Linnstaedt Lab

The Linnstaedt Lab focuses on three main areas of research, with all projects committed to improving the recovery process for individuals who have experienced trauma.

  1. Determine molecular mechanisms driving increased chronic pain and posttraumatic stress symptom development following trauma exposure in women. For these studies we are testing specific hypotheses regarding transcriptional control mechanisms that might differ in men and women. For instance, one question we are asking is whether sex hormones such as 17-β-estradiol or testosterone alter expression of genes that are pathogenic for chronic pain and/or posttraumatic stress. In order to test these hypotheses, we use a variety of methodological techniques, including bioinformatic modeling, association analyses using human cohort data, molecular and cell culture studies, and behavioral studies.
  2. Develop a clinically useful objective biomarker of chronic pain and posttraumatic stress development. For this project we are currently using high dimensional variable selection and support vector machines to develop a predictive algorithm that defines individuals at high risk of developing adverse outcomes following both motor vehicle collision trauma and sexual assault trauma. The development of this algorithm uses both clinical data collected from participants in our studies, along with genomic and transcriptomic data assessed in the early aftermath of trauma exposure.
  3. Determine genetic risk factors for individual susceptibility to posttraumatic adverse outcomes. We are fortunate to have genetic data on a large number of individuals from longitudinal studies of adverse outcome development following motor vehicle collision and sexual assault trauma. We use this cohort data to ask directed questions about individual susceptibility to chronic pain and posttraumatic stress symptom development. With these types of studies we have been able to show that genetic variants in important stress system genes such as ADRA2A (catecholaminergic system) and FKBP5 (HPA axis) influence vulnerability to chronic pain and posttraumatic stress following trauma. We have also been able to show the molecular mechanism through which some of these alleles affect individual variation in disease pathogenesis. Future studies will continue to examine pathways of genes as well as individual genes that are associated with posttraumatic adverse outcomes.


The current team at Linnstaedt Lab