p38 activation occurs mainly in microglia in the P301S Tauopathy mouse model

Tauopathies are a group of neurodegenerative diseases characterized by the accumulation of hyperphosphorylated tau protein in the brain. Many of these pathologies also present an inflammatory component determined by the activation of microglia, the resident immune cells of the brain. p38 MAPK is one...

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Bibliographic Details
Authors: Perea, Juan R.; García, Esther; Vallés-Saiz, Laura; Cuadros, Raquel; Hernández Pérez, Félix; Bolós, Marta; Ávila, Jesús
Format: Article
Publication date:2022
Country:España
Institution:Universidad Autónoma de Madrid
Repository:Biblos-e Archivo. Repositorio Institucional de la UAM
Language:English
OAI Identifier:oai:repositorio.uam.es:10486/719204
Online Access:http://hdl.handle.net/10486/719204
https://dx.doi.org/10.1038/s41598-022-05980-8
Access Level:Open access
Keyword:Tauopathies
p38 mitogen-activated protein kinases
Microglia
Alzheimer's disease
Hippocampus
Biología y Biomedicina / Biología
Description
Summary:Tauopathies are a group of neurodegenerative diseases characterized by the accumulation of hyperphosphorylated tau protein in the brain. Many of these pathologies also present an inflammatory component determined by the activation of microglia, the resident immune cells of the brain. p38 MAPK is one of the molecular pathways involved in neuroinflammation. Although this kinase is expressed mainly in glia, its activation in certain neurodegenerative diseases such as Alzheimer's Disease has been associated with its ability to phosphorylate tau in neurons. Using the P301S Tauopathy mouse model, here we show that p38 activation increases during aging and that this occurs mainly in microglia of the hippocampus rather than in neurons. Furthermore, we have observed that these mice present an activated microglial variant called rod microglia. Interestingly, p38 activation in this subpopulation of microglia is decreased. On the basis of our findings, we propose that rod microglia might have a neuroprotective phenotype in the context of tau pathology