Deliberately Forgetting Memories – Easy for Someby Carla Clark, PhD | April 20, 2014
We have all had memories that, at some point in time, we wished we could forget. Many newly published studies highlight the neurological and molecular mechanisms behind choosing to forget and suggest why disrupting this process may lead to unhealthy aging and serious mental disorders. It seems, that to some degree, one does find eternal sunshine in a spotless mind.
Our autobiographical memories are integral to both making sense of the past and making predictions for the future, as well as providing an understanding of who we are as individuals. Having a lack of control over autobiographical memory retrieval and which memories enter our conscious awareness is debilitating for those suffering from clinical conditions such as depression, phobia or post-traumatic stress disorder. Conversely, research suggests that possessing the ability to deliberately choose which autobiographical memories we retain, may be pivotal to our mental health, well-being and sense of self.
The existence of memory repression, a Freudian concept, where unwanted memories are forgotten by pushing them into the unconscious, has remained controversial for more than a century. In recent years, however, research has centred upon a “think/no-think” paradigm, providing proof-of-principle that it is possible to train people to systematically forget previously learned material. The idea is simple; participants memorize word pairs and are then shown the first word and asked to either recall the second word or consciously try to avoid thinking about it.
fMRI studies identified two separate mechanisms for the forgetting of unwanted memories, suppression and substitution, involving two separate neural pathways. Brain activity was observed while participants who had previously learned associations between pairs of words tried to forget the memories by either recalling alternative memories (substitution) or blocking them out (suppression). For memory suppression, the hippocampus, which is the key player in remembering past events, is inhibited by the dorsolateral prefrontal cortex, thus inhibiting memory retrieval. Substituting memories, on the other hand, activates specific areas of the prefrontal cortex which are involved in consciously willing our attention to focus on specific memories in the presence of distracting unwanted ones.
So, we can actively forget using at least two different neural mechanisms of mnemonic control, but how relevant is forgetting random words to real life situations? Well the buck doesn’t stop there. The think/no-think task was extended into the realms of autobiographical memory, revealing that training people to not think about a memory results in a loss of specific details about that memory. When asked to recall a memory they had previously tried to intentionally forget, the main gist of the story remained. However, about 11 per cent less detail was recalled on average. Interestingly, for the never-been-depressed student subjects, the intentional memory loss effect was stronger for negative autobiographical memories, with positive memories being retained more strongly, despite trying to forget them.
However, the most recent addition to the think/no-think research looked at individual differences in forgetting, over both short and long time periods. Researchers were able to predict which students were most likely to be successful “forgetters” 12 to 13 months after the think/no-think training, based on how well they were able to forget immediately after training. This indicates that obtaining ‘the eternal sunshine of a spotless mind’ by forgetting negative memories at will may be easier for some than others, giving them the ability to forget more successfully for longer. This may indicate that these individuals are less likely to suffer rebound effects from traumatic experiences.
Hot off the press is new evidence that shows how memory loss is actively regulated at the molecular level. The study drew attention to a protein in a model organism for neural development, the nematode Caenorhabditis elegans, called musashi (MSI-1). In MSI-1 mutants, where expression of the protein is prevented, memory loss was inhibited. This memory loss inhibition brought about by MSI-1’s absence, caused an increase in the levels of a protein complex called Arp2/3, which is involved in the growth of dendritic spines and in establishing strong synapses.
The researchers presented a model for the active forgetting of memories, where MSI-1 regulates neuroplasticity and de-stabilizes neural connections associated with the memory by inhibiting levels of Arp2/3. This subsequently reduces the size, complexity and activity of the associated synapses. The existence of human MSI-1 homologues, indicates that actively choosing to forget a memory may also involve musashi regulated de-stabilization of neural connections associated with that memory in humans.
It’s likely that future research will attempt to characterize the precise mechanisms involved in humans and may result in the development of drugs for the prevention of abnormal memory loss in diseases such as Alzheimer’s and Parkinson’s. On the flip side, such research may also prove useful in the treatment of depression and post-traumatic stress disorder, where there is therapeutic value in improving our ability to forget. Nonetheless, we are someway off the development of Eternal Sunshine-esque technologies for complete and specific erasure of unwanted memories.
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Hadziselimovic N, Vukojevic V, Peter F, Milnik A, Fastenrath M, Fenyves BG, Hieber P, Demougin P, Vogler C, de Quervain DJ, Papassotiropoulos A, & Stetak A (2014). Forgetting Is Regulated via Musashi-Mediated Translational Control of the Arp2/3 Complex. Cell, 156 (6), 1153-66 PMID: 24630719
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