Can we pick and choose which memories to keep?
The current issue of Neuron features a new study on selective memory erasure. It comes from a group of Chinese researchers, led by Joe Tsien, who have successfully targeted and destroyed specific memories in mice. Now, there’s a possibility that they will adapt their method for human use.
In fact, a team of scientists that includes Roger Pitman, a psychiatrist at Harvard, and Karim Nader, a neuroscientist at McGill, is already much farther along in the effort to reshape human memories. Last year, they published findings suggesting certain drugs might be able to affect the way in which traumatic events are remembered if administered shortly afterward. Now, they are looking for a way to refashion memories even years after they were created. Recently they received a grant from the Department of Defense, which has a vested interest in their line of research, as more and more American troops are returning from Iraq and Afghanistan with post-traumatic stress disorder.
The researchers discovered that reactivating memories in mice with excessive amounts of a particular enzyme caused the memories to be destroyed.
Though their methods are different, the Chinese researchers are capitalizing on the same thing as Pitman’s team: the relatively recent discovery that memories are not written in permanent ink.
We forget the vast majority of things that happen to us. Experiences must be processed and reprocessed in order to become long-term memories. Now research shows that even those memories we do hold on to are subject to revision every time we recall them.
Here’s an example: Four years ago, let’s say, on a hot August morning, you were walking down the street, rushing to make the light, and arguing with your mother on your cell phone. Something caused this episode to stick with you—maybe you found $50 on the sidewalk, or maybe you unconsciously associated it with summer in New York. But when, four years later, you are reminded of it, it is possible that you will inadvertently revise the events of that morning -- your mother was there with you, for instance, or it wasn’t August, it was April, and unseasonably warm.
Even more surprising, perhaps, is that simply as a result of remembering it, that morning could disappear from your memory altogether. Recent research has revealed that ‘reactivating’ a memory causes it to change form in the brain—it returns to a pliable, impermanent state. In order for it to once again regain something approaching permanency, various proteins must be produced by various brain cells. Durability is every bit up for grabs when an old memory is reactivated as when a new one is first on the brink of being formed.
Seizing upon this momentary blank slate that memory reactivation offers, Roger Pitman, Karim Nader and their colleagues are running clinical trials on drugs that have the potential to disarm traumatic memories. Their work has focused on Propranolol, a beta-blocker that has been on the market for several years to treat hypertension. As Dr. Nader explains, by targeting only the emotional component of a memory, the treatment that he and his team are developing will change memories, not erase them.
This works because when we remember something that happened to us, we’re remembering not just the event itself, but also the way we felt as that event was taking place. These feelings are stored separately, in the brain region called the amygdala. Injecting someone with a drug that specifically targets the amygdala, and then prompting him or her to recall the traumatic experience, can change the memory from one that invokes a wave of grief and horror to a more benign, matter-of-fact recollection.
Dr. Nader says that their goal in treating trauma victims is “just to decrease the emotional intensity of the memory so that it goes back down to within the range of a normal bad memory.”
The new Chinese study joins this growing trend in neuroscience. Joe Tsien and his colleagues use genes instead of drugs, but they too are taking advantage of what is now understood about memory reactivation. Rather than administer drugs to their experimental mice, however, Tsien’s team altered their genes to produce an excess of one particular enzyme, called CaMKII. The researchers discovered that reactivating memories in mice with excessive amounts of this enzyme caused the memories to be destroyed.
One major consideration for all of these studies is specificity—how to target one memory without affecting others. Tsien’s group says it successfully targeted single, isolated memories, but what they mean is that their experimental mice forgot that a particular training chamber would deliver an electrical shock. The mouse brain, clearly, does not deal in nuances—a sliver of moldy cheese forgotten on the floor might make for a festive occasion, but it’s no madeleine. Another unknown: how long will the treatment effects last? The hope, with both methods, is to permanently alter the targeted memory to rule out the possibility that it could one day resurface. Tsien and colleagues say that their genetic intervention succeeded in erasing memories in the long-term, but in the mouse world, long-term means two weeks.
As for Pitman’s team, it is also early to know how durable the effects of drugs like Propranolol are on memory revision. In fact, unlike his colleague Karim Nader, Roger Pitman refused to comment on their findings so far. When reached by phone, he said it was too soon to make any definitive pronouncements.
“Call me in six months,” he said, before hanging up.
Apparently, he’s optimistic.
