Is the rejuvenation or deletion of memory using brain-computer interface technology possible? 

 

We’ll go through how this is possible for rejuvenating memories first. Alzheimer’s is a disease that is the cause of millions of seniors forgetting their memories. Memory works with connections formed between neurons. The neurons become damaged, they lose connections to each other, and eventually die; that’s how you lose memories. Dementia results from changes that cause neurons and their connections to stop working. The parts in your brain that control memory are the amygdala, the hippocampus, the cerebellum, and the prefrontal cortex. EEG technology is found to take the biosignals from the postsynaptic potentials of pyramidal neurons in the neocortex and allocortex (two types of cerebral cortex in the hippocampus). The hippocampus is one of the brain areas affected by Alzheimer's (AD). In the early stages of AD, the hippocampus shows rapid loss of its tissue, which is associated with functional disconnection from other parts of the brain. AD causes the brain to shrink up and the brain cells die (the first being the memory cells). Let’s focus on the hippocampus, the part of the brain that connects AD and brain-computer interface technology. A machine could be developed to restore memories with this key component. A technology such as this was first demonstrated on rodents since we are alike in many ways in the brain. Scientists have developed, (a) a multi-input, multi-output nonlinear dynamical model to mimic signal processing properties of hippocampal circuit, and (b) a double-layer multi-resolution classification model to decode memory contents from hippocampal activities. These are the 2 basics for any hippocampal memory prosthesis. These results showed that electrical stimulation delivered to the hippocampus can restore and enhance short-term and long-term memory functions. Let’s get more into that. How could you decode these memory contents into a language that’s understandable? A person’s brain uses a pattern of wavelengths to store memories. fMRI scans trained decoding software to map individual speech and thought patterns, recognizing brain signals and translating into words or phrases. Non-invasive BCI can only go a long way when decoding languages, currently they can only identify small words or construct short sentences with simple phrases. There was a study conducted with a decoder mapping out brain images from individuals reading and they’d associate it with a word. This activated three parts of the brain, speech, association and prefrontal. The problem was that each region produced a different sentence, but they all discussed similar ideas. The decoder did convey the intended thought. This mere study is important. Theoretically, if the brain was able to bring back certain memories, we should be able to delete them as well. If doing so is possible, it wouldn’t be deleting all of the memory. Since the memory of a certain event isn’t only present in one area of the brain, but stored in different smaller parts. The brain has created special mechanisms for editing memories, and so memories are to be degraded. Researchers have tried to enhance this using certain drugs. The recopters they’ve targeted include, the glucocorticoid, glutamatergic, adrenergic, cannabinoid, serotonergic, and glycine receptors. Deep brain stimulation (DBS) of the hippocampus is proposed for enhancement of memory impaired by injury or disease. Patients under epilepsy treatment were implanted with depth electrodes capable of recording neurosignals. Many preclinical DBS models can be addressed in epilepsy patients undergoing inside the skull monitoring for seizure localization, since they already have electrodes implanted in brain areas of interest. Even though epilepsy is usually not a memory disorder targeted by DBS, the studies can nevertheless model other memory-impacting disorders, such as Traumatic Brain Injury (TBI). These results showed that hippocampal stimulation for memory facilitation was more helpful for subjects who had previously suffered a brain injury. This delayed-match-to-sample (DMS) memory task while hippocampal ensembles from CA1 and CA3 cell layers were recorded to estimate a multi-input, multi-output (MIMO) model of CA3-to-CA1 neural encoding and a memory decoding model (MDM) to decode memory information from CA3 and CA1 neuronal signals. These are more or less the techniques, and technology that would help us reach this point in the field of neuroscience. Let’s move onto the working steps for the rejuvenation of memories.

 

 

 

Working steps : Part I

The process of creating a brain computer interface for the rejuvenation of memories is unknown and hasn’t been looked into as much as we would need for medical reasons. Electroencephalography- based systems are the key to this project. Specifically, deep brain stimulation (DBS). These systems have been researched and experimented to help a number of neurological and neurodegenerative disorders. This neuromodulation technique has emerged as an accurate treatment for disorders such as epilepsy, Parkinson's disease, post-traumatic amnesia, and Alzheimer's disease, as well as neuropsychiatric disorders such as depression, obsessive-compulsive disorder, and schizophrenia. Now, deep brain stimulation is a closed-loop interface, and in the past, people have been prompted to try out open-brain interfaces. These itself are less likely to work due to the distance between the headgear and the brain cells for memory restoration. Closed-brain interface is more convenient due to the more difficult reading of the brain's circuits during cognitive processes. Yet, these are especially useful for neuromotor issues. A unique dataset with electrodes would be inserted into the hippocampus to test for a presence of a pattern that is the phase of the hippocampal theta oscillation which modulates gamma oscillations in the cortex. This represents a neuro mechanism that promotes the organization of interregional oscillatory activities, this has never been observed in humans. Next, there would be a focus on hippocampal gamma power as a `biomarker' and use a dataset in which open-loop DBS is applied to the posterior cingulate cortex (PCC). The encoding of episodic memory would evaluate the feasibility of hippocampal power by a control of stimulation. In the simulation framework, the demonstrated proposed BCI system achieves effective control of hippocampal gamma power. Lastly, the further developed PCC-applied binary-noise (BN) DBS paradigm targets the neuromodulation of both hippocampal theta and gamma oscillatory power. The utilization of a nonlinear autoregressive with an input neural network as the plant paired with a proportional derivative controller. The nonlinear device delivers a stimulation pattern to achieve desired oscillatory power level. This also shows the capacity of architecture in controlling both hippocampal theta and gamma power. Outlining further experimentation to test our BCI system and compare our findings to emerging closed-loop neuromodulation strategies. (This experiment was conducted by Dr. David Xiaoliang Wang, from the Southern Methodist University, credits go to him and his team) 

 

Working steps : Part 2

BCI devices in the brain would be able to “delete” memories interlinked with certain smells, memories from depression, or any psychiatric disorders. Just as we discussed in the working steps part 2, the most frequently used device is the DBS (Deep brain stimulation). Neural implants can restore or improve certain functions lost or impaired through traumatic brain injury, infection, or other insults to the brain. Instead of enabling the formation of new memories, could a device implanted in the brain erase memories that have been encoded, consolidated, and reconsolidated? DBS can modulate dysfunctional circuits mediating sensorimotor, cognitive, and emotional processing. Theoretically, this or a similar stimulating technique could selectively erase a pathological fear memory by inactivating neurons and synapses constituting the memory trace. This could disrupt memory stored as information in the brain. Erasing fear memories identified as the source of anxiety, panic, phobia, and post-traumatic stress disorder could be an effective therapy when they fail to respond to other treatments (Pitman, 2015). They can use fMRI to measure changes in neural activity and synaptic connectivity following different memory connections. Hypothetically, stimulation from a DBS could reduce activity in neurons constituting the emotionally charged memory trace conditioned responses to stimulate stimuli and open a subject to unlearn pathological behavior. In psychiatric disorders, the trace of a memory of a disturbing or traumatizing event is stuck in the brain beyond any short-term adaptive function. This ruins the memory network regulating fear and results in pathological thought and behavior. Anxiety, panic, phobia, and PTSD are disorders of memory content associated with the emotional part of the memory. The problem is not an inability to form memories, but the inability to extinguish them.

 

The source of these disorders is hyperactivity in the basolateral amygdala of the fear memory network. This occurs when a negative emotional memory of a fearful experience or a series of such experiences forms and solidifies in the brain through the processes of consolidation and REconsolidation. One theory of fear memory consolidation following a traumatic experience is that the memory embeds in the amygdala. The memory becomes more firmly embedded in this brain region from behavior in which the subject learns to link a stimulus with another stimulus. Memories must be updated constantly to remain stored in the brain. Updating memories consists in reconsolidating them after retrieval. One goal of memory research is to interfere with reconsolidation during or immediately after retrieval in order to weaken or erase a traumatic memory trace. Memories are labile and easy to alter at this time. 

An effective way of blocking them would be to eradicate the emotional representation of the memory. During retrieval, infusion of a protein synthesis inhibitor such as anisomycin in this brain region might disrupt reconsolidation and effectively erase the memory trace. This or a similar acting drug would also interfere with long-term potentiation (LTP) and the transcription factor cyclic-response element-binding protein (CREB) that regulate protein synthesis in the formation and retention of memories. If they were effective, these processes would rule out the possibility of repeating a heightened emotional reaction to stimuli associated with the memory trace because there would no longer be any trace in the brain. (Agren et al., 2012).

 

A major challenge to pharmacological erasure of memory is the selectivity of this. Many memories of fearful experiences are adaptive and critical.  Not all fear memories are pathological or maladaptive. Because of the distributed and non-discriminating effects of psychotropic drugs, a drug intended to erase the trace could have unintended expanding effects and impair normal functions of the fear memory system. A drug infused in the brain could alter both targeted and non-targeted nuclei in the system and alter normal emotional processing. This could also introduce a new psychopathology.

 

The focused action of deep brain electrical stimulation of the neurons within the memory trace might be able to overcome the problem of selectivity. They precisely target the neurons within the trace and electrical stimulation could reduce the risk of effects on adaptive fear memories and more on positive emotional memories. This could prevent expanding effects on neurons  unrelated to the problematic memory. Unlike thermoelectric and radiofrequency neural ablation, electrical stimulation could erase the trace without destroying brain tissue.

 

The selectivity problem is a problem about localization. The main question is whether a particular maladaptive fear memory would be localized enough for DBS to erase it while leaving adaptive fear memories intact. One hypothesis that could support the idea of selectively erasing a maladaptive fear memory is that functional imaging could reveal higher levels of activation in the nuclei associated with that memory when a subject was asked to recall the traumatic experience as the source of it (Pitman et al., 2002; Pitman, 2015). DBS could target these nuclei for inactivation and erasure.

 

Even if imaging showed localized metabolic overactivation in nuclei associated with the memory, there are questions about whether DBS could inactivate it. Although many studies have confirmed the neuromodulating effects of DBS, the mechanisms of action of the technique are not well understood. DBS increased glucose metabolism in the entorhinal cortex of a group of epilepsy patients and enhanced learning and spatial memory. (Lozano et al., 2016). The goal of using DBS to enhance certain types of memory in these studies is in contrast to the goal of using DBS to erase other types of memory. Enhancing memory would require activating metabolically underactive nuclei associated with LTP, CREB, and protein synthesis. Erasing memory would require inhibiting metabolically overactive nuclei associated with these same processes. The second mechanism would be similar, in some ways, to the effects of high-frequency DBS on metabolically overactive circuits in treatment-resistant depression (Mayberg et al., 2005). One significant difference between DBS for depression and DBS for memory erasure, is that the target in the second case would be more discrete. Whether DBS enhanced memory or erased it would depend on the frequency of the electrical current delivered to the targeted nuclei and its effect on the neurons constituting the memory trace.

 

Suppose that investigators could use electrical stimulation from a device implanted in the brain to erase not just pathological fear memories but also less emotionally charged memories of disturbing experiences. If the emotional representation of some of these memories was localized in discrete limbic nuclei, the critical neurons, and excitatory synapses could be inactivated and the memory trace erased by DBS, should it be?

As we continue to push the boundaries of brain-computer interface (BCI) technology, we find ourselves standing on the border of a new era in neuroscience. The ability to manipulate memories, whether through their restoration or deletion, promises to revolutionize healthcare and mental health treatment. Memory restoration could provide individuals suffering from Alzheimer’s, dementia, and other cognitive impairments with a chance to regain lost connections. The potential to erase traumatic memories opens up new avenues for treating disorders like PTSD, anxiety, and depression.

 

Technology itself is still evolving, and the consequences of manipulating memory on such a fundamental level are largely unknown. The precision required to selectively restore or delete memories without unintended effects on other aspects of cognition or personality is a significant challenge. We must consider whether such interventions could unintentionally alter a person’s character, decision-making, or moral compass. How do we figure out the line between healing and harm when dealing with the most intimate parts of the human experience?

 

Remembering choices and actions can haunt one for years and make someone indecisive when choosing between courses of action in the present and future. Yet memories of these mistakes and of more emotionally disturbing experiences are absolutely necessary for character development and growth. They promote this development by activating the moral emotions of remorse and regret. They also enable us to reflect on our motivational states in forming and executing action plans that promote moral sensitivity toward others. Disturbing memories can provide decision-making that are necessary for effective rational and moral agency. 

 

Research into manipulating the content of memory has been limited to animal models. Psychiatric researchers will have to address many theoretical and technical challenges in moving from animal to first-in-human studies. Functional neuroimaging will be critical in identifying changes in brain activity correlating with a weakened or erased memory trace at neuronal and synaptic levels. The most important question is whether the critical neurons can be altered at a localized, discrete level. The idea of erasing a particular pathological fear memory with DBS or similar implantable electrical stimulation devices is still speculative. 

 

While these technologies advance, we will need a collective, multidisciplinary approach to ensure that their application is both responsible and beneficial. Neuroscientists, ethicists, psychologists, and policymakers must work together to develop guidelines that balance the potential therapeutic benefits of BCI technology with the preservation of personal identity, autonomy, and dignity. We ask ourselves not only if we can manipulate memory, but whether we should, and under what circumstances.

Ultimately, the future of BCIs and memory manipulation presents a profound opportunity to enhance human life in ways we never thought possible. But as we navigate this uncharted territory, it is essential that we proceed with caution and a deep awareness of the profound impact that altering memory could have on an individual’s sense of self and on society as a whole. The road ahead is filled with both promise and peril, and the choices we make in the coming years will shape the very fabric of our humanity.

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First, I want to thank God for guiding me spirtually and giving me the motivation to finish my project. He helped me with everything, and all my thanks go to Him. Second, I want to thank my school; Mountain View Academy. They gave me the materials and workplace to finish my research, and for never giving up on me. Specifically, Mrs. Kale for always helping me and being an expentional teacher everyday. She never gives up on her students, and she continues to give me more chances with my science fair. I want to thank my parents as well for listening to me ramble on about science and for never giving up on my schoolwork. My last thanks go to my siblings and my close frends. My sister stayed up day and night proofreading my rough draft (s) and kept giving me advice. The same goes to my friends, who never looked down on me and helped me strive to the top.