Changes in DNA methylation linked to traumatic memories and PTSD

[stumbleupon design=”horizontal_large”] [fbshare type=”button”] [twitter style=”horizontal” float=”left”] In my first post I touched on a few things including an MS drug, memory, changes in DNA, and epigenetics. Well, here is another related post about a research paper published today in Journal of Neuroscience discussing epigenetics and how it again relates to memory, but this time to the memory of traumatic events. I think it’s a good follow up to the MS post and I also think the paper has some really interesting conclusions.

Today researchers out of Switzerland, Germany, and the Netherlands (University of Basel, University of Ulm, University of Konstanz, and University of Nijmegen), published a paper in Journal of Neuroscience discussing how epigenetics and DNA methylation alter traumatic memories in male survivors of the Rwandan genocide. In the study, Vukojevic et al. studied the role of a glucocorticoid receptor gene, NR3C1, in PTSD risk and traumatic memory. Stress hormones and their signaling, including glucocorticoid receptor signaling, have been implicated in memory processes. For this reason, the authors chose to study how epigenetic changes of NR3C1 relate to intrusive memories.

In the paper, the authors first show that an important region of the NR3C1 gene, the NGFI-A binding site, shows increased DNA methylation, an epigenetic change (change in DNA without a change in the DNA code) that helps turn genes off. This increased methylation was associated with less intrusive traumatic memories in male survivors of the Rwandan genocide. Importantly, the study shows that the epigenetic changes were specific to memory and not to other symptoms of PTSD such as avoidance or arousal.

Another important experiment of the study showed that  the increased methylation of NR3C1 was associated with decreased expression of this gene, a result that is consistent with methylation’s role in turning genes off. Additionally, the increased methylation in male subjects was also associated with changes in brain area activation as measured by fMRI.

It is now becoming clear how epigenetic mechanisms contribute to memory encoding, consolidation, and retrieval. The  ability to control gene expression by epigenetic modifications allows for an additional layer of control over what proteins are made and when they are made, in this case, proteins needed to make, store, or access memories. The findings of this study point to a gene manipulation that can lead to less intrusive traumatic memories, a manipulation that could potentially be the target for future therapy.

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