (AD) risk factor TREM2 increases dementia risk, we created Trem2R47H KI rats. Trem2R47H rats were engineered to produce human Aβ to define human-Aβ-dependent and -independent pathogenic mechanisms triggered by this variant. Interestingly, pre- and peri-adolescent Trem2R47H rats present increased brain concentrations of TNF-α, augmented glutamatergic transmission, suppression of Long-term-Potentiation (LTP), an electrophysiological surrogate of learning and memory, but normal Aβ levels. Acute reduction of TNF-α activity with a neutralizing anti-TNF-α antibody occludes the boost in amplitude of glutamatergic transmission and LTP suppression observed in young Trem2R47H/R47H rats. Thus, the microglia-specific pathogenic Trem2 variant boosts glutamatergic neuronal transmission and suppresses LTP by increasing brain TNF-α concentrations, directly linking microglia to neuronal dysfunction. Future studies will determine whether this phenomenon represents an early, Aβ-independent pathway that facilitates dementia pathogenesis in humans.
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The Apph allele enables the physiological production of human Aβ instead of rodent Aβ from the endogenous rat App gene.
“The Apph allele enables the physiological production of human Aβ instead of rodent Aβ from the endogenous rat App gene [43–49].”
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Self-citationTREM2-H157Y Increases Soluble TREM2 Production and Reduces Amyloid PathologyPreprint
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izydorczak, M., Oumov, M., Udhwani, M. V., Fostok, F., Coronas‐Samano, G., Sanganahalli, B. G., Hermán, P., Hyder, F., & Verhagen, J. V. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.04.20.649712
Tajiri, M., Omi, H., Inoue, A., Etani, H., Sawada, T., Iino, Y., & Yagishita, S. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.06.16.659241
Additional file 1 of Trem2 H157Y increases soluble TREM2 production and reduces amyloid pathology
Qiao, W., Chen, Y., Zhong, J., Madden, B. J., Charlesworth, C. M., Martens, Y. A., Liu, C.-C., Knight, J., Ikezu, T. C., Kurti, A., et al. (2023) · Figshare · doi:10.6084/m9.figshare.22608512
Additional file 2 of Trem2 H157Y increases soluble TREM2 production and reduces amyloid pathology
Qiao, W., Chen, Y., Zhong, J., Madden, B. J., Charlesworth, C. M., Martens, Y. A., Liu, C.-C., Knight, J., Ikezu, T. C., Kurti, A., et al. (2023) · Figshare · doi:10.6084/m9.figshare.22608515
Additional file 10 of Trem2 H157Y increases soluble TREM2 production and reduces amyloid pathology
Qiao, W., Chen, Y., Zhong, J., Madden, B. J., Charlesworth, C. M., Martens, Y. A., Liu, C.-C., Knight, J., Ikezu, T. C., Kurti, A., et al. (2023) · Figshare · doi:10.6084/m9.figshare.22608542
Additional file 7 of Trem2 H157Y increases soluble TREM2 production and reduces amyloid pathology
Qiao, W., Chen, Y., Zhong, J., Madden, B. J., Charlesworth, C. M., Martens, Y. A., Liu, C.-C., Knight, J., Ikezu, T. C., Kurti, A., et al. (2023) · Figshare · doi:10.6084/m9.figshare.22608530
Additional file 5 of Trem2 H157Y increases soluble TREM2 production and reduces amyloid pathology
Qiao, W., Chen, Y., Zhong, J., Madden, B. J., Charlesworth, C. M., Martens, Y. A., Liu, C.-C., Knight, J., Ikezu, T. C., Kurti, A., et al. (2023) · Figshare · doi:10.6084/m9.figshare.22608524
Additional file 4 of Trem2 H157Y increases soluble TREM2 production and reduces amyloid pathology
Qiao, W., Chen, Y., Zhong, J., Madden, B. J., Charlesworth, C. M., Martens, Y. A., Liu, C.-C., Knight, J., Ikezu, T. C., Kurti, A., et al. (2023) · Figshare · doi:10.6084/m9.figshare.22608521
Additional file 3 of Trem2 H157Y increases soluble TREM2 production and reduces amyloid pathology
Qiao, W., Chen, Y., Zhong, J., Madden, B. J., Charlesworth, C. M., Martens, Y. A., Liu, C.-C., Knight, J., Ikezu, T. C., Kurti, A., et al. (2023) · Figshare · doi:10.6084/m9.figshare.22608518
Additional file 6 of Trem2 H157Y increases soluble TREM2 production and reduces amyloid pathology
Qiao, W., Chen, Y., Zhong, J., Madden, B. J., Charlesworth, C. M., Martens, Y. A., Liu, C.-C., Knight, J., Ikezu, T. C., Kurti, A., et al. (2023) · Figshare · doi:10.6084/m9.figshare.22608527
Additional file 9 of Trem2 H157Y increases soluble TREM2 production and reduces amyloid pathology
Qiao, W., Chen, Y., Zhong, J., Madden, B. J., Charlesworth, C. M., Martens, Y. A., Liu, C.-C., Knight, J., Ikezu, T. C., Kurti, A., et al. (2023) · Figshare · doi:10.6084/m9.figshare.22608539
Additional file 8 of Trem2 H157Y increases soluble TREM2 production and reduces amyloid pathology
Qiao, W., Chen, Y., Zhong, J., Madden, B. J., Charlesworth, C. M., Martens, Y. A., Liu, C.-C., Knight, J., Ikezu, T. C., Kurti, A., et al. (2023) · Figshare · doi:10.6084/m9.figshare.22608536
Yin, T., Metkar, S. K., Yeşiltepe, M., & D'adamio, L. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.04.28.721316
Self-citationMedeiros, E. B., Monteiro, I. D. O., Kluwe‐Schiavon, B., Possamai, O. L., Fenilli, G. P., Keller, G. S., Lídio, A. V., Casagrande, D. D., Souza, C. S. M., Silveira, G. D. B., et al. (2026) · Probiotics and Antimicrobial Proteins · doi:10.1007/s12602-026-11104-9
Pyrazolo[3,4-b]pyridine: a privileged scaffold for the synthesis of anti-Alzheimer’s agents
Waly, O. M., El‐Sayed, S. M., Ghaly, M. A., & El‐Subbagh, H. I. (2026) · Future Journal of Pharmaceutical Sciences · doi:10.1186/s43094-026-01006-6
Neurons as cytokine sensors in the central nervous system
Kahn, A., Binkle-Ladisch, L., Sonner, J. K., & Friese, M. A. (2026) · Trends in Immunology · doi:10.1016/j.it.2026.07.012
Yi, Z., Zhou, N., Sun, Z., Liu, X., & Chen, C. (2026) · Public Health Nursing · doi:10.1111/phn.70154
- Authors
- Ren, S., Yao, W., Tambini, M. D., Yin, T., Norris, K. A., & D'Adamio, L.
- Affiliations
- Rutgers, The State University of New Jersey (US)
- Corresponding author
- D'Adamio, Luciano
- Venue
- eLife
- Publisher
- eLife Sciences Publications, Ltd
- Published
- 2020-06-24
- Volume
- 9
- ISSN
- 2050-084X (ISSN-L)
- PMC
- PMC7338048
- OpenAlex
- W3037953859
- Cited by
- 68
- References
- 43
- Citations by year
- 2026: 10 · 2025: 12 · 2024: 5 · 2023: 19 · 2022: 6 · 2021: 11 · 2020: 5
- FWCI
- 3.96
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- eLife (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 (R01AG063407, RF1AG064821)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- TREM2, Alzheimer's disease, microglia, TNF-α, glutamatergic neurotransmission, long-term potentiation, learning and memory, amyloid-beta, anti-TNF-alpha antibody, dementia risk, neuronal dysfunction
- MeSH terms
- Aging, Animals, Female, Gene Expression Regulation, Genotype, Macrophages, Male, Membrane Glycoproteins, Receptors, Immunologic, RNA, Messenger, Tumor Necrosis Factor-alpha, Genetic Variation, Cytokines, Microglia, Long-Term Potentiation, Glutamic Acid, Rats
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