Our interest in schizophrenia targets a wide range of brain dysfunction including basic sensory-perceptual and cognitive functions. Development of biomarker for schizophrenia: Electrophysiological markers of sensory processing, observable in human event-related potentials, hold great promise to establish so-called endophenotypes-quantifiablemeasures of risk for schizophrenia. We assess the integrity of the early visual event-related- components (ERP) in clinically unaffected first-degree relatives of patients with schizophrenia, schizophrenia patients, and healthy control participants in the development of biomarkers. Relationship between dysbindin risk variants and sensory-level deficits: Variation at the dysbindin gene (DTNBP1) has been associated with increased risk for schizophrenia. Using electrophysiological markers of sensory processing, we explore the relationship between dysbindin risk variants and sensory-level deficits. A deficit in early visual ERP associated with a dysbindin risk haplotype presents functional confirmation of its deleterious effect on brain activity. Building on evidence of dysbindin's role in higher cognitive function, these early visual processing deficits suggest a generalized role for dysbindin in brain function and is likely to be part of the mechanism by which illness susceptibility is mediated.
How do emotions modulate neural activity related to inhibitory control in schizophrenic patients with and without a history of violence? It is well established that emotionally charged situations
affect our behavior. Preliminary electrophysiological data from a currently ongoing project suggest that schizophrenic patients with a history of violence gain from an emotionally charged situation such that cortical circuitry related to inhibitory control are reinstated, allowing them to exert improved control over their behavior.