| Literature DB >> 26362308 |
Elísabet Alcocer-Gómez1, Cristina Ulecia-Morón2, Fabiola Marín-Aguilar3, Tatyana Rybkina2, Nieves Casas-Barquero4, Jesús Ruiz-Cabello5, Bernhard Ryffel6, Lionel Apetoh7,8,9, François Ghiringhelli7,8,9, Pedro Bullón3, José Antonio Sánchez-Alcazar1, Angel M Carrión10, Mario D Cordero11,12,13.
Abstract
Depression is a major public health concern in modern society, yet little is known about the molecular link between this condition and neuroinflammation. The inflammasome complex was recently shown to be implicated in depression. The present study shows the implication of NLRP3 inflammasome in animal model of stress-induced depression. Accordingly, we show here that in the absence of a NLRP3 inflammasome, prolonged stress does not provoke depressive behaviors or microglial activation in mice or dampen hippocampal neurogenesis. Indeed, NLRP3 deletion or inhibition of microglial activation impairs the stress-induced alterations associated with depression. According to these findings in animal model, the inflammasome could be a target for new therapeutic interventions to prevent depression in patients.Entities:
Keywords: Depression; Inflammasome; Microglia; Stress
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Year: 2015 PMID: 26362308 DOI: 10.1007/s12035-015-9408-7
Source DB: PubMed Journal: Mol Neurobiol ISSN: 0893-7648 Impact factor: 5.590