Department of Psychology

Our research is concerned with understanding neurocognitive, emotional, and interpersonal processes during the early or prodromal phase, initial course and chronic phase of schizophrenia. Although there is substantial evidence of genetic liability or risk for schizophrenia, determining the genetic basis for the disorder has proved to be elusive. Along with other investigators, we are attempting to identify neurocognitive and affective abnormalities that reflect central and autonomic nervous system dysfunction which, in turn, may indicate vulnerability or genetic risk for schizophrenia. In addition to identifying vulnerability or risk factors, we are studying the contribution of stress and emotional reactivity to the expression and course of schizophrenia; our goal is to identify processes that lead from vulnerability for the illness to an episode of schizophrenia. The methods that we use include 128-channel dense array recordings to examine event-related brain potential (ERP) and EEG activity, psychophysiological measures of heart rate activity, electrodermal activity, the startle eye blink reflex and the post auricular reflex, measures of neuroendocrine response as well as interview and behavioral measures of clinical symptoms, life stress and coping.

Current Research Projects

Stress and Emotional Reactivity in Schizophrenia

Although theory and research on schizophrenia suggest that stress contributes to its etiology, expression and course, the processes that lead from vulnerability for schizophrenia to an episode of illness remain poorly understood. This project seeks to improve our understanding of stress and emotional reactivity in individuals who are vulnerable for schizophrenia, and to clarify the mechanisms that influence when and how patients react to stress. By focusing on patients in the prodromal, first episode and chronic phases of schizophrenia, there is the unique opportunity to examine how stress and emotional reactivity might contribute to the onset and progression of illness and to school, work and social functioning. This research is one of four projects within the NIMH-funded Center for Neurocognition and Emotion in Schizophrenia at UCLA that fosters collaborative efforts between researchers from the fields of psychology, psychiatry and other disciplines.

Attentional and Affective Modulation of Sensory Gating in Schizophrenia

This research project involves a series of studies that examine the influence of attention, emotion and stress on sensory gating or filtering in patients with a recent-onset or chronic course of schizophrenia. Investigators hypothesize that the sensory overload, cognitive fragmentation and conceptual disorganization frequently observed in schizophrenia patients may reflect a failure of normal filtering or gating mechanisms, and they have applied various measures to study this phenomenon. One measure that has been found to be well suited for examining impairments associated with sensory gating is the P50 component of the event-related brain potential (ERP), with P50 suppression serving as an operational definition of gating. P50 suppression is of considerable interest among clinical researchers not only because it appears to index neurophysiological substrates underlying the sensory overload observed in schizophrenia patients but because it also appears to be a promising indicator of genetic vulnerability for schizophrenia.

Vulnerability Indicators during the Prodromal and Recent-Onset Phases of Schizophrenia

Abnormalities of attention and sensory perception have long attracted the interest of researchers who study schizophrenia because such disturbances appear to be defining features of the illness. Researchers hypothesize that the sensory overload, cognitive fragmentation and conceptual disorganization frequently observed in schizophrenia patients reflects a failure of normal filtering or sensory gating mechanisms. Two measures that are being applied to examine impairments in sensory gating are the P50 component of the event-related brain potential and prepulse inhibition of the startle eye blink reflex. The aim of our research is to extend consideration of sensory gating deficits in schizophrenia to the study of early symptomatic manifestations of psychosis.

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