Can we decode memories?

Premise: I don't have a strong background in neuroscience or human biology, so I would ask you to answer like you would at a 5 years old child. I have done a couple of research on the web, as well as here on StackExchange, but the answers that I have found are either pretty old or difficult to understand for me.

I have read that memories are not stored in a unique place in our brain.

  • If you knew the region where the particular memory you are looking for is, would you be able to decode it?

Example: Let's say that someone said to you something you perfectly remember even after a few years. Since you remember the exact words, I suppose that those words are stored in our brain somehow. Is it possible to retrieve what those words were?

To summarize my question, what do we know (and don't know) about how we encode memories?

Thank you all.

Given recent advances in AI related neuroscience, I can easily imagine a future where it is possible to decode thoughts and impressions. In fact, we are already nearly there.

It seems like the limitation is not the decoding of memories, but their detection or measurement: While you are seeing an image and the brain actively is working on it its perception, causing your neurons to fire in certain patterns that can physically be measured with fMRI, there is the possibility to decode some information out of these signals. Same if you remember a scene in your memory.

However, I don't see any theoretical potential to read memories out of inactive/dead brains. So I hardly can imagine that any machines can read anything that's not currently happening in the brain. Maybe your brain can be stimulated somehow and its response can be read, but in the end you need physical measurements.

Scientists decode brain waves to eavesdrop on what we hear

Neuroscientists may one day be able to hear the imagined speech of a patient unable to speak due to stroke or paralysis, according to University of California, Berkeley, researchers.

These scientists have succeeded in decoding electrical activity in the brain's temporal lobe -- the seat of the auditory system -- as a person listens to normal conversation. Based on this correlation between sound and brain activity, they then were able to predict the words the person had heard solely from the temporal lobe activity.

"This research is based on sounds a person actually hears, but to use it for reconstructing imagined conversations, these principles would have to apply to someone's internal verbalizations," cautioned first author Brian N. Pasley, a post-doctoral researcher in the center. "There is some evidence that hearing the sound and imagining the sound activate similar areas of the brain. If you can understand the relationship well enough between the brain recordings and sound, you could either synthesize the actual sound a person is thinking, or just write out the words with a type of interface device."

"This is huge for patients who have damage to their speech mechanisms because of a stroke or Lou Gehrig's disease and can't speak," said co-author Robert Knight, a UC Berkeley professor of psychology and neuroscience. "If you could eventually reconstruct imagined conversations from brain activity, thousands of people could benefit."

In addition to the potential for expanding the communication ability of the severely disabled, he noted, the research also "is telling us a lot about how the brain in normal people represents and processes speech sounds."

Pasley and his colleagues at UC Berkeley, UC San Francisco, University of Maryland and The Johns Hopkins University report their findings Jan. 31 in the open-access journal PLoS Biology.

Help from epilepsy patients

They enlisted the help of people undergoing brain surgery to determine the location of intractable seizures so that the area can be removed in a second surgery. Neurosurgeons typically cut a hole in the skull and safely place electrodes on the brain surface or cortex -- in this case, up to 256 electrodes covering the temporal lobe -- to record activity over a period of a week to pinpoint the seizures. For this study, 15 neurosurgical patients volunteered to participate.

Pasley visited each person in the hospital to record the brain activity detected by the electrodes as they heard 5-10 minutes of conversation. Pasley used this data to reconstruct and play back the sounds the patients heard. He was able to do this because there is evidence that the brain breaks down sound into its component acoustic frequencies -- for example, between a low of about 1 Hertz (cycles per second) to a high of about 8,000 Hertz -that are important for speech sounds.

Pasley tested two different computational models to match spoken sounds to the pattern of activity in the electrodes. The patients then heard a single word, and Pasley used the models to predict the word based on electrode recordings.

"We are looking at which cortical sites are increasing activity at particular acoustic frequencies, and from that, we map back to the sound," Pasley said. He compared the technique to a pianist who knows the sounds of the keys so well that she can look at the keys another pianist is playing in a sound-proof room and "hear" the music, much as Ludwig van Beethoven was able to "hear" his compositions despite being deaf.

The better of the two methods was able to reproduce a sound close enough to the original word for Pasley and his fellow researchers to correctly guess the word.

"We think we would be more accurate with an hour of listening and recording and then repeating the word many times," Pasley said. But because any realistic device would need to accurately identify words heard the first time, he decided to test the models using only a single trial.

"This research is a major step toward understanding what features of speech are represented in the human brain" Knight said. "Brian's analysis can reproduce the sound the patient heard, and you can actually recognize the word, although not at a perfect level."

Knight predicts that this success can be extended to imagined, internal verbalizations, because scientific studies have shown that when people are asked to imagine speaking a word, similar brain regions are activated as when the person actually utters the word.

"With neuroprosthetics, people have shown that it's possible to control movement with brain activity," Knight said. "But that work, while not easy, is relatively simple compared to reconstructing language. This experiment takes that earlier work to a whole new level."

Based on earlier work with ferrets

The current research builds on work by other researchers about how animals encode sounds in the brain's auditory cortex. In fact, some researchers, including the study's coauthors at the University of Maryland, have been able to guess the words ferrets were read by scientists based on recordings from the brain, even though the ferrets were unable to understand the words.

The ultimate goal of the UC Berkeley study was to explore how the human brain encodes speech and determine which aspects of speech are most important for understanding.

"At some point, the brain has to extract away all that auditory information and just map it onto a word, since we can understand speech and words regardless of how they sound," Pasley said. "The big question is, What is the most meaningful unit of speech? A syllable, a phone, a phoneme? We can test these hypotheses using the data we get from these recordings."

Coauthors of the study are electrical engineers Stephen V. David, Nima Mesgarani and Shihab A. Shamma of the University of Maryland Adeen Flinker of UC Berkeley's Helen Wills Neuroscience Institute and neurologist Nathan E. Crone of The Johns Hopkins University in Baltimore, Md. The work was done principally in the labs of Robert Knight at UC Berkeley and Edward Chang, a neurosurgeon at UCSF.

Chang and Knight are members of the Center for Neural Engineering and Prostheses, a joint UC Berkeley/UCSF group focused on using brain activity to develop neural prostheses for motor and speech disorders in disabling neurological disorders.

The work is supported by the National Institute of Neurological Disorders and Stroke of the National Institutes of Health and the Humboldt Foundation.


Since time immemorial, humans have tried to understand what memory is, how it works and why it goes wrong. It is an important part of what makes us truly human, and yet it is one of the most elusive and misunderstood of human attributes.

The popular image of memory is as a kind of tiny filing cabinet full of individual memory folders in which information is stored away, or perhaps as a neural super-computer of huge capacity and speed. However, in the light of modern biological and psychological knowledge, these metaphors may not be entirely useful and, today, experts believe that memory is in fact far more complex and subtle than that

It seems that our memory is located not in one particular place in the brain, but is instead a brain-wide process in which several different areas of the brain act in conjunction with one another (sometimes referred to as distributed processing). For example, the simple act of riding a bike is actively and seamlessly reconstructed by the brain from many different areas: the memory of how to operate the bike comes from one area, the memory of how to get from here to the end of the block comes from another, the memory of biking safety rules from another, and that nervous feeling when a car veers dangerously close comes from still another. Each element of a memory (sights, sounds, words, emotions) is encoded in the same part of the brain that originally created that fragment (visual cortex, motor cortex, language area, etc), and recall of a memory effectively reactivates the neural patterns generated during the original encoding. Thus, a better image might be that of a complex web, in which the threads symbolize the various elements of a memory, that join at nodes or intersection points to form a whole rounded memory of a person, object or event. This kind of distributed memory ensures that even if part of the brain is damaged, some parts of an experience may still remain. Neurologists are only beginning to understand how the parts are reassembled into a coherent whole.

The human brain, one of the most complex living structures in the universe, is the seat of memory

Neither is memory a single unitary process but there are different types of memory. Our short term and long-term memories are encoded and stored in different ways and in different parts of the brain, for reasons that we are only beginning to guess at. Years of case studies of patients suffering from accidents and brain-related diseases and other disorders (especially in elderly persons) have begun to indicate some of the complexities of the memory processes, and great strides have been made in neuroscience and cognitive psychology, but many of the exact mechanisms involved remain elusive.

This website, written by a layman for the layman, attempts to piece together some of what we DO know about the enigma that is…The Human Memory.Hypertension affects the cardiovascular system as well as the blood flow to the brain. This can cause many symptoms including memory loss.


This project describes how to utilize the memory formation mechanism discovered in recent years together with optogenetics, a technology used to manipulate human brain cells, to cure Post-traumatic Stress Disorder (PTSD).

It has been discovered that memory is stored in brain cells called neurons that physically reside together, rather than scattered throughout the brain. Such groups of brain cells are called engrams, referring to where memory is stored. As a result, it is possible to target an engram. We can manipulate them in such a way that people can forget specific memories either temporarily or permanently. Since only specific brain cells related to specific memories are targeted, all the other memories are intact. However, that isn&rsquot the best part. We can plant good memories into the human brain as well!

The above are achieved via optogenetics, a technology using light to control neurons, the brain cells responsible for processing and transmitting information. The process starts with identification of the neurons associated with a particular engram that is responsible for a specific piece of memory. Then, light sensitive opsins are inserted into the engram, turning the neurons in that area light sensitive. After that, fiber optics or micro LEDs are implanted to target the light sensitive neurons. The light is controlled by a microchip to turn on or off those neurons to manipulate memory.

For forgetting a specific memory, the light is activated to control the neurons that release certain chemicals, such as alpha-CaM kinase II, that erase memories. Alternatively, the light can also be used to deactivate neurons responsible for memory storage, preventing the memory from being recalled.

For implanting good memories, the process is more complicated. The subject is prepared with memories of good feelings, such as a delicious dinner being served. Later, the subject is put in another environment, such as the dirty small room where his poor family lives. The light is then turned on to recall the good feeling in this environment, effectively creating the false memory that the good feeling took place in this environment. As a result, the subject likes this environment.

After the traumatic memory is removed, and the good memory is implanted, the PTSD patients are able to escape from the previous event, and restore their life.

Fear triggers many split-second reactions in the body to prepare to defend against the incoming danger or to avoid it. This &ldquofight-or-flight&rdquo response is a normal and healthy reaction meant to protect a person from harm. But in post-traumatic stress disorder (PTSD), this reaction has altered or damaged. People who have PTSD experience fear and stress even after the danger has passed for a very long time. It interferes with everyday life, because these people cannot stop the recollection of the horrifying memories that happened.

Most people who see traumatic events don&rsquot develop PTSD, but nonetheless, PTSD develops after an event that involved harm or the threat of harm. The person who develops PTSD could be a victim or witness of the terrifying event, but the person will experience the event over and over. Currently, the main treatments are to visit a psychologist or counselor to help the brain &ldquoget over&rdquo the event, or to go to a psychiatrist to take some medication to help alleviate the stress. There are many other therapies such as art therapy to relieve stress indirectly.

Symptoms of PTSD may include re-living the event, avoidance of things that remind you of the traumatic event, negative changes toward beliefs and attitudes, and feeling keyed up.

As shown in the diagram here, many Americans have experienced trauma. About 60% of men and 50% of women experience at least one traumatic event. Of those who do, about 8% of men and 20% of women will develop PTSD. For some events, like combat and sexual assault, more people develop PTSD.

3.5% of adults in USA are estimated to be suffering from post-traumatic stress disorder (PTSD) over the course of a given year. A new effective treatment would mark a milestone for mental-health and well-being.

The Cause

Studying parts of the brain involved in dealing with fear and stress helps researchers to better understand possible causes of PTSD. One such brain structure is the amygdala, known for its role in emotion, learning, and memory. The amygdala appears to be active in fear acquisition, or learning to fear an event (such as touching a hot stove), as well as in the early stages of fear extinction, or learning not to fear. Another such brain structure is the hippocampus. The hippocampus is important for forming memories, but in people with PTSD, the hippocampus has a significantly lower volume.

Stathmin is necessary for the creation of fear memories. Some people have more stathmin in the brain than others, and thus are more prone to PTSD. GRP is another signaling chemical in the brain released during emotional events. A lack of GRP may result in less capability to cope with the traumatic event. Serotonin also plays a role in the happiness of the person. If serotonin levels are low, then the person is more likely to develop PTSD.

Storing fear extinction memories and dampening the original fear response appears to involve the prefrontal cortex area of the brain, involved in tasks such as decision-making, problem-solving, and judgment. Certain areas of the prefrontal cortex play slightly different roles.

How Memory Works

The term &ldquoengram&rdquo is used to describe where memory is stored. There are many engrams in different regions of the brain, each used for a different purpose. For instance, the amygdala is responsible for fear memories and the interpositus nucleus is responsible for conditioned stimulus.

Through experiments in mice, researchers discovered that neurons associated with memory can be boosted with a protein called CREB, and memories can be erased with a protein called alpha-CaM kinase II. Also, those neurons can be activated to form false memory.


For short term memories, a protein called Kinase A is produced. However, sometimes, Kinase A is produced in such abundance that it causes MAPK, another protein, to be produced. MAPK causes a protein called CREB to be produced. CREB is essential for forming long-term memories.


Evolution of human beings allows people to forget things because the quality of life rests with the selective erasure of memory. Recent research suggests that fear memories can be near instantly erased and that specific proteins have significant powers to abolish them. This happens through production of a protein called alpha-CaM kinase II. Scientists have found that this protein can be used for selective deletion of fear memories in mice.

False Memory

People are found to have false memory too. For example, in many court cases, defendants were found guilty based on testimony from witnesses who were sure of their recollections, but DNA evidence proved otherwise. Researchers in MIT found that by reactivating neurons associated with a particular memory, false memory could be planted into the brains of mice.

Implanting Memory

Specific memories, such as a visit to a friend, are saved in interconnected neurons called an engram. When that memory is being recalled, the engram becomes active. On the other hand, when those exact neurons are reactivated in someone else&rsquos head, another person can experience that memory.

Also, memories are interlinked. For example, if somebody walks on a quiet street every day, that environment is stored in the person&rsquos memory. If that person is robbed on that street one day, the terrible experience is linked to the memory of that street. Hence, the next time the person walks on the same street, that person will feel unease.

Based on the theory above, a group of neuroscientists in MIT let by Nobel Laureate Susumu Tonegawa successfully implanted false memories in mice&rsquos brain.

Tonegawa and his group first put a mouse in a chamber. While the mouse is memorizing the chamber, they marked the mouse&rsquos engram in the hippocampus with a special protein called ChR2. Now they know which neurons in the engram is involved for memorizing the chamber. Those neurons are marked in white dots as shown in the picture.

Next, they put the mouse in a second chamber that is very different from the first chamber. Simultaneously, Tonegawa and his group activated the neurons marked in the previous step with a technology called optogenetics.

We will talk about optogenetics in a separate section. This technology allows people to use light to activate specific neurons being targeted. While those neurons are activated, the mouse recalls the environment in the first chamber, even though they are physically in the second chamber. At the same time, the mouse is electrocuted. This caused a memory of fear to be stored in the mouse&rsquos memory.

Now, the mouse is placed back into chamber 1, where they never actually experienced an electrical shock before. The mouse froze, as if it were electrocuted in Chamber 1. The false memory was successfully implanted into the mouse&rsquos brain!


The technology proposed on this website brings health back to patients suffering from PTSD. They can now choose what memory to forget, and what memory to implant. It provides fairness to the people who were not lucky enough to experience the happy life other people did. They can have a chance to choose a better memory, and a better life. Large expenses spent on caring for and helping cure PTSD patients can be saved. Furthermore, those people are willing back to school or the workplace, allowing them to contribute to society.

However, there are always two sides to a coin, and this solution is no exception. An instantly thought of one will be the fear of mind control. This technique provides a free pass to an apocalypse where everyone&rsquos brains are enslaved. When this technology is employed for illegal purposes, people&rsquos memory can be wiped out for illegal motives, and fake memories leading to criminal activities can be injected.

This will also lead to a lot of debatable topics. For example, if a person has any wrongdoing based on his manipulated memory, who is to be responsible? Who is responsible to make the final decision on which part of the memory shall be erased? Who is responsible for the consequences of the new memories being implanted? If the technology is defective, creating unwanted effects on the user&rsquos memory and causing unwanted behaviors, who takes the responsibility? Do parents have the right to decide whether their children should forget certain things, and remember certain fake memories instead?

Essentially, we have to ask ourselves a very fundamental question: do we wish for the human being&rsquos mind to be programmable like a computer? Is it a positive or negative thing to have such technology available?


1. Anastasiades, Christoph. "How to Build a Responsive HTML5 Website - a Step by Step Tutorial." Lingulocom How to Build a HTML5 Website from Scratch Part 1 Comments. Lingulo, 11 May 2013. Web. 5 Apr. 2014.

2. "Brain Trust." Discover Mar. 2009: n. pag. Web.

3. "Building a Better Brain." Discover Apr. 2012: n. pag. Web.

4. Costandi, Moheb. "Where Are Old Memories Stored in the Brain?" Scientific American Global RSS. Scientific American, 10 Feb. 2009. Web. 10 Apr. 2014.

Researchers See What Memory Looks Like in Brain

The researchers engineered microscopic probes that light up synapses in a living neuron in real time by attaching fluorescent markers onto synaptic proteins. The fluorescent markers allow them to see live excitatory and inhibitory synapses for the first time and, importantly, how they change as new memories are formed. The findings are published in the journal Neuron.

The synapses appear as bright spots along dendrites. As the brain processes new information, those bright spots change, visually indicating how synaptic structures in the brain have been altered by the new data.

“When you make a memory or learn something, there’s a physical change in the brain. It turns out that the thing that gets changed is the distribution of synaptic connections,” Dr Arnold explained.

The probes behave like antibodies, but they bind more tightly and are optimized to work inside the cell – something that ordinary antibodies can’t do.

“Using mRNA display, we can search through more than a trillion different potential proteins simultaneously to find the one protein that binds the target the best,” Dr Roberts said

The probes, named FingRs, are attached to green fluorescent protein, a protein isolated from jellyfish that fluoresces bright green when exposed to blue light. Because FingRs are proteins, the genes encoding them can be put into brain cells in living animals, causing the cells themselves to manufacture the probes.

The design of FingRs also includes a regulation system that cuts off the amount of FingR-GFP that is generated after 100 percent of the target protein is labeled, effectively eliminating background fluorescence – generating a sharper, clearer picture.

These probes can be put in the brains of living mice and then imaged through cranial windows using two-photon microscopy.

Can we imitate organisms' abilities to decode water patterns for new technologies?

The shape of water. Can it tell us about what drives romance? Among fish, it might. Eva Kanso, a professor of Aerospace and Mechanical Engineering at the USC Viterbi School of Engineering studies fluid flows and almost like a forensic expert, Kanso, along with her team, is studying how aquatic signals are transported through the water.

When it comes to mating, tiny crustaceans called copepods are one of the most abundant multi-cellular organisms, says Kanso, the Zohrab Kaprielian Fellow in Engineering.

To locate their mate, male copepods search for and follow the hydrodynamic and chemical trail of the female. Scientists like Kanso believe aquatic organisms transmit and read information through the movements they make and the wakes they leave behind in the water. Harbor seals, for example, have been shown to track the wake of a moving object, even when the seal is blindfolded and initially acoustically-masked. Researchers believe the flow of water encodes a pattern of information—a type of language by which an organism can call another to mate, use to avoid predators or even in the case of salmon, begin upstream migration.

Just as a seagull's footprint in the sand is different than a human's, every moving body in the water generates a different pattern or wake based on certain factors such as the size of the body that created it or the speed at which it is moving (a fast-swimming and scared animal might generate a distinct wake by the more frequent and faster beat of its tail). Kanso would like to understand how these water flow patterns are perceived at a local level, by an organism or a bio-inspired vehicle, and decode them to ascertain what's happening in the water at a larger scale.

Eva Kanso, a professor of Aerospace and Mechanical Engineering at the USC Viterbi School of Engineering studies fluid flows and almost like a forensic expert, Kanso, along with her team, is studying how aquatic signals are transported through the water. Credit: Brendan Colvert, Mohamad Alsalman, Eva Kanso

Using a computational physics model, Kanso, and PhD students Brendan Colvert and Mohamad Alsalman, generated various fluid flow patterns, then using machine learning, trained an algorithm to correctly identify these fluid patterns, achieving 99 percent accuracy. By doing this, the researchers developed an algorithm to, in a sense, mimic an aquatic sensory intelligence with regards to the patterns created in water. It is one of the first instances in which machine learning was applied to characterizing patterns in fluid flows.

Why does it matter? Consider how technologies have evolved based on the way a bat generates awareness of an environment. Just as sonar waves are used by submarines to actively probe their environment, there could be navigational uses for knowledge of water patterns under the sea. Without GPS, underwater vehicles equipped with sensors that are trained with such algorithms could, in principle, detect vehicles of a particular size and speed, known to generate certain flow patterns. By the same token, understanding the patterns that make a given wake detectable could help design underwater vehicles that leave behind inconspicuous wakes.

Kanso and her team are now testing these algorithms on real-life data and extending their scope to spatially-distributed networks of sensors that have the potential to create more robust and accurate maps of the flow patterns.

The article was recently published in Bioinspiration & Biomimetics.

Memory fail controlled by dopamine circuit, study finds

Scripps Research, Florida Neuroscience Professor Ron Davis, PhD, has discovered a mechanism underlying transient forgetting. Credit: Scripps Research

In a landmark neurobiology study, scientists from Scripps Research have discovered a memory gating system that employs the neurotransmitter dopamine to direct transient forgetting, a temporary lapse of memory which spontaneously returns.

The study adds a new pin to scientists' evolving map of how learning, memory and active forgetting work, says Scripps Research Neuroscience Professor Ron Davis, Ph.D.

"This is the first time a mechanism has been discovered for transient memory lapse," Davis says. "There's every reason to believe, because of conservation biology, that a similar mechanism exists in humans as well."

The study, "Dopamine-based mechanism for transient forgetting," appears Wednesday in the journal Nature.

Everyone has experienced transient forgetting. A name sits on the tip of our tongue, but resurfaces only after a meeting. We walk into a room and forget why we entered—until we leave. Annoying, to be sure. But does it represent a mental glitch, or is absentmindedness a feature of a normal brain? Was the elusive memory erased and somehow restored, or merely hidden for a time? Exactly how transient forgetting worked was unknown until now.

To derive an answer, Davis' team worked in the common fruit fly, a model favored by neurobiologists for decades due to its relatively simple brain structure, ease of study and translatability to more complex animals.

The team put their flies through a series of training exercises, teaching them to associate an odor with an unpleasant foot shock. They then watched as several interfering stimuli, such as a blue light or a puff of air, distracted the flies so they forgot the odor's negative association, temporarily. Interestingly, stronger stimulation led to longer lasting periods of forgetting.

Martin Sabandal, a graduate student in the lab of neuroscientist Ron Davis, PhD, at Scripps Research, co-authored the new study on transient forgetting. Credit: Scripps Research

Additional biochemical studies revealed a single pair of dopamine-releasing neurons in the flies, called PPL1-α2α'2, which directed the transient forgetting. Dopamine sent from other neurons didn't have the same effect. The neurons activated dopamine receptors called DAMB on axons extending from neurons in the memory-processing center of the fruit fly brain, called its mushroom body.

Activation of the transient forgetting circuit did not erase the flies' long-term memory recall, suggesting that transient forgetting doesn't affect permanent, consolidated memory traces, or engrams, that are acquired over time, Davis says.

Intriguingly, they found the flies' memory performance was restored after the transient forgetting period lifted, says the paper's first author, John Martin Sabandal, a Scripps Research graduate student, who worked with staff scientist Jacob Berry, Ph.D., at the team's lab in Jupiter, Florida.

"Could we perform better if certain memories are suppressed over others—could we learn or adapt to situations better? Nobody knows. Those are the type of questions that will be explored in the future," Sabandal says. "We found, provisionally, there is a potential memory reserve that is just unable to be expressed at a particular moment."

The mechanisms underlying long-term memory acquisition and consolidation have been thoroughly studied over the past 40 years, Davis says, but forgetting has been overlooked until recently. It's proving to be a fascinating field. In 2012 Davis' group found a mechanism directing permanent forgetting, finding it is an ongoing, active process, one apparently needed for healthy brain function.

"You can imagine that we have thousands of memories that occur every day in our lifetime, and the brain does not have the capability of remembering, or encoding, all of those memories. So there is a need to erase those memories that are irrelevant to our existence and our daily lives," Davis says.

Taken together, it's increasingly clear that much of what we think of as memory loss is not a result of broken connections or age-related decline, but an important feature, one necessary for survival, Davis says. Much more work lies ahead, he adds.

"We now know that there is a specific receptor in the memory center that receives the transient forgetting signal from dopamine. But we don't yet know what happens downstream. What does that receptor do to the physiology of the neuron that temporarily blocks memory retrieval? That's the major next goal, to understand how this block in retrieval occurs through the activation of this dopamine receptor," Davis says. "We are just at the very beginning of understanding how the brain causes transient forgetting."

In experiments echoing mice behavior, researchers emulate how brains recognize specific smells


The hippocampus in the medial temporal lobe plays important roles in learning and memory.

The clinical studies on Patient H.M in 1953 showed the significant functions of the medial temporal lobe. Patient H.M. underwent surgical removal of the medial temporal lobes. This resulted to anterograde amnesia (difficulty of forming new memories) and neologism (forming and/or using new words). However, procedural memories, semantic memories, speech, reading and writing were all left unaffected.

Situated in the medial temporal lobe, the hippocampus is responsible for the consolidation of short term memory and long term memory. In particular, the hippocampus is responsible for the formation of new memories related to experiences events, also known as autobiographical or episodic memories. Declarative memories, those that can be verbalized more explicitly than episodic memories, are formed but not stored in the hippocampus. These memories as well as past events are believed to be stored in the frontal and temporal lobes.

There are two hippocampi in the brain, one in the left hemisphere and the other one on the right. When one of these hippocampi are damaged and the other one is left intact, the person can still experience almost normal memory functioning. However, severe damage or removal of both hippocampi as in the case of Patient H.M. results to anterograde amnesia.

A process called long-term potentiation (LTP) occurs in the hippocampus. LTP refers to the increase in neural responsivity. Recent research studies proved that LTP is involved in spatial learning.

False memories aren't always cause for concern

Many were skeptical of the theory at first, as adults tend to do better than children at almost everything. But that's perhaps because we rely on our minds a lot, and any suggestion they are not to be trusted, or they get less accurate as we age, is a frightening prospect.

In reality, even though all of us will have manufactured false memories at some point, according to Reyna, we get along just fine.

From an evolutionary perspective, it might even be beneficial for us to get better at relying on gist memory.

For example, Reyna's research found that gist memory helps people make healthier decisions in terms of risk taking. If we went through life only looking at things objectively in a black-and-white sense, we might see things mathematically, and go for the highest expected value every time.

The Allais paradox — a choice problem designed by Maurice Allais in 1953 — helps explain this. In the problem, people are given the choice of taking Gamble A, which was a 100% chance of $1 million, or Gamble B, which offers a 89% of $1 million, a 10% chance of $5 million, and a 1% chance of nothing.

From an economic perspective, if you do all the maths, the highest expected value is actually Gamble B. But that doesn't mean most people go for it. In fact, most people choose Gamble A and walk away with $1 million for sure — because why wouldn't you?

"Most people say wait a minute, a whole lot of money is better than the possibility of getting nothing — which is gist," said Reyna. "The gist and the tendency to pick things in that way goes up in age to adulthood. It's not about maximising the money, it's about looking at these categorical possibilities.

"That bottom line realisation is what drives your preference there. Just like the gist drives your memory for the words in the word test."

Reyna said that false memories can make people concerned about the way they see the world, but they shouldn't think of it this way. Rather than thinking of imperfect memory being a negative impact of ageing, it's more likely to be something that actually helps us make safer, more informed choices.

"People can rely on gist very well in the world," she said. "The average college student has a very affluent memory on average, but they have all sorts of inaccuracies too, they just don't realise it. So it's not that memory is this stable accurate record all the time. We just have that illusion because our minds fill in the gaps."

Gist memory is another way our brains have shown how good they are at adapting to our surroundings. That's not to say the idea of losing your memory as a result of dementia is any less scary, but until that point, it isn't something you should necessarily worry about.

"Folks as they age will have good days and bad days, they'll have days where they don't remember the literal details, but they can compensate a lot by relying on their memory for gist," Reyna said. "So I think as we get older we shouldn't be quite as concerned that our memories are somehow broken. They were never really fully intact to begin with."