Modulation of astrocyte reactivity improves functional deficits in mouse models of Alzheimer’s disease
Open accessAbstract
Astrocyte reactivity and neuroinflammation are hallmarks of CNS pathological conditions such as Alzheimer's disease. However, the specific role of reactive astrocytes is still debated. This controversy may stem from the fact that most strategies used to modulate astrocyte reactivity and explore its contribution to disease outcomes have only limited specificity. Moreover, reactive astrocytes are now emerging as heterogeneous cells and all types of astrocyte reactivity may not be controlled efficiently by such strategies.Here, we used cell type-specific approaches in vivo and identified the JAK2-STAT3 pathway, as necessary and sufficient for the induction and maintenance of astrocyte reactivity. Modulation of this cascade by viral gene transfer in mouse astrocytes efficiently controlled several morphological and molecular features of reactivity. Inhibition of this pathway in mouse models of Alzheimer's disease improved three key pathological hallmarks by reducing amyloid deposition, improving spatial learning and restoring synaptic deficits.In conclusion, the JAK2-STAT3 cascade operates as a master regulator of astrocyte reactivity in vivo. Its inhibition offers new therapeutic opportunities for Alzheimer's disease.
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Only a subset, often a mix of A1 and A2 or pan-reactive transcripts, are upregulated in astrocytes from brains of study participants with HD or AD, or from several mouse models of acute injuries and chronic diseases of the CNS.
“Importantly, only a subset, often a mix of A1 and A2 or pan-reactive transcripts, are upregulated in astrocytes from brains of study participants with HD74 or AD75,76, or from several mouse models of acute injuries and chronic diseases of the CNS42,69,76,77.”
From Reactive astrocyte nomenclature, definitions, and future directions (2021) · cites this paper as [42]
The Results section (‘SOCS3 normalizes multiple reactive astrocyte markers in AD mice’; page unavailable) reports induced pan-reactive, A1 and A2 markers in astrocytes from an AD mouse model, supporting the mixed-marker portion of the claim. This paper does not establish that pattern in astrocytes from human AD participants or across several models of acute CNS injury and chronic disease. The HD portion is attached to a different citation. (LLM, conf=0.84)
Experimental — accuracy not yet measuredInterventional strategies such as classical pharmacology, genetic manipulation, and biomaterials are available tools to modify pathological signaling in reactive astrocytes for therapeutic purposes.
“Finally, interventional strategies such as classical pharmacology56,98, genetic manipulation42,56, and biomaterials99 are available tools to modify pathological signaling in reactive astrocytes for therapeutic purposes.”
From Reactive astrocyte nomenclature, definitions, and future directions (2021) · cites this paper as [42]
The Discussion section reports that astrocyte-targeted viral gene transfer altered JAK2–STAT3 signaling in Alzheimer’s disease mouse models, supporting genetic manipulation as an intervention. The cited paper does not establish classical pharmacology as a tool for this purpose; the biomaterials example is attached to a different citation. (LLM, conf=0.85)
Experimental — accuracy not yet measuredManipulation of reactive astrocytes has resulted in improved outcomes, worse outcomes, and no change in mouse models of AD and MS.
“For example, the manipulation of reactive astrocytes has resulted in improved outcomes38,42,43, worse35 outcomes, and no change44 in mouse models of AD and MS40,45,46.”
From Reactive astrocyte nomenclature, definitions, and future directions (2021) · cites this paper as [42]
Blocking astrocyte reactivity has positive effects on AD pathology.
“On the other hand, blocking astrocyte reactivity has demonstrated positive effects on pathology (Ceyzeriat et al., 2018; Reichenbach et al., 2019).”
From Inhibition of the mitochondrial pyruvate carrier in astrocytes reduces amyloid and tau accumulation in the 3xTgAD mouse model of Alzheimer's disease (2024) · cites this paper as Ceyzeriat et al., 2018
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The Role of Astrocytes in Synapse Loss in Alzheimer's Disease: A Systematic Review
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Regulatory T cells decrease C3-positive reactive astrocytes in Alzheimer-like pathology
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Kater, M. S. J., Badia‐Soteras, A., van Weering, J. R. T., Smit, A. B., & Verheijen, M. H. G. (2023) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2023.1085690 · Cited by 24 · see citing works
STAT3 Drives GFAP Accumulation and Astrocyte Pathology in a Mouse Model of Alexander Disease
Hagemann, T. L., Coyne, S., Levin, A., Wang, L., Feany, M. Β., & Messing, A. (2023) · Cells · doi:10.3390/cells12070978 · Cited by 24 · see citing works
Phosphorylated Tau 181 Serum Levels Predict Alzheimer’s Disease in the Preclinical Stage
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The rise of astrocytes: are they guardians or troublemakers of the brain disorder?
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Ceyzériat, K., Zilli, T., Millet, P., Koutsouvelis, N., Dipasquale, G., Fossey, C., Cailly, T., Fabis, F., Frisoni, G. B., Garibotto, V., et al. (2022) · Journal of Neuroinflammation · doi:10.1186/s12974-022-02673-x · Cited by 21 · see citing works
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- Authors
- Ceyzériat, K., Ben Haim, L., Denizot, A., Pommier, D., Matos, M., Guillemaud, O., Palomares, M.-A., Abjean, L., Petit, F., Gipchtein, P., Gaillard, M.-C., Guillermier, M., Bernier, S., Gaudin, M., Aurégan, G., Joséphine, C., Déchamps, N., Veran, J., Langlais, V., Cambon, K., Bemelmans, A. P., Baijer, J., Bonvento, G., Dhenain, M., Deleuze, J.-F., Oliet, S. H. R., Brouillet, E., Hantraye, P., Carrillo-de Sauvage, M.-A., Olaso, R., Panatier, A., & Escartin, C.
- Affiliations
- Université Paris-Sud (FR)
- Université de Bordeaux (FR)
- Commissariat à l'Énergie Atomique et aux Énergies Alternatives (FR)
- Corresponding author
- Escartin, Carole
- ORCID
- Venue
- Acta Neuropathologica Communications
- Published
- 2018-10-16
- Volume
- 6
- Issue
- 1
- Pages
- 104-104
- ISSN
- 2051-5960 (ISSN-L)
- PMC
- PMC6190663
- OpenAlex
- W2897601491
- Cited by
- 256
- References
- 86
- Citations by year
- 2026: 18 · 2025: 38 · 2024: 50 · 2023: 38 · 2022: 30 · 2021: 40 · 2020: 31 · 2019: 11
- FWCI
- 9.22
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Acta Neuropathologica Communications (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Fédération pour la Recherche sur le Cerveau
- Agence Nationale de la Recherche (2010-JCJC-1402-1; 2011-BSV4-021-03; ANR-16-TERC-0016-01, 2011-INBS-0011)
- Fondation Vaincre Alzheimer (FR-15015)
- Association France Alzheimer and Fondation de France
- 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
- astrocyte activation, Alzheimer's disease, JAK2/STAT3 signaling, neuroinflammation, viral gene delivery, amyloid deposition, spatial learning deficits, synaptic dysfunction, therapeutic target
- MeSH terms
- Suppressor of Cytokine Signaling 3 Protein, Alzheimer Disease, Animals, Apolipoproteins E, Astrocytes, Disease Models, Animal, Glial Fibrillary Acidic Protein, Hippocampus, Male, Mice, Transgenic, Mutation, Amyloid beta-Peptides, Aspartic Acid Endopeptidases, Amyloid beta-Protein Precursor, Maze Learning, Excitatory Postsynaptic Potentials, Extracellular Signal-Regulated MAP Kinases, STAT1 Transcription Factor, Mice, Janus Kinase 2, Presenilin-1, Amyloid Precursor Protein Secretases
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