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The specific aim of this proposal is to investigate the neurophysiological mechanisms of oxytocin's (OT) prosocial effects in patients with schizophrenia and healthy subjects using magnetoencephalography. Hypothesis A: When OT is administered to patients with schizophrenia, fear-related amygdala hyperreactivity and fusiform gyrus (FG) and anterior cingulate cortex (ACC) hypoactivity will be normalized. Hypothesis B: When OT is administered to patients with schizophrenia, the decreased functional connectivity (FC) between the amygdala, FG, and ACC will be normalized. By elucidating the neurophysiological mechanisms of OT administration on emotional face processing, investigators will bee able to: 1. understand the pathophysiology of the functionally debilitating social cognitive deficits of schizophrenia, 2. test the efficacy of OT in normalizing the neural abnormalities underlying these social deficits, and 3. develop and optimize novel treatments for these currently untreatable deficits.
San Francisco, California