Explore the words cloud of the SOCIALBRAINCIRCUITS project. It provides you a very rough idea of what is the project "SOCIALBRAINCIRCUITS" about.
The following table provides information about the project.
Coordinator |
FONDAZIONE ISTITUTO ITALIANO DI TECNOLOGIA
Organization address contact info |
Coordinator Country | Italy [IT] |
Total cost | 168˙277 € |
EC max contribution | 168˙277 € (100%) |
Programme |
1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility) |
Code Call | H2020-MSCA-IF-2017 |
Funding Scheme | MSCA-IF-EF-ST |
Starting year | 2018 |
Duration (year-month-day) | from 2018-09-01 to 2020-08-31 |
Take a look of project's partnership.
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1 | FONDAZIONE ISTITUTO ITALIANO DI TECNOLOGIA | IT (GENOVA) | coordinator | 168˙277.00 |
Also known as velocardiofacial or DiGeorge syndrome, 22q11.2 deletion syndrome (22q11.2DS) is currently considered as the highest genetic-based vulnerability factor for neuropsychiatric disorders, such as autism spectrum disorder, attention deficit hyperactivity disorder, anxiety disorders and schizophrenia. Noteworthy, this microdeletion leads to a wide range of peripheral and central symptoms, including severe deficits in face memory and social cognition, which remain incurable to date. Thus, the present proposal aims at delineating the neuroanatomical substrates of social behavior in order to identify new therapeutic avenues for social deficit in velocardiofacial syndrome and its associated neuropsychiatric disorders. To this purpose, we will use a very solid murine model of 22q11.2DS, the LgDel/- mouse, which similarly displays deficits in social interaction, to investigate the respective interventions of the oxytocin (OT) and the dopamine (DA) system in the implementation of normal versus altered social behavior, at critical time periods (first post-natal days and adolescence). Specifically, preliminary findings from the host laboratory suggest that early alterations of the OT system, by preventing proper GABA switch in the medial prefrontal cortex (mPFC), leads to abnormal mPFC regulation of DA function in the nucleus accumbens and/or amygdala, and subsequent social deficits at adulthood in LgDel/- mice. We will address this hypothesis by using a multidisciplinary strategy encompassing genetics, molecular biology, biochemistry, tracing methods, cell culture, as well as viral and behavioral approaches. The originality of the present project, which resides in our will to identify the developmental trajectories of social behavior, together with a reciprocal transfer of theoretical, practical and transferrable skills between the host laboratory and me, will allow me to develop independent research projects and a competitive research career.
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The information about "SOCIALBRAINCIRCUITS" are provided by the European Opendata Portal: CORDIS opendata.