Recent analyses of a particular gene shed new light on “memory extinction” – the neuronal process whereby certain memories are gradually replaced by new ones. According to researchers from the Massachusetts Institute of Technology, a more sophisticated understanding of the gene may eventually inspire efforts to control harmful and unwanted memories. The findings could thus have significant bearing on future post-traumatic stress disorder (PTSD) treatment.

Published in the journal Neuron, the new study examined how a gene known as Tet1 regulates a variety of mechanisms associated with memory extinction. According to senior author Li-Huei Tsai, the regulatory gene could hold the key to suppressing debilitating memories.

"If there is a way to significantly boost the expression of these genes, then extinction learning is going to be much more active," he said in a press release.

To test the hypothesis, the researchers examined mice subjects in which the Tet1 gene had been suppressed. Together with a control group, the knockout mice were conditioned to fear a particular cage in which they were administered a mild shock.

Initially, the experiment showed no significant difference between the subjects without Tet1 and those with regular levels, as both groups were able to form the memory without complications. But while the normal mice gradually overcame their fear once the danger element was removed, the knockout mice appeared to retain it. According to the researchers, their genetic configuration made it impossible for new memories to replace the old one.

"What happens during memory extinction is not erasure of the original memory," Tsai explained. "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."

The correlation between Tet1 and memory extinction suggests that the gene could have a therapeutic potential for individuals suffering from PTSD. By supplementing treatment programs with a reliable way to boost Tet1 expression, therapist would facilitate the introduction of new memories and the formation of positive associations. For this reason, Tsai and his colleagues’ findings may prove indispensable in the battle against the debilitating condition that currently affects 7.7 million Americans.

Garrett A. Kaas, Chun Zhong, Dawn E. Eason, Daniel L. Ross, Raj V. Vachhani, Guo-li Ming, Jennifer R. King, Hongjun Song, J. David Sweatt. TET1 Controls CNS 5-Methylcytosine Hydroxylation, Active DNA Demethylation, Gene Transcription, and Memory Formation. Neuron, 2013