Deletion of FKBP5 alters stress-related parameters in mice

Posttraumatic stress disorder (PTSD) is a common and debilitating psychiatric disease. Estimates of the prevalence of PTSD in populations experiencing potentially traumatic events range from 1% to 15% for current PTSD and 10% to 39% for lifetime PTSD (1) indicating that although a substantial amount of individuals exposed to a traumatic event develop PTSD, most individuals do not. Beside the severity of trauma and the extent of peritraumatic social support, inborn or acquired constitutional factors could explain why only some exposed individuals develop PTSD. Latter assumption fueled the performance of several genetic association studies in patients and animal models that revealed a set of interesting candidate genes mostly linked to either the fields of neurotransmission, neurode-/regeneration or HPA-axis modulation. Nevertheless, some of these trials achieved contradictory findings possibly resulting from confounding variables like co-morbidities, types of trauma and, supposedly, yet unknown non – genomic constitutional variables. These discrepancies demand the need for further and more comprehensive clinical research trials hopefully contributing to the improvement of current therapeutic options. Here we present the conceptual design of the Munich PTSD Biomarker Research Study – a clinical research trial started in March 2009at the Max Planck Institute of Psychiatry. 1. Neurocognitive risk factors for PTSD, Orr S.P., Pitman R., in: Risk Factors for PTSD, 1999, p.125–43