The objective of the project is to implement, in a biologically-supported way, an intranasal oxytocin (OXT) treatment to ameliorate the still incurable social, cognitive and immune system deficits characterizing the 22q11.2 microdeletion syndrome (22q11.2DS). Specifically, we will identify the selective behavioral domains, as well as the central and peripheral immune system components ameliorated by perinatal or adolescent exposure to OXT in the LgDel/+ 22q11.2DS mouse model. Then, we will disentangle the specific brain-immune connections involved in the rescue process. Our preliminary evidence indicates that in 22q11.2DS mice, which embed the well conserved full hemideletion found in 22q11.2DS patients, perinatal OXT exposure ameliorates some social and immune developmental trajectories. However, the extend of the ameliorative effects in other social, cognitive and immune system deficits, as well as the role played by the brain-immune interconnections in the mechanisms of rescue is unknown. The expected output is the establishment of a new strategy to correct altered developmental trajectories in 22q11.2DS, at the same time providing new knowledge on OXT immunomodulatory effects and immune-brain communication as the base of psychiatric-relevant phenotypes and treatments.
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Improving developmental trajectories in 22q11.2 deletion syndrome by oxytocin: focus on anti-inflammatory effects.