Changes in the Effective Connectivity of the Social Brain When Making Inferences About Close Others vs. the Self.

Previous research showed that the ability to make inferences about our own and other's mental states rely on common brain pathways; particularly in the case of close relationships (e.g., romantic relationships).

Brain circuits involved in understanding our own and other's internal states in the context of romantic relationships.

Social interactions require the capacity to understand both our and other's internal states. These semi-independent skills, the ability to understand oneself and others, seem to rely on the same type of representations and recruit similar brain areas. In this study, we looked at the neural basis of self and other processing in the context of an interaction with a significant other.

Using resting-state DMN effective connectivity to characterize the neurofunctional architecture of empathy.

Neuroimaging studies in social neuroscience have largely relied on functional connectivity (FC) methods to characterize the functional integration between different brain regions. However, these methods have limited utility in social-cognitive studies that aim to understand the directed information flow among brain areas that underlies complex psychological processes. In this study we combined functional and effective connectivity approaches to characterize the functional integration within the Default Mode Network (DMN) and its role in self-perceived empathy.

Quantification of mutant E-cadherin using bioimaging analysis of in situ fluorescence microscopy. A new approach to CDH1 missense variants.

Missense mutations result in full-length proteins containing an amino acid substitution that can be neutral or deleterious, interfering with the normal conformation, localization, and function of a protein. A striking example is the presence of CDH1 (E-cadherin gene) germline missense variants in hereditary diffuse gastric cancer (HDGC), which represent a clinical burden for genetic counseling and surveillance of mutation carriers and their families. CDH1 missense variants can compromise not only the function of E-cadherin but also its expression pattern.