Inflammation, glia and schizophrenia-related phenotypes

The activation of innate immune pathways has been identified as a pathogenic factor contributing to schizophrenia and other neuropsychiatric diseases. Activation of the NLRP3 inflammasome pathway has been shown to contribute to several neurodegenerative diseases and probably to the pathological sequelae of innate immune activation in schizophrenia. Therefore, NLRP3 inhibitor therapies could be considered a therapeutic intervention in this disease. However, the timing, site and duration of the NLRP3 activation still need to be known in order to delineate the best treatment periods. The objectives of this line of work are:

1. Study of the involvement of NLRP3 inflammasome in glial cell activation during brain development in young animals exposed to infectious (MIA mouse model) and non-infectious agents. 
2. Study of the impact of abnormal inflammasome activation due to a modification of microglia functions on brain development in a MIA model. 
3. Evaluation of the specific involvement of the NLRP3 inflammasome in a schizophrenia-like phenotype (MIA model) by using activation inhibitors. 
4. Analysis of the regulation of inflammasome activities and processes at the appropriate time during development and its benefit for therapeutic intervention in schizophrenia.