It all comes down to the gene known as Tet1. It pilots memory by altering levels of DNA methylation (a biomechanical process that controls access to genes). In an MIT experiment, researchers discovered that mice with normal levels of Tet1 could eventually forget that a particular cage gave them a shock, while those with low levels of Tet1 did not forget. Theoretically, that could mean that shellshocked war victims or PTSD sufferers might have low levels of Tet1, thus making it hard for them to form to make new memories to combat their old, painful ones. But it's not just a matter of replacement. "What happens during memory extinction is not erasure of the original memory," says Li-Huei Tsai, director of MIT’s Picower Institute for Learning and Memory. "The old trace of memory is telling the mice that this place is dangerous. But the new memory informs the mice that this place is actually safe. There are two choices of memory that are competing with each other." In other words, it allows you to more appropriately choose how to weigh between good and bad memories.
The question then becomes: So how do we return patients' Tet1 levels to normal, helping them to forget? This is the next phase of the experiment, and the answers are likely a few years away. But learning how to forget is the first step in knowing what, and when, to remember. [Gizmodo]