Les Drs Nicolas Cermakian et Patricia Pelufo Silveira obtiennent un financement d’amorçage Ludmer-MI4

Félicitations aux Drs Nicolas Cermakian et Patricia Pelufo Silveira pour leur récente obtention d'un fonds d’amorçage Ludmer-MI4! Cette subvention vise à soutenir de nouveaux projets de recherche en santé ciblant le rôle de l'infection, de l'immunité et/ou du microbiome dans le développement, la prévention ou le traitement de troubles mentaux. Le projet financé s'intitule, Maternal immune activation and circadian disruption as risk factors for mental disorders – using transcriptomics to identify individual differences in susceptibility. 

Nous souhaitons aux Drs Cermakian et Silveira, ainsi qu'à leurs collaborateurs, Drs Lalit Srivastava et Tie Yuan Zhang, succès dans leurs travaux.

Résumé du projet

Schizophrenia is a severe neurodevelopmental disorder with lifetime prevalence ~1%. The occurrence of neurodevelopmental disorders such as schizophrenia and autism spectrum disorders rely on a combination of risk factors, including genetic variants and environmental factors. Exposure to prenatal infections is associated with increased risk for neurodevelopmental disorders. For example, influenza infection during pregnancy first trimester leads to a 7-fold risk of the offspring to develop schizophrenia. Up to 80% of patients with schizophrenia show disrupted sleep and circadian rhythms. This led us to propose circadian disturbances as a possible risk factor for schizophrenia, which our recent findings in mice support. This is important because circadian alterations are common in our modern-day societies (e.g. in shift workers, but also, for a large proportion of the population, with modern lifestyle involving irregular schedules of activity, light exposure and meal timing). Here we plan to identify mechanisms underlying this interaction between an immune-related risk factor (maternal infection) with a new environmental risk factor (circadian disruption). We will study the cellular and molecular bases for this interaction, by looking at the impact of the risk factors on gene expression at the cellular level in mouse brains. Furthermore, to underscore the translational potential of this research, we will use gene expression data to develop a new polygenic score as a tool to detect individual differences in susceptibility to these schizophrenia risk factors in human populations. This work will allow designing novel strategies, taking circadian rhythms into consideration, to prevent schizophrenia and other psychiatric conditions.

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