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Título: | Microglial hyperreactivity evolved to immunosuppression in the hippocampus of a mouse model of accelerated aging and Alzheimer’s Disease traits |
Autor: | Molina-Martínez, Patricia CSIC; Corpas, Rubén CSIC ORCID; García-Lara, Elisa CSIC ORCID; Cosín-Tomás, Marta CSIC ORCID; Cristòfol, Rosa CSIC ; Kaliman, Perla CSIC; Solà, Carme CSIC ORCID; Molinuevo, José Luis; Sánchez-Valle, Raquel; Antonell, Anna; Lladó, Albert; Sanfeliu, Coral CSIC ORCID | Palabras clave: | Neuroinflammation SAMP8 mice Autosomal dominant Alzheimer’s disease (ADAD) Sporadic earlyonset Alzheimer’s disease (sEOAD) Triggering receptor expressed on myeloid cells 2 (TREM2) |
Fecha de publicación: | 28-ene-2021 | Editor: | Frontiers Media | Citación: | Frontiers in Aging Neuroscience 12: 622360 (2021) | Resumen: | Neuroinflammation is a risk factor for Alzheimer’s disease (AD). We sought to study the glial derangement in AD using diverse experimental models and human brain tissue. Besides classical pro-inflammatory cytokines, we analyzed chitinase 3 like 1 (CHI3L1 or YKL40) and triggering receptor expressed on myeloid cells 2 (TREM2) that are increasingly being associated with astrogliosis and microgliosis in AD, respectively. The SAMP8 mouse model of accelerated aging and AD traits showed elevated pro-inflammatory cytokines and activated microglia phenotype. Furthermore, 6-month-old SAMP8 showed an exacerbated inflammatory response to peripheral lipopolysaccharide in the hippocampus and null responsiveness at the advanced age (for this strain) of 12 months. | Versión del editor: | http://dx.doi.org/10.3389/fnagi.2020.622360 | URI: | http://hdl.handle.net/10261/260338 | DOI: | 10.3389/fnagi.2020.622360 | Identificadores: | doi: 10.3389/fnagi.2020.622360 e-issn: 1663-4365 |
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