Trauma processing: Does it depend on the genes?

The body's own regulation of a particular gene is associated with a reduced risk of developing post-traumatic stress disorder after a terrible experience.

Lower risk of PTSD observed with a stronger NTRK2 regulation

The body's own regulation of a particular gene is associated with a reduced risk of developing post-traumatic stress disorder after a terrible experience. In particular, traumatic memories of the experience are less pronounced. This was reported by researchers from the University of Basel, Switzerland, in the journal PNAS.

Traumatic experiences such as an accident, rape, or torture can be deeply engraved in the memory and even years later cause symptoms of post-traumatic stress disorder. The stress hormone cortisol plays an important role in regulating these memory processes. This has been shown by studies conducted by the research team of Prof. Dr. Dominique de Quervain at the University of Basel, among others.

In their current work, de Quervain's team took a closer look at the genes involved in the signal transmission of cortisol. They determined the extent to which these genes are chemically regulated by so-called methyl groups on the DNA genetic molecule. Vanja Vucojevic, one of the main authors of the study, examined this DNA methylation in two groups of trauma victims, namely 463 survivors of the civil war in Uganda and 350 survivors of the genocide in Rwanda.

In both groups, those individuals who had stronger regulation of the NTRK2 gene had a lower risk of developing posttraumatic stress disorder. Conversely, the researchers were able to rule out with a high degree of probability that the trauma itself leads to a change in the regulation of this gene: There was no correlation between the severity of the trauma and the extent of DNA methylation, which suggests that the latter already existed before the trauma.

A weaker memory

Several basic studies had already shown that the NTRK2 gene plays an important role in memory formation. Indeed, in the current study, people with stronger regulation of this gene had fewer traumatic memories. In addition, the researchers found that the regulatory mechanism - i.e. DNA methylation at the NTRK2 gene - was also related to memory in a control group of 568 non-traumatized people. Thus, people with stronger methylation of this gene had a poorer memory of previously seen images. In addition, during the memory tests, they showed altered brain activity in the regions important for memory.

The results suggest that increased regulation of the NTRK2 gene reduces memory formation. As a result, terrible experiences bury themselves less strongly in the memory and thus the risk of developing post-traumatic stress disorder is reduced. The researchers hope that the discovered mechanism will contribute to the development of new therapies. These could also be useful in cases of pre-existing post-traumatic stress disorder by preventing the recurring horrible memories from further cementing the traumatic memory.

The current study is part of the Basel Genetic Memory Project taking place within the Transfaculty Research Platform Molecular and Cognitive Neurosciences (MCN), which is led by Prof. Andreas Papassotiropoulos and Prof. Dominique de Quervain. The aim is to transfer results from basic research into clinical projects as quickly as possible.

Vanja Vukojevic, David Coynel, Navid Reza Ghaffari, Virginie Freytag, Thomas Elbert, Iris-Tatjana Kolassa, Sarah Wilkeri, James L. McGaugh, Andreas Papassotiropoulos, and Dominique J.-F. de Quervain. NTRK2 methylation is related to reduced PTSD risk in two African cohorts of trauma survivors. PNAS (2020), doi: 10.1073/pnas.2008415117