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 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 also perceptual processes that represent “basic building blocks” of affective and social functions. Examples of our recent work are summarized below.

Medial Temporal Lobe & Salience Networks in Schizophrenia

Our early studies tested the hypothesis that overactivity of a salience detection/memory network (which includes the hippocampus and amygdala) represents a core abnormality of schizophrenia. 

Fear and Extinction Learning & Memory

Recent studies in our lab aim to identify the mechanisms underlying changes in salience detection/fear inhibition that may generate or contribute to psychotic symptoms in schizophrenia. Studies using a Pavlovlian fear conditioning and extinction paradigm showed that patients with schizophrenia exhibit  abnormalities in context-dependent extinction memory or "safety signaling." Impaired safety signaling may give rise to delusions in these patients. 

Psychosis has long been thought to involve a disruption of the representations of social information, including knowledge about the self and others. It has been recently established that a network of midline cortical regions are critically involved in generating these representations. To investigate whether the function of these regions is altered in psychotic illness, we studied this network using a classical self-reference fMRI task and a resting-state functional connectivity analysis in a cohort of patients with schizophrenia and demographically-matched control subjects. This investigation revealed an anterior-to-posterior shift in self-referential-related fMRI activity in this midline network, with overactivity of the posterior cingulate and reduced activity of the medial prefrontal cortex in the patients, compared to the controls. The posterior cingulate region showed reduced connectivity with medial prefrontal cortex in the schizophrenia group compared to the controls, suggesting that weakening of this pathway may contribute to social cognition deficits in schizophrenia. Also, these findings suggest that lower-level perceptual processes that contribute to self/other processing may be disrupted in psychotic patients. 

Higher-Level and Lower-Level Social Cognition

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Massachusetts General Hospital 

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