---
title: "Memory erasure"
chunk: 2/3
source: "https://en.wikipedia.org/wiki/Memory_erasure"
category: "reference"
tags: "science, encyclopedia"
date_saved: "2026-05-05T04:23:40.242517+00:00"
instance: "kb-cron"
---

=== Disruption of molecular mechanisms ===
There is a growing amount of information that has shown that memory depends largely on the brain's synaptic plasticity, with a large part of this being dependent on its ability to maintain long-term potentiation (LTP). Studies on LTP have also started to indicate that there are several molecular mechanisms that may be at the basis of memory storage. 
A more recent approach to erasing memories and the associations the brain makes with objects is disrupting specific molecular mechanisms in the brain that are actively keeping memories active.
Recovering methamphetamine (meth) addicts have reported that the sight of certain objects such as a lighter, gum or drug paraphernalia can cause massive cravings that can sometimes lead to a break in their mental strength and cause them to relapse. This indicates that long-term memories can be called upon by various different associations that were made with the memory without the conscious effort of the person. With an increasing belief that memories are largely supported by functional and structural plasticity deriving from F-actin polymerization in postsynaptic dendritic spines at excitatory synapses. Recent research has been done to target this F-actin polymerization by using direct actin depolymerization or a myosin II inhibitor to disrupt the polymerized F-actin associated with METH memory associations. The study indicated types of associations can be disrupted days to weeks after consolidation. Although the depolymerization techniques had no effect on food reward based associations or shock based associations the results demonstrate the idea that meth associated memories' actin cytoskeleton is constantly changing making it uniquely sensitive to depolymerization during the maintenance phase. This is some of the first evidence showing that memories made with different associations are actively maintained using different molecular substrates. These results also show that the actin cytoskeleton may be a promising target for selective disruption of unwanted long-term memories.

=== Selective memory suppression ===
Selective memory suppression is the idea that someone can consciously block an unwanted memory. Several different therapeutic techniques or training have been attempted to test this idea with varied success. Many of these techniques focus on blocking the retrieval of a memory using suppression techniques to slowly teach the brain to suppress the memory. Although some of these techniques have been useful for some people it has not been shown to be a clear cut solution to forgetting memories.  Because these memories are not truly erased but merely suppressed the question of how permanent the solution is and what actually happens to the memories can be troubling for some.
Selective memory suppression is also something that can occur without a person being consciously aware of suppressing the creation and retrieval of unwanted memories. When this occurs without the person knowing it is usually referred to as memory inhibition; the memory itself is called a repressed memory.

==== Interruption of memory reconsolidation ====

One of the ways scientists have attempted to erase these memories through suppression is by interrupting the reconsolidation of a memory. Reconsolidation of a memory is when a person recalls a memory, usually a fearful one, it becomes susceptible to alteration, and then gets stored again. This has led many researchers to believe that this time period is the best time for memories to be altered or erased. Studies have shown that through behavioral training results showed that they were able to erase memories by tampering with memories during the reconsolidation phase.

=== Destruction of neurons ===
With evidence showing that different memories excite different neurons or system of neurons in the brain the technique of destroying select neurons in the brain to erase specific memories is also being researched. Studies have started to investigate the possibility of using distinct toxins along with biotechnology that allows the researchers to see which areas of the brain are being used during the reward learning process of making a memory to destroy target neurons. In a paper published in 2009, authors showed that neurons in the lateral amygdala that had a higher level of cyclic adenosine monophosphate response element-binding protein (CREB) were activated primarily over other neurons by fear memory expression. This indicated to them that these neurons were directly involved in the making of the memory trace for that fear memory. They then proceeded to train mice using auditory fear training to produce a fear memory. They proceeded to check which of the neurons were overexpressing CREB and then, using an inducible diphtheria-toxin strategy, they destroyed those neurons, resulting in persistent and strong memory erasure of the fear memory.
Researchers have also found that the levels of the neurotransmitter, acetylcholine, can also effect which memories are most prominent in our minds.
Due to the lack of understanding of the brain this technique of destroying neurons may have a much larger effect on the patient than just the removal of the intended memories. Due to this complex nature of the brain treatment that would stun the neurons instead of destroying them could be another approach that could be taken.

=== Optogenetics ===
A way of selectively erasing memories may be possible through optogenetics, a type of gene therapy that targets specific neurons. In 2017, researchers at Stanford demonstrated a technique for observing hundreds of neurons firing in the brain of a live mouse, in real time, and have linked that activity to long-term information storage. By using a virus to trigger production of a light-sensitive protein in neurons linked to a fear, they could erase the memory by weakening the pathways using light.