by Emma Kornberg
art by Tanisha Reddy
We’ve all been there – while reviewing for a final exam in the winter, we look at material from September and think, I used to know this. The information was in your brain at some point, right? Where definitions could once be recalled at lightning speed, we find only hazy traces of vague familiarity. Where did these memories go? More broadly, if everyone forgets to some extent, is it perhaps possible there are implications of remembering too much?
Memory shapes our perception of the world, informing the decisions we make. This includes the relationships we choose to pursue, the places we visit, and the habits we engage in – all based on past experiences. Theoretically, memory is limitless. We have a seemingly never-ending ability to learn over time, through making mistakes and being exposed to new things. Why is it, then, that we forget?
It turns out that there are benefits to forgetting – it helps us prioritize relevant information without having to sort through a sea of random memories. If remembering everything was truly optimal for humans, everyone would probably have a photographic memory. Yet, the concept of a perfectly photographic memory is debated and rare [1].
There are neurobiological and control-related mechanisms specifically designed to help us forget, indicating that the selectiveness of memory could be evolutionarily advantageous. Moreover, people with disorders such as post-traumatic stress disorder (PTSD) and major depressive disorder (MDD) experience intrusive and uncontrollable memories in their daily lives that can make regular functioning incredibly difficult. This implies that the disruption of mechanisms underlying forgetting and memory actually could have serious implications.
What is memory and where is it stored?
Memory is described as a long-term change in behavior based on a past experience. “Long-term” means longer than the experience during which it was formed, thus influencing future decisions [2]. For example, if a person goes to a coffee shop and experiences poor-quality coffee, they probably will not go again because they remember it tasting bad. This past experience influences future behavior.
The neurological basis of these longer-term changes is thought to lie in engram neurons, which are groups of neurons involved in transforming information from sensory experiences into memories that we can draw upon [3]. These neurons are located across brain regions involved in memory processing, such as the hippocampus, amygdala, and prefrontal cortex [2]. The role of engram neurons can help us understand where memories are neurally stored, as their collective reactivation is how we recall memories [4].
Which memories are kept and which are forgotten?
Importantly, engram neurons are use-dependent. Walking home daily from work is a repeated and meaningful route, so we remember it better than the walk to the random restaurant we visited once a year ago. In fact, we reach a certain point where the route feels rather automatic, whereas directing to a new location requires more attention. The network of engram neurons strengthened with repeated firing, to the point where signaling is much faster, giving us that “auto-pilot” feeling of navigating home [5].
On the biological level, synaptic plasticity is the way neurons are able to alter their
connection strength with other neurons by changing their structure [6]. Long-term potentiation (LTP) is the strengthening of a synapse due to repeated use, making the signal faster, while long-term depression (LTD) refers to the weakening of unused synapses [7]. This system is adaptive—the repeated route home is an example of LTP, while the largely forgotten one-time restaurant visit is an example of LTD. Forgetting involves microglia, a type of support cell in the brain that prunes unused synapses that have gone through LTD [8].
Engram neurons are usually highly excitable, or very likely to fire action potentials, which enables them to support learning throughout development because they are engaging in synaptic plasticity [2]. The stages that engram neurons follow are categorized as the general memory processes of encoding: the acquisition of an experience into short-term memory; consolidation, the process of storing it into long-term memory; and retrieval, the recalling of the experience from long-term memory [2, 9].
Synaptic plasticity is crucial for memory regulation, which is why repeated action potentials are necessary [7, 10]. Plasticity involves making physical changes to synaptic structure, which makes synapses larger, or more numerous, in order to increase the surface area between two neurons and encourage an action potential. It can also include making membrane channels involved in transmitting action potentials more numerous, which also increases the likelihood of neural firing [10]. Both processes can induce LTP.
Adaptive Active Forgetting in the Memory Process
Forgetting can either be a passive or active process. The passive process is unintentional, where information becomes less available for us to access [11]. Passive forgetting includes the following: retroactive interference, a process in which new information affects already encoded memories, retrieval-induced forgetting, where recalling an item decreases the ability to recall related items, and passive decay over time, which is a form of LTD [12]. For instance, a person might unintentionally forget their last address from many years ago because they have a new one. When recalling the old one, they might include some numbers from the current one, which is retroactive interference—new information affecting older information.
On the other hand, active forgetting is deliberate and adaptive, pruning the brain of unnecessary information [11]. Interestingly, this is partly why sleep plays such a crucial role in memory—not only does it allow for organized consolidation, but also helps clear out irrelevant information during active forgetting [7]. Active forgetting can be adaptive during the consolidation stage of memory, where we solidify short-term memories into long-term memory, so we can prioritize relevant information based on rewards or threat avoidance [12]. This model suggests that a tag, or mental note, can be placed on relevant information that signals synapses to strengthen, or to trigger LTP. The tag can be defined either in the moment, during the encoding of the memory, or afterwards as new information is learned [12]. For example, let’s say we are sitting in a lecture passively listening and copying down sparse notes, when the professor announces that this material will be on an exam. This causes us to pay more active attention, take more thorough notes, and ask questions to enhance understanding. The addition of this new information, that this material will be tested, causes us to tag it as relevant and meaningful—we want to earn the reward of a good grade and avoid the threat of a bad one.
Biological Memory Limits
Intuitively, we know that remembering every single thing is not the most practical, as we would spend time parsing through layers of information to find the most relevant pieces. Going back to the example of a home address, imagine being asked for the current street and remembering every single street name we’ve ever seen or heard - it would take a long time to pick out the specific one we need. Forgetting that irrelevant information, all the other streets we’ve ever known, is beneficial to finding the most relevant piece. There seems to also be a biological need to limit memory formation, as we have memory suppressor and enhancer genes that play important roles in information acquisition, consolidation, and forgetting [13].
Acquisition suppressors have an especially crucial influence on limiting memory, as they stop information from initially entering short-term memory, also called working memory [13]. This type of memory is fleeting, having limits on both the duration and capacity of information; it depends on the rehearsal of the experience [14]. Imagine you are on the phone with someone dictating a phone number to you. After you hang up, you verbally repeat this number to yourself while you find a pencil and paper to write it down. During that verbal repetition, those numbers are being stored in your short-term memory.
Acquisition suppressors, then, work largely to inhibit that original memory formation. They can affect genes that control inhibitory neurotransmitters, such as GABA or acetylcholine, reducing a neuron’s ability to fire an action potential [15]. Altering the associated neurotransmitter receptors can alter the representation of a particular experience in the brain, limiting its ability to be preserved. Acquisition suppressors also work to set a limit on neuronal excitability, or its capacity to fire an action potential, using small non-coding RNAs called microRNAs. These microRNAs help regulate gene expression to limit the number of synaptic vesicles filled with neurotransmitters, crucial for triggering an action potential [15]. These all affect the strength of the synapses related to the memory circuit [13].
Information moves from short to long-term memory through synaptic plasticity strengthening and solidifying connections to make future firing faster [16]. This will crystallize it into long-term memory on an engram-level as well as on a more cerebrally-integrated level, moving across different brain regions, where it can be recalled from later on [17, 18]. Consolidation suppressors therefore work to stop irrelevant information from entering long-term memory.
Forgetting and Learning
Just as memory is important for learning, forgetting is important for behavioral flexibility, such as eliminating a pattern that is no longer useful, or learning a better way to do something. Forgetting the information underlying non-advantageous behavior could prove useful to many organisms. For example, when we adapt to a new environment or face change, it may be helpful to prioritize the new information and forget some of the old conditions to limit hindrances, essentially “updating” to the current situation.
Another possible advantage is promoting accurate association—having mental connections to everything around us would be overwhelming! Accurate association is socially useful as well, because the ability to recognize faces, remember names, and recall context is beneficial. This connects back to accurate association of meaningful information, as we are better able to distinguish between the connections we make [13].
Implications of Remembering “Too Much”
Certain memories are densely packed with emotion, like a familial death, beautiful wedding, or painful breakup. For the most part, we are able to control these types of memories so they don’t interfere with our daily focus. Sure, occasionally the scent of a late-grandma’s perfume can trigger emotional memories, but they are not incredibly frequent or intrusive in the long-term. An inability to control the unintentional remembering of stored memories can be associated with unhealthy rumination (excessive dwelling on negative feelings), and symptoms of various mental disorders, including anxiety and depressive disorders, obsessive-compulsive disorder (OCD), and post-traumatic stress disorder (PTSD) [19].
What we are doing when we control emotion-triggering memories is actually inhibiting mechanisms associated with the automatic nature of remembering [19]. Inhibition increases when the brain prunes information to prioritize what is important, as mentioned earlier, but may also be engaged more consciously to prevent disruptive or particularly evocative memories [20]. An example of conscious inhibition is ignoring distractions during a task that requires focus, such as a test; some neural activity in certain brain regions and pathways are suppressed as the attention is intentionally elsewhere. Since encoding did not occur in these situations, meaning the “distracting” information was never solidified as a memory, that information will likely not be remembered. This, there is an evident intentionality that comes with remembering and forgetting).
One study involving memory-retrieval suppression found that intrusions, or unwanted memories interfering with awareness despite intentional efforts to stop them, sharply decreased across repeated suppression attempts [20]. This finding is meaningful because it suggests that strengthening inhibitory control and increasing awareness plays a role in active forgetting, so as to prune useless or distracting information. PTSD is thought to be partly related to deficits in inhibitory control, manifesting after an individual is exposed to a traumatic event such as war, abuse, or death [21]. It is characterized by recurrent and uncontrollable trauma-related memories [22]. People with the most severe PTSD symptoms seem to have the least ability in suppressing memory retrieval [21]. It has also been found that decreased inhibitory control could indicate a predisposition to the development of PTSD; thus, a screening tool such as a self-perceived thought-control ability test could be helpful in highlighting the degree of risk [21].
How does this inhibitory control in people with PTSD compare to people without PTSD on the biological level? Retrieval suppression involves the prefrontal cortex, a region of the brain associated with decision-making and self-control, as well as the hippocampus, another region typically associated with memory [23].
In people with PTSD, there are often abnormalities in activity and structure in these areas as well as in their neural pathways [5]. Memory traces are the most vulnerable to being disrupted during reactivation, as they are easily altered and can be influenced by things such as newly-learned information [20]. Thus, memories are dynamic and can be changed by the strengthening or weakening of their traces in the brain through LTP and LTD, disrupting associations with negative feelings (such as fear), and actually reconsolidating, or restabilizing, new ones [24]. Research now suggests that it may be beneficial to combine this with inhibitory control, to strengthen the awareness an individual has surrounding their memories and practice suppressing memory retrieval [21].
Like PTSD, major depressive disorder (MDD) is also associated with deficits in inhibitory control, manifesting in difficulty managing negative information-processing and pruning no-longer-useful negative information [25]. MDD is often characterized by the tendency to intensely ruminate on and frequently access negative memories and thoughts, among other symptoms [26]. Research suggests that in depressed individuals, suppression-induced forgetting proves to be more challenging on account of regular rumination, perhaps making it more difficult to disrupt memory traces [27]. Furthermore, findings suggest that people with and without depression differ in their brain activity when trying to suppress unwanted memories [25]. However, more research is necessary to explore what these differences signify [25].
Inhibitory control can be challenging to apply as a simple treatment for mental health disorders because of how interconnected brain regions are, especially during memory formation [28]. Areas involved in memory-processing and consolidation form traces that can reactivate during recall and retrieval. For example, the amygdala is a structure associated with emotional salience, and the visual cortex is associated with visual processing, both of which play roles in memory encoding (as the experience includes sensory details) [29]. Applying this to inhibitory control, repeatedly engaging in retrieval suppression can disrupt the traces formed during the memory formation, reducing the sensory associations and making it less intrusive [19].
Appreciating Our Ability to Forget
Overall, it is clear that the inability to selectively prune information and memories in the brain can have severe implications on mental health. Our ability to control intense memories, such as those associated with fear or negative emotions, is crucial for maintaining cognitive functioning [30]. Unwanted memories that rampantly pop up during a person’s daily function are intrusive and distracting, affecting their quality of life. Biological mechanisms supporting the ability to actively and passively forget encourage prioritization and constant updating of old information, while discouraging rumination and the keeping of non-useful or non-essential information in order to move forward.
Our forgetting is actually quite adaptive, allowing us to place relevant information at the forefront of our minds to help make advantageous decisions and apply past learning. Through this process, we have the ability to move forward after facing difficult situations that can come as a part of life. Thus, while we may view forgetting as a human flaw, wishing to have perfectly photographic memories, it is important to appreciate it as ultimately useful, helping to focus our attention on things that matter to us.
REFERENCES:
1. Brady, T. F., Konkle, T., Alvarez, G. A., & Oliva, A. (2008). Visual long-term memory has a massive storage capacity for object details. Proceedings of the National Academy of Sciences of the United States of America, 105(38), 14325–14329. https://doi.org/10.1073/pnas.0803390105
2. Guskjolen, A., & Cembrowski, M. S. (2023). Engram neurons: Encoding, consolidation, retrieval, and forgetting of memory. Molecular Psychiatry, 1–13. https://doi.org/10.1038/s41380-023-02137-5
3. Tonegawa, S., Morrissey, M. D., & Kitamura, T. (2018). The role of engram cells in the systems consolidation of memory. Nature Reviews Neuroscience, 19(8), 485–498. https://doi.org/10.1038/s41583-018-0031-2
4. Josselyn, S. A., & Tonegawa, S. (2020). Memory engrams: Recalling the past and imagining the future. Science (New York, N.Y.), 367(6473), eaaw4325. https://doi.org/10.1126/science.aaw4325
5. Kennedy, M. B. (2016). Synaptic Signaling in Learning and Memory. Cold Spring Harbor Perspectives in Biology, 8(2), a016824. https://doi.org/10.1101/cshperspect.a016824
6. Ho, V. M., Lee, J.-A., & Martin, K. C. (2011). The Cell Biology of Synaptic Plasticity. Science, 334(6056), 623–628. https://doi.org/10.1126/science.1209236
7. Langille, J. J. (2019). Remembering to Forget: A Dual Role for Sleep Oscillations in Memory Consolidation and Forgetting. Frontiers in Cellular Neuroscience, 13. Retrieved from https://www.frontiersin.org/articles/10.3389/fncel.2019.00071
8. Zacher, A. C., Hohaus, K., Felmy, F., & Pätz-Warncke, C. (2023). Developmental profile of microglia distribution in nuclei of the superior olivary complex. Journal of Comparative Neurology, n/a(n/a). https://doi.org/10.1002/cne.25547
9. Winters, B. D., Saksida, L. M., & Bussey, T. J. (2008). Object recognition memory: Neurobiological mechanisms of encoding, consolidation and retrieval. Neuroscience & Biobehavioral Reviews, 32(5), 1055–1070. https://doi.org/10.1016/j.neubiorev.2008.04.004
10. Citri, A., & Malenka, R. C. (2008). Synaptic Plasticity: Multiple Forms, Functions, and Mechanisms. Neuropsychopharmacology, 33(1), 18–41. https://doi.org/10.1038/sj.npp.1301559
11. Davis, R. L., & Zhong, Y. (2017). The Biology of Forgetting—A Perspective. Neuron, 95(3), 490–503. https://doi.org/10.1016/j.neuron.2017.05.039
12. Cowan, E. T., Schapiro, A. C., Dunsmoor, J. E., & Murty, V. P. (2021). Memory consolidation as an adaptive process. Psychonomic Bulletin & Review, 28(6), 1796–1810. https://doi.org/10.3758/s13423-021-01978-x
13. Noyes, N. C., Phan, A., & Davis, R. L. (2021). Memory Suppressor Genes: Modulating Acquisition, Consolidation, and Forgetting. Neuron, 109(20), 3211–3227. https://doi.org/10.1016/j.neuron.2021.08.001
14. Cowan, N. (2008). What are the differences between long-term, short-term, and working memory? Progress in brain research, 169, 323–338. https://doi.org/10.1016/S0079-6123(07)00020-9
15. Teleanu, R. I., Niculescu, A.-G., Roza, E., Vladâcenco, O., Grumezescu, A. M., & Teleanu, D. M. (2022). Neurotransmitters—Key Factors in Neurological and Neurodegenerative Disorders of the Central Nervous System. International Journal of Molecular Sciences, 23(11), 5954. https://doi.org/10.3390/ijms23115954
16. Dubnau, J., Chiang, A.-S., & Tully, T. (2003). Neural substrates of memory: From synapse to system. Journal of Neurobiology, 54(1), 238–253. https://doi.org/10.1002/neu.10170
17. Born, J., & Wilhelm, I. (2012). System consolidation of memory during sleep. Psychological Research, 76(2), 192–203. https://doi.org/10.1007/s00426-011-0335-6
18. Hardt, O., & Nadel, L. (2018). Systems consolidation revisited, but not revised: The promise and limits of optogenetics in the study of memory. Neuroscience Letters, 680, 54–59. https://doi.org/10.1016/j.neulet.2017.11.062
19. Hu, X., Bergström, Z. M., Gagnepain, P., & Anderson, M. C. (2017). Suppressing Unwanted Memories Reduces Their Unintended Influences. Current Directions in Psychological Science, 26(2), 197–206. https://doi.org/10.1177/0963721417689881
20. Levy, B. J., & Anderson, M. C. (2012). Purging of Memories from Conscious Awareness Tracked in the Human Brain. The Journal of Neuroscience, 32(47), 16785–16794. https://doi.org/10.1523/JNEUROSCI.2640-12.2012
21. Catarino, A., Küpper, C. S., Werner-Seidler, A., Dalgleish, T., & Anderson, M. C. (2015). Failing to Forget. Psychological Science, 26(5), 604–616. https://doi.org/10.1177/0956797615569889
22. Clark, I. A., & Mackay, C. E. (2015). Mental Imagery and Post-Traumatic Stress Disorder: A Neuroimaging and Experimental Psychopathology Approach to Intrusive Memories of Trauma. Frontiers in Psychiatry, 6. https://doi.org/10.3389/fpsyt.2015.00104
23. Pica, G., Chernikova, M., Pierro, A., Giannini, A. M., & Kruglanski, A. W. (2018). Retrieval-Induced Forgetting as Motivated Cognition. Frontiers in Psychology, 9. Retrieved from https://www.frontiersin.org/articles/10.3389/fpsyg.2018.02030
24. Kim, G. S., Smith, A. K., Nievergelt, C. M., & Uddin, M. (2018). Neuroepigenetics of Post-traumatic Stress Disorder. Progress in molecular biology and translational science, 158, 227–253. https://doi.org/10.1016/bs.pmbts.2018.04.001
25. Sacchet, M. D., Levy, B. J., Hamilton, J. P., Maksimovskiy, A., Hertel, P. T., Joormann, J., … Gotlib, I. H. (2017). Cognitive and neural consequences of memory suppression in major depressive disorder. Cognitive, Affective & Behavioral Neuroscience, 17(1), 77–93. https://doi.org/10.3758/s13415-016-0464-x
26. Marx, W., Penninx, B. W. J. H., Solmi, M., Furukawa, T. A., Firth, J., Carvalho, A. F., & Berk, M. (2023). Major depressive disorder. Nature Reviews Disease Primers, 9(1), 1–21. https://doi.org/10.1038/s41572-023-00454-1
27. Dillon, D. G., & Pizzagalli, D. A. (2018). Mechanisms of Memory Disruption in Depression. Trends in Neurosciences, 41(3), 137–149. https://doi.org/10.1016/j.tins.2017.12.006
28. Bazinet, V., Hansen, J. Y., & Misic, B. (2023). Towards a biologically annotated brain connectome. Nature Reviews Neuroscience, 1–14. https://doi.org/10.1038/s41583-023-00752-3
29. Zheng, J., Anderson, K. L., Leal, S. L., Shestyuk, A., Gulsen, G., Mnatsakanyan, L., … Lin, J. J. (2017). Amygdala-hippocampal dynamics during salient information processing. Nature Communications, 8(1), 14413. https://doi.org/10.1038/ncomms14413
30. Engen, H. G., & Anderson, M. C. (2018). Memory Control: A Fundamental Mechanism of Emotion Regulation. Trends in Cognitive Sciences, 22(11), 982–995. https://doi.org/10.1016/j.tics.2018.07.015
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