DOPAMINE FUNCTION AND CEREBRAL GLUCOSE METABOLISM IN PSYCHOTIC DEPRESSION

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. It is now possible to apply brain imaging methodology to investigate the neurochemical basis of psychotic depressive disorder and the mechanims underlying the clinical response to glucocorticoid antagonists. Psychotic depression has not been extensively studied with neuroimaging methods. The neurobiology of psychotic depression is an important area of investigaton as it is associated with greater cognitive impairment, treatment resistance and mortality than non-psychotic depression. The purpose of the study described in the protocol is to evaluate the effects of mifepriustone treatment on cerebral glusose metabolism and dopamine (D2) receptor availability in patients with psychotic depression. Specifically, patients who are enrolled in the IRB approved treatment protocol "A Phase III, Randomized, Double-Blind, Placebo-Controlled Study of Safety and Efficacy of C-1073 (Mifepristone) in Patients with Major Depressive Disorder with Psychotic Features who are not receiving Antidepressants or Antipsychotics" will undergo neuroimaging procedures prior to and following treatment. This study will involve two Positron Emission (PET) scanning sessions (baseline and at the end of one week of treatment with mifepristone). Each PET scan session lasts approximately three hours. Each scan session involves one scan with [11C]-raclopride and one scan with [18F]-FDG. An MR scan will be performed for region of interest localization and for the correction of the PET data for cerebral atrophy. It is hypothesized that mifepristone treatment will result in increased cortical glucose metabolism and increased D2 receptor binding compared to placebo treated patients.