THE ROLE OF CORTISOL DYSREGULATION IN DEPRESSION AND HIPPOCAMPAL DYSFUNCTION

这个子项目是众多研究子项目之一

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. Depression, memory dysfunction, and hippocampal atrophy are associated with poorly controlled seizures in patients with temporal lobe epilepsy (TLE). However, little is known about the interrelationships among these factors and their potential mechanisms of action. Research has implicated cortisol in memory dysfunction and hippocampal cell loss in non-epileptic patients with depression. However, no published studies have examined the role cortisol may play in these factors in patients with TLE. The objective of this initial investigation is to examine the role of cortisol in depression, memory dysfunction, and hippocampal atrophy in 40 patients with medically intractable TLE and to evaluate a multivariate model to determine if cortisol mediates the relationships among these variables. All participants will complete neuropsychological examinations (including depression and memory measures) and MRI studies and have their cortisol levels measured. It is anticipated that patients with elevated cortisol levels will have significantly more depressive symptoms, lower memory scores, and lower hippocampal volumes than patients with normal range cortisol. It is further anticipated that the proposed multivariate model will be supported, demonstrating that cortisol is an important mediator. Successful completion of this research will provide valuable information about the role of cortisol in depression, memory dysfunction, and hippocampal atrophy in patients with TLE and provide a model for better understanding how these factors may work synergistically in TLE. The acquisition of such knowledge is critical to understanding the potential neuroendocrinological underpinnings of these factors and may provide strong implications for the medical treatment and management of TLE patients.