Schizophrenia
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.
Emotion-Cognition Interaction:
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.