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The overall, long-term goal of much of our work is to understand the basic neurobiological mechanisms that are altered in serious mental illnesses, such as schizophrenia, which give rise to some of the core symptoms of these disorders (e.g. delusions, depression, and social dysfunction). The central hypothesis tested in our studies is that many of these symptoms emerge from disruptions of processes supporting emotional function and/or social cognition. Thus, to test this model, we have conducted studies in a range of populations examining emotional memory mechanisms and perceptual processes that represent “basic building blocks” of affective and social functions.
In a parallel line of research, we have studied these same processes in individuals who have some degree of transdiagnostic risk for serious mental illness, including those with low-level psychotic experiences (subclinical psychotic symptoms) and first-degree relatives of people with psychiatric illnesses (e.g., schizophrenia, depression). The goal of this work is to identify objective markers of risk which can be used in the future in early detection and prevention tools -- to identify individuals who might benefit from preventive interventions. At the same time, we are also developing and evaluating behavioral interventions that might reduce liability for future illness or disability by increasing resilience in at-risk individuals.
Examples of our recent work are summarized below.
Changes in Social Perception and Behavior
Lower-level social perception and behavior
Deficits in social cognition are some of the strongest predictors of daily functioning in individuals with schizophrenia. Moreover, consistent links between changes in social cognitive processes and both the positive and negative symptoms of schizophrenia have been reported. We have studied both higher-order and basic, non-verbal forms of social cognition. One manifestation of a non-verbal social behavior is "personal space" -- the distance that individuals prefer to maintain from others. Our recent findings suggest that some individuals with schizophrenia and healthy subjects, particularly those who prefer to spend more time alone (with higher levels of social anhedonia), show abnormalities in personal space-related behaviors.
Investigating Personal Space in Virtual Reality
Deficits in Inhibition of Limbic Circuitry
Overactivity and impaired habituation of the medial temporal lobe in schizophrenia
One long-standing theory about psychosis is that it arises from a deficit in inhibition of the medial temporal lobe. We have found evidence for this deficit in fMRI studies of the responses of the hippocampus and amygdala to face stimuli—with findings of overactivity and impaired habituation of the medial temporal lobe to emotional facial expressions in individuals with schizophrenia.
The Neural Basis of Illness Risk and Resilience
At-risk Phenotypes
We have been investigating neural correlates of several “at-risk phenotypes”, including subclinical psychotic symptoms (such as subclinical delusional ideas), familial risk for psychosis or depression (i.e., having a relative with one of these disorders), and those with a history of childhood trauma, with the goal of identifying objective, neural markers of risk that could be used as quantitative targets of preventive treatments.
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