THY-Tau22 mouse model accumulates more tauopathy at late stage of the disease in response to microglia deactivation through TREM2 deficiency
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The role played by microglia has taken the center of the stage in the etiology of Alzheimer's disease (AD). Several genome-wide association studies carried out on large cohorts of patients have indeed revealed a large number of genetic susceptibility factors corresponding to genes involved in neuroinflammation and expressed specifically by microglia in the brain. Among these genes TREM2, a cell surface receptor expressed by microglia, arouses strong interest because its R47H variant confers a risk of developing AD comparable to the ε4 allele of the APOE gene. Since this discovery, a growing number of studies have therefore examined the role played by TREM2 in the evolution of amyloid plaques and neurofibrillary tangles, the two brain lesions characteristic of AD. Many studies report conflicting results, reflecting the complex nature of microglial activation in AD. Here, we investigated the impact of TREM2 deficiency in the THY-Tau22 transgenic line, a well-characterized model of tauopathy. Our study reports an increase in the severity of tauopathy lesions in mice deficient in TREM2 occurring at an advanced stage of the pathology. This exacerbation of pathology was associated with a reduction in microglial activation indicated by typical morphological features and altered expression of specific markers. However, it was not accompanied by any further changes in memory performance. Our longitudinal study confirms that a defect in microglial TREM2 signaling leads to an increase i…
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TREM2 loss-of-function studies have yielded conflicting outcomes in the context of tau pathology.
“TREM2 loss-of-function studies have also yielded conflicting outcomes in the context of tau pathology.”
From TREM2-Deficient Microglia Attenuate Tau Spreading In Vivo (2023) · cites this paper as [15]
In the THY-Tau22 transgenic model, TREM2 deletion increases tau hyperphosphorylation and aggregation at advanced stages of pathology.
“Furthermore, in the THY-Tau22 transgenic model that overexpresses human tau carrying the G272V and P301S mutations, it was shown that TREM2 deletion increases tau hyperphosphorylation and aggregation at advanced stages of pathology [15].”
From TREM2-Deficient Microglia Attenuate Tau Spreading In Vivo (2023) · cites this paper as [15]
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Role of T-cell immunity in the pathophysiology of Alzheimer’s disease and other Tauopathies
Matta, K. (2024) · theses.fr (ABES) · doi:10.70675/cea4fe5ez67c3z4445z92f7z39af62ba059b
Mercado, C., Amaro, A., Martínez-Pinto, J., Vidal, R., Jury, N., & Lasagna‐Reeves, C. A. (2026) · Journal of Neuroinflammation · doi:10.1186/s12974-026-04065-x
- Authors
- Vautheny, A., Duwat, C., Aurégan, G., Joséphine, C., Hérard, A.-S., Jan, C., Mitja, J., Gipchtein, P., Gaillard, M.-C., Buée, L., Blum, D., Hantraye, P., Bonvento, G., Brouillet, E., Cambon, K., & Bemelmans, A.-P.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Inserm (FR)
- Corresponding author
- Bemelmans, Alexis-Pierre
- ORCID
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 2021-07
- Volume
- 155
- Pages
- 105398
- ISSN
- 0969-9961 (ISSN-L)
- OpenAlex
- W3160918637
- Cited by
- 28
- References
- 54
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 7 · 2023: 8 · 2022: 2 · 2021: 3
- FWCI
- 3.14
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Neurobiology of Disease (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- French National Research Agency
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- TREM2, tauopathy, Alzheimer's disease, microglial activation, neuroinflammation, amyloid plaques, neurofibrillary tangles, memory performance, disease progression
- MeSH terms
- Animals, Disease Models, Animal, Female, Humans, Longitudinal Studies, Male, Membrane Glycoproteins, Mice, Inbred C57BL, Mice, Transgenic, Receptors, Immunologic, tau Proteins, Microglia, Maze Learning, Thy-1 Antigens, Tauopathies, Mice
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