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Changing Your Mind about PTSD

by
Scope Correspondent

Do you have a memory you’d rather forget? If you do, chances are that over time it will seem to fade away as you begin to associate the words or places or smells that trigger that unpleasant recollection with a more positive experience. Researchers call this process fear memory extinction, but that’s a bit of a misnomer. We actually don’t delete memories; we write new ones called extinction memories that come to mind faster than our older associations. Our brains accomplish this trick by flipping genetic switches on and off in the process of learning and forming the new memory.

Recently, researchers at MIT identified a molecular mechanism that contributes to memory extinction. They did so using mice lacking a single gene that helps regulate a part of our genetic control system, a chemical process called methylation. Surprisingly, those mutant mice were unable to forget fearful memories.

Methylation is a chemical coating of the DNA that cells can use to keep genes locked in the reference section of our DNA libraries. It acts as a stop sign that prevents the molecules needed to switch the gene on from interacting with the DNA. Until recently, it was thought to be fairly static, particularly in the brain, and maintained in the same places throughout generations of cells. But the MIT study shows that methylation can change rapidly in our brains while they are recalling fear-associated memories.

“The very fact that DNA methylation may regulate something so specific is peculiar, and the idea that DNA methylation can regulate cognition is super new,” said Dr. Andrii Rudenko, lead author of the study.
Proper DNA methylation in memory extinction seems to play a role in humans, too. In an unrelated study of roughly 5000 human PTSD patients, Professor Kerry Ressler and his colleagues at Emory University have found unique methylation patterns in PTSD sufferers, indicating that DNA methylation in the wrong places could be part of the disease.

These studies don’t yet have direct clinical applications, but researchers hope that continued advances in the field might lead to improved treatments for psychiatric disorders caused by a persistent memory that refuses to be replaced – such as phobias, addiction relapses, and post-traumatic stress disorder (PTSD).

Today, PTSD treatment relies on exposure-based therapy, which tries to train the brain to replace the negative memory associated with a particular stimulus with a benign one. But pharmaceuticals which could target the methylation patterns of only the appropriate genes could enhance the effect of therapy, even if they would likely not entirely replace it. “It would basically be helping someone get over a bad experience in the way they would do it normally, and they don’t have to be on drugs for a long time,” said Dr. James Stafford, a researcher at NYU unaffiliated with the MIT study.

Beyond possible applications, however, the research suggests scientists may have to rewire their thinking about how stable methylation is in the brain. The research confirms that “very little in the brain is static, it’s constantly reinventing itself,” said Dr. Ressler.

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