MedicalResearch.com Interview with:
Rainbo Hultman, PhD
Postdoctoral Research Associate
Laboratory for Psychiatric Neuroengineering, Principal Investigator
Affective Cognitive and Addiction Disorders (ACAD) Research Group
Department of Psychiatry and Behavioral Sciences
Center for Neuroengineering Duke University Medical Center
Durham, NC 27710
Medical Research: What are the main findings of the study?
Dr. Hultman: Using a mouse model of stress-induced psychiatric dysfunction, we found that the brainwave patterns in two key brain regions (prefrontal cortex, PFC and amygdala, AMY) encode for susceptibility to such dysfunction. Furthermore, such susceptibility can be predicted from the brainwave patterns in these regions before the onset of stress.
Medical Research: Were any of the findings unexpected?
Dr. Hultman: While we hypothesized that there may be differences in stress-susceptible brains prior to chronic stress, we were surprised to find this especially strong relationship between electrical activity in the prefrontal cortex before stress with social behavior after chronic stress.
Medical Research: What should clinicians and patients take away from your report?
Dr. Hultman: A number of psychiatric disorders can be caused or made worse by stress (e.g. major depressive disorder, schizophrenia, PTSD). Here we find that even among genetically identical animals, chronic stress can impact the brain differentially across individuals. One hopeful aspect of our findings is that there is something detectably different about these individuals’ brains even before the onset of stress. Future studies will be aimed at developing biomarkers to determine who is likely to have an adverse response to stress and make lifestyle and treatment plans accordingly before the onset of disorder.
Medical Research: What recommendations do you have for future research as a result of this study?
Dr. Hultman: This study really opens up the door to a number of different types of studies that can be done in the pursuit of mechanisms and biomarkers for susceptibility to maladaptive psychiatric responses to chronic stress. For example, it has not been possible previously to study which genes are highly expressed in a susceptible individual prior to the onset of stress. By having a neurophysiological biomarker of stress-susceptibility, we can ask questions about what other predictors of stress response may exist, and then target such mechanisms for developing therapies.