Can we delineate cognitive processes involved in social attention?
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As an instrumental skill for maintaining positive social relationships, social attention is critical for understanding and learning about people, yet it is unclear whether there are distinct subdomains of endogenous (automatic) and exogenous (directed) social attention. This project aims to characterize these aspects of social attention across brain and behavior measurements in a large and diverse sample of adolescents. This information will improve our conceptualization of social attention, as well as mapping social attention abilities to individual differences in real-world sociocognitive abilities and biological factors.
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Are social attention and social motivation distinct in autism and social anxiety?
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We rely on brain mechanisms of social attention to learn and understand the actions of others, yet these abilities are disrupted in autism spectrum disorder (ASD) and social anxiety disorder (SAD). Similar to the NIMH project described above, we are interested in measuring whether there are shared mechanisms within these areas of social cognition -- but also if there are unique patterns or subgroups for ASD and/or SAD.
Social attention brain mechanisms are in large part automatic, but may also be driven by differences in social motivation (e.g, the intrinsic desire to engage and connect with others). However, although heavily featured in the context of social impairments in ASD, the concept of social motivation is poorly defined in healthy or non-clinical populations. Graduate student Nicole Friedman is leading our efforts to better understand social motivation. |
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Linking gene, brain, and behavior: How do attention brain biomarkers relate to behaviors in children with disruptive GRIN2B mutations?
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GRIN2B is a gene that encodes proteins that together form a receptor that manages how brain signals are sent in the brain. Disruptions to the GRIN2B gene are associated with neurodevelopmental disorders (including autism spectrum disorder), hypotonia, seizures, and speech and behavior difficulties. However, the connection between preclinical animal models of GRIN2B and the human profiles of these phenotypes is less clear. The objective of this project is to establish a candidate biological indicator (“biomarker”) to the clinical and behavioral profile of children with disruptive GRIN2B mutations.
We are targeting an electroencephalography (EEG) attention response known as the P3a as a candidate biomarker. We predict the P3a will relate to attention and sensory behaviors in children with disruptive GRIN2B mutations. |
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Linking gene, brain, and behavior: Do distinct phenotypes of SCN2A (loss vs gain of function) exhibit unique attention biomarkers?
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SCN2A is a gene that encodes proteins that regulate action potentials in the brain, particularly during early development. However, there are two different SCN2A phenotypes based upon where the genetic disruption is located: (1) Children with a loss-of-function variant exhibit features of ASD and broad intellectual disabilities, whereas (2) children with a gain-of-function variant exhibit a strong infantile epileptic encephalopathy (IEE) phenotype characterized by seizures early in life.
We are targeting an electroencephalography (EEG) attention response known as the P3a as a candidate biomarker. Here, we will specifically look how the P3a signal changes over time (i.e., habituation response) with a prediction that the IEE response will be distinct from the loss-of-function and ASD response. |
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