This question is inspired by a question I answered on Health.

Can we erase problematic memories to aid recovery from depression?

A depressed person asked how to erase specific unpleasant memories in order to manage his depression. My answer was basically "that's impossible, here is how you deal with these memories instead". And then somebody asked in the comments why it is impossible.

I thought of tackling this question and realized I can't do it well. My best attempt was something like, "First, you have to find out which millions of neurons (out of the billions the person has) light up together to represent 'a memory', and we don't have a method for brain imaging with that resolution. Second, you have to stop them from activating in exactly that combination, while preserving their ability to activate in any other combination, and we have no idea how to achieve that". But this level of explanation does not satisfy me. It is very vague, and I'm not even certain it's correct.

To our best knowledge, what would we have to do if we wanted to erase a specific memory of an event happening to a person? And how far is our technology from achieving each of the steps needed?


3 Answers 3


The notion of "selective memory loss" as erasing problematic memories presumes the existence of engrams, which is a theoretical localized, biological basis for memory. Despite exhaustive searching, we have not found any evidence of engrams in any animal with a nervous system, however. To the best of our knowledge, it's therefore impossible to erase memories, because there is nothing to erase―we have more or less concluded that engrams do not exist. Bruce (2001) aptly summarized Karl Lashley's seminal findings on the matter:

In his well-known article “In Search of the Engram” published in 1950, Karl Spencer Lashley summarized his 33 years of research and theory on memory and the brain. He concluded that (1) memories are not localized but are instead distributed within functional areas of the cortex and (2) memory traces are not isolated cortical connections between inputs and outputs. Though not the first time he had expressed such convictions, their reiteration in this article was backed by Lashley's estimable reputation and expressive power and they have taken firm root in the collective knowledge of today's memory and neuropsychological research community.

We cannot have "selective memory loss", at least not in the sense of erasing individual memories, because there is no such thing as "a memory" in any tangible sense. In modern cognitive science, such as Baddeley's multi-modal model, memory is not so much considered a neural warehouse of remembrances as it is a distributed and generative process. It's not a question of technology.


  • Bruce, D. (2001). Fifty years since Lashley's In search of the Engram: refutations and conjectures. Journal of the History of the Neurosciences, 10(3), 308-318.

A phenomenon called "memory reconsolidation" has received considerable attention over the last 15 years. This is about activation (retrieval) causing memories to temporarily enter a labile state in which they can be manipulated, even erased. Most of the research has been with animals, especially rodents, but there are a number of studies on humans and there has been great interest in the possibility of developing therapies for anxiety-related disorders like PTSD and for self-destructive behaviors like drug addiction.

Memories are believed to be encoded by the strengthening of synapses between the members of a population of neurons. According to reconsolidation theory, when a memory is recalled, the corresponding synapses enter a labile state in which they can be manipulated by different kinds of intervention, including certain drugs and also exposure to new information that may update or contradict the original memory.

To the extent that this line of research leads to practical therapies, it is interesting to note that the experimenter/therapist doesn't need to know which neurons are being manipulated.

Here are a few entry points into the reconsolidation literature:

A good overview of the field: Hardt, O., Einarsson, E. Ö., & Nader, K. (2010). A bridge over troubled water: reconsolidation as a link between cognitive and neuroscientific memory research traditions. Annual review of psychology, 61, 141–167.

In Humans: Schiller, D., & Phelps, E. A. (2011). Does Reconsolidation Occur in Humans? Frontiers in Behavioral Neuroscience, 5. doi:10.3389/fnbeh.2011.00024

The study that ignited the recent wave of interest in reconsolidation: Nader, K., Schafe, G. E., & Le Doux, J. E. (2000). Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval. Nature, 406(6797), 722–726. http://doi.org/10.1038/35021052

  • $\begingroup$ Thanks for this answer, Peter. To further clarify the extent of reconsolidation research in non-human animals, do you know the reference for the anisomycin and memory reconsolidation in rats studies off the top of your head? Although not human, I think it would help OP to see "how far we are from achieving" their goal. $\endgroup$ Commented May 19, 2015 at 23:48
  • 2
    $\begingroup$ I added the reference to my answer above. Anisomycin, a protein synthesis inhibitor, is too toxic to use in human studies, but there has been some interesting work with the beta blocker propranolol, see for example Schiller, D., Monfils, M.-H., Raio, C. M., Johnson, D. C., LeDoux, J. E., & Phelps, E. A. (2010). Preventing the return of fear in humans using reconsolidation update mechanisms. Nature, 463(7277), 49–U51. doi.org/10.1038/nature08637 $\endgroup$ Commented May 20, 2015 at 0:10

Chemical Methods

There is a little bit of research going into selective erasure of traumatic memories (targeted at people with severe anxiety disorders such as PTSD) by targeting synaptic plasticity. This has a long timeline on human use but has interesting potential.


Synapse-specific long-term plasticity underlying memory involves the targeting of plasticity-related proteins (PRPs) to activated synapses. If distinct tags and PRPs are used for different forms of plasticity, one could selectively remove distinct forms of memory. Using a stimulation paradigm in which associative long-term facilitation (LTF) occurs at one input and non-associative LTF at another input to the same postsynaptic neuron in an Aplysia sensorimotor preparation, we found that each form of LTF is reversed by inhibiting distinct isoforms of protein kinase M (PKM), putative PRPs, in the postsynaptic neuron. [...] Thus, the activity of distinct PRPs and tags in a postsynaptic neuron contribute to the maintenance of different forms of synaptic plasticity at separate inputs, allowing for selective reversal of synaptic plasticity and providing a cellular basis for developing therapeutic strategies for selectively reversing maladaptive memories.


In the rat cortex, long-term associative memories vanished rapidly after local application of an inhibitor of the protein kinase C isoform, protein kinase M zeta (PKMζ). The effect was observed for at least several weeks after encoding and may be irreversible. In the neocortex, which is assumed to be the repository of multiple types of long-term memory, persistence of memory is thus dependent on ongoing activity of a protein kinase long after that memory is considered to have consolidated into a long-term stable form.

There are also some other chemicals that, when interrupted, hinder memory consolidation and reconsolidation.


We found that oral administration of the β-adrenergic receptor antagonist propranolol before memory reactivation in humans erased the behavioral expression of the fear memory 24 h later and prevented the return of fear.


Memories formed through association with methamphetamine (METH), but not associations with foot shock or food reward, were disrupted by a highly-specific actin cycling inhibitor when infused into the amygdala during the post-consolidation maintenance phase. This selective effect of depolymerization on METH-associated memory was immediate, persistent and did not depend upon retrieval or strength of the association. Inhibition of non-muscle myosin II also resulted in a disruption of METH-associated memory.


By employing an inducible and reversible chemical-genetic technique, we find that transient alphaCaMKII overexpression at the time of recall impairs the retrieval of both newly formed one-hour object recognition memory and fear memories, as well as 1-month-old fear memories

https://doi.org/10.1111/JABR.12031 (meta-analysis that "suggests that disruption of glutamate signaling under reconsolidation parameters is sufficient to erase drug-related memories")

Electroconvulsive therapy has also been used with some success

https://pubmed.ncbi.nlm.nih.gov/25093782/ (removes memories of traumatic car crash, n=1)


Despite accumulating evidence for a reconsolidation process in animals, support in humans, especially for episodic memory, is limited. Using a within-subjects manipulation, we found that a single application of electroconvulsive therapy following memory reactivation in patients with unipolar depression disrupted reactivated, but not non-reactivated, memories for an emotional episode in a time-dependent manner. Our results provide evidence for reconsolidation of emotional episodic memories in humans.

https://www.science.org/doi/10.1126/science.160.3827.554 (the first study that showed some potential for electroconvulsion -> memory erasure, in rats)


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3677482/ (memories reconsolidation can be interrupted by distraction and/or replacing memories with incorrect memories)


Thus, as previously demonstrated in rodents, fear memory suppression resulting from behavioral disruption of reconsolidation is amygdala-dependent also in humans, which supports an evolutionarily conserved memory-update mechanism.

This is not a conclusive list of memory erasure experiments, but it should provide an overview of the some of the methods that are being investigated

Some of these papers have been mentioned above, but I include them here for completeness.


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