How can memories be erased

When the longer exposure occurred, the memory was re-saved in a weaker form. This, they say, stops the fear from returning so easily.

The researchers believe that this could strengthen techniques for dealing with anxiety and phobias in cases where exposure alone does not provide a long-term solution. To complement cognitive approaches, some scientists have suggested using drugs to remove bad memories or the fear-inducing aspect that is associated with them.

In one study , people with a fear of heights took D-cycloserine before a virtual reality exposure therapy. One week, and again 3 months later, their stress levels were lower than before. In other research , when a group of people with PTSD took propranolol at the time of consolidating a memory, for example, just after recounting a bad experience, they had fewer stress symptoms the next time the memory was activated.

Researchers in New York carried out tests on rats that showed it is possible to erase single memories from the brain, by delivering a drug known as U, while leaving the rest of the brain intact. In a mouse study published in Nature in , scientists used a drug known as an HDACi to erase epigenetic markers in the DNA that enable bad memories to live on.

This could help people, for example, with PTSD. She starts, she says, by telling someone that when they were young, they committed a crime, then adding layers of information until the person can no longer decipher reality from imagination. Shaw says she does this to highlight how some interrogation methods can be abused.

Healthy people could use them to erase an inconvenient event from the mind. Perpetrators of crimes could give memory-erasing drugs to people to make them forget events. After all, some bad memories serve a purpose. They can prevent people from making the same mistakes again, or guide their actions on similar occasions in the future.

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How to forget unwanted memories. Medically reviewed by Timothy J. Legg, Ph. How do memories form? Why are bad memories so vivid? Substituting memories Changing contexts Weakening memories that cause phobias A drug for forgetting? Implanting false memories Everyone has memories they would rather forget, and they may know the triggers that bring them bouncing back.

Share on Pinterest Some memories can lead to fears and phobias. Substituting memories. Share on Pinterest Unwanted memories can lead to anxiety. The new study tested that hypothesis by stimulating two sensory neurons connected to a single motor neuron of the marine snail Aplysia; one sensory neuron was stimulated to induce an associative memory and the other to induce a non-associative memory. They found that each memory could be erased -- without affecting the other -- by blocking one of the PKM molecules.

In addition, they found that specific synaptic memories may also be erased by blocking the function of distinct variants of other molecules that either help produce PKMs or protect them from breaking down. The researchers say that their results could be useful in understanding human memory because vertebrates have similar versions of the Aplysia PKM proteins that participate in the formation of long-term memories.

Future studies in preclinical models are needed to better understand how PKMs are produced and localized at the synapse before researchers can determine which drugs may weaken non-associative memories. Materials provided by Columbia University Medical Center. Note: Content may be edited for style and length.

Science News. Farah , Margaret H. Hastings , Wayne S. Sossin , Samuel Schacher. Current Biology , DOI: Reconsolidation can also be disrupted pharmacologically. The beta-adrenergic receptor antagonist propranolol can also block the consolidating action as represented by altered physiological responses associated with a fear response like heart rate and skin conductance by blockade of beta adrenergic receptors in humans.

In essence, one might surmise that by attenuating its emotional salience, the drug takes the sting out of the memory while leaving its cognitive trace intact. Even so, stress or other environmental factors can trigger a return of a heightened fear response read this article and this article , and not all subjects can be trained so that the conditioned stimulus no longer signals danger.

Theoretically, a more effective form of reconsolidation blockade would be one that not only weakened but also erased the emotional representation of the memory. Because reconsolidation is thought to require protein synthesis, a drug that interfered with protein synthesis could block reconsolidation. Infusion of a protein synthesis inhibitor, such as anisomycin perhaps in areas like the basolateral amygdala, during memory retrieval might prevent reconsolidation and effectively erase — not just weaken — any trace of the memory read this article and this article.

This would eliminate any possibility of reactivating a fear response because there would be no representation to be reactivated. This intervention has been used only in animal models.

Because it is still a hypothetical intervention for humans, any claims about memory erasure must be made tentatively. There are a number of challenges in using this intervention as therapy. One problem is that the longer a memory has been stored in the brain, the more difficult it is to destabilize and alter it with the exception of memory retrieval in which the memory must be reconsolidated. Retrieval does not always trigger reconsolidation and the labile state necessary for memory disruption.

Also, older and stronger memories may be less susceptible to disruption after retrieval due to increased synaptic strength from the effects of protein synthesis and long-term potentiation over extended periods read this article and this article. To be effective, reconsolidation blockade would have to occur not long after the memory had been encoded and consolidated. Another challenge is selectivity. While, in theory, implicit memories such as those involved in fear conditioning versus explicit memories employ different neural pathways, the question still remains whether it would be possible to erase a particular memory in the fear system while leaving other memories intact.

Not all memories of fearful events are maladaptive or pathological. Many are adaptive and critical for survival by enabling us to recognize and respond appropriately to external threats. Unless it could target a specific memory in a specific node of a specific neural circuit, it is not known whether a protein synthesis inhibitor aimed at erasing it would have unintended and unforeseeable expanding effects that might disable normal adaptive functions in the fear memory system or even beyond that system with off-target effects.

This might expose the subject to even greater harm than the psychological harm caused by the memory targeted for deletion. As with any other interventions in the brain, these risks have to be weighed against the potential benefit, which could be substantial in some psychiatric disorders.

Among their adverse psychological effects, fear memories can impair rational and moral agency by interfering with the deliberative ability to form and execute action plans and recognize and respond to reasons for or against certain actions. If we could and should erase the emotionally charged memories associated with psychopathologies, then why stop there? Why not also erase episodic memories that are not pathological but only unpleasant or disturbing? While not as harmful as fear memories associated with mental disorders, persistent unpleasant episodic memories may still cause harm.

Erasing these memories may be even more challenging neurophysiologically than erasing a traumatic emotional memory. Traumatic emotional memory and episodic memory are separated into implicit and explicit memory systems involving different mechanisms.