Memory

Memory is the faculty of the mind by which data or information is encoded, stored, and retrieved when needed. It is the retention of information over time for the purpose of influencing future action.^[1] If past events could not be remembered, it would be impossible for language, relationships, or personal identity to develop.^[2] Memory loss is usually described as forgetfulness or amnesia.^{[3][4][5][6][7][8]}

Memory is often understood as an informational processing system with explicit and implicit functioning that is made up of a sensory processor, short-term (or working) memory, and long-term memory.^[9] This can be related to the neuron. The sensory processor allows information from the outside world to be sensed in the form of chemical and physical stimuli and attended to various levels of focus and intent. Working memory serves as an encoding and retrieval processor. Information in the form of stimuli is encoded in accordance with explicit or implicit functions by the working memory processor. The working memory also retrieves information from previously stored material. Finally, the function of long-term memory is to store through various categorical models or systems.^[9]

Declarative, or explicit memory, is the conscious storage and recollection of data.^[10] Under declarative memory resides semantic and episodic memory. Semantic memory refers to memory that is encoded with specific meaning.^[2] Meanwhile, episodic memory refers to information that is encoded along a spatial and temporal plane.^[11][12][13] Declarative memory is usually the primary process thought of when referencing memory.^[2] Non-declarative, or implicit, memory is the unconscious storage and recollection of information.^[14] An example of a non-declarative process would be the unconscious learning or retrieval of information by way of procedural memory, or a priming phenomenon.^[2][14][15] Priming is the process of subliminally arousing specific responses from memory and shows that not all memory is consciously activated,^[15] whereas procedural memory is the slow and gradual learning of skills that often occurs without conscious attention to learning.^[2][14]

Memory is not a perfect processor and is affected by many factors. The ways by which information is encoded, stored, and retrieved can all be corrupted. Pain, for example, has been identified as a physical condition that impairs memory, and has been noted in animal models as well as chronic pain patients.^{[16][17][18][19]} The amount of attention given new stimuli can diminish the amount of information that becomes encoded for storage.^[2] Also, the storage process can become corrupted by physical damage to areas of the brain that are associated with memory storage, such as the hippocampus.^[20][21] Finally, the retrieval of information from long-term memory can be disrupted because of decay within long-term memory.^[2] Normal functioning, decay over time, and brain damage all affect the accuracy and capacity of the memory.^[22][23]

Sensory memory holds information, derived from the senses, less than one second after an item is perceived. The ability to look at an item and remember what it looked like with just a split second of observation, or memorization, is an example of sensory memory. It is out of cognitive control and is an automatic response. With very short presentations, participants often report that they seem to "see" more than they can actually report. The first precise experiments exploring this form of sensory memory were conducted by George Sperling (1963)^[24] using the "partial report paradigm." Subjects were presented with a grid of 12 letters, arranged into three rows of four. After a brief presentation, subjects were then played either a high, medium or low tone, cuing them which of the rows to report. Based on these partial report experiments, Sperling was able to show that the capacity of sensory memory was approximately 12 items, but that it degraded very quickly (within a few hundred milliseconds). Because this form of memory degrades so quickly, participants would see the display but be unable to report all of the items (12 in the "whole report" procedure) before they decayed. This type of memory cannot be prolonged via rehearsal.

Three types of sensory memories exist. Iconic memory is a fast decaying store of visual information, a type of sensory memory that briefly stores an image that has been perceived for a small duration. Echoic memory is a fast decaying store of auditory information, also a sensory memory that briefly stores sounds that have been perceived for short durations.^[25][26] Haptic memory is a type of sensory memory that represents a database for touch stimuli.

Short-term memory, not to be confused with working memory, allows recall for a period of several seconds to a minute without rehearsal. Its capacity, however, is very limited. In 1956, George A. Miller (1920–2012), when working at Bell Laboratories, conducted experiments showing that the store of short-term memory was 7±2 items. (Hence, the title of his famous paper, "The Magical Number 7±2.") Modern perspectives estimate the capacity of short-term memory to be lower, typically on the order of 4–5 items,^[27] or argue for a more flexible limit based on information instead of items.^[28] Memory capacity can be increased through a process called chunking.^[29] For example, in recalling a ten-digit telephone number, a person could chunk the digits into three groups: first, the area code (such as 123), then a three-digit chunk (456), and, last, a four-digit chunk (7890). This method of remembering telephone numbers is far more effective than attempting to remember a string of 10 digits; this is because we are able to chunk the information into meaningful groups of numbers. This is reflected in some countries' tendencies to display telephone numbers as several chunks of two to four numbers.

Short-term memory is believed to rely mostly on an acoustic code for storing information, and to a lesser extent on a visual code. Conrad (1964)^[30] found that test subjects had more difficulty recalling collections of letters that were acoustically similar, e.g., E, P, D. Confusion with recalling acoustically similar letters rather than visually similar letters implies that the letters were encoded acoustically. Conrad's (1964) study, however, deals with the encoding of written text. Thus, while the memory of written language may rely on acoustic components, generalizations to all forms of memory cannot be made.

The storage in sensory memory and short-term memory generally has a strictly limited capacity and duration. This means that information is not retained indefinitely. By contrast, while the total capacity of long-term memory has yet to be established, it can store much larger quantities of information. Furthermore, it can store this information for a much longer duration, potentially for a whole life span. For example, given a random seven-digit number, one may remember it for only a few seconds before forgetting, suggesting it was stored in short-term memory. On the other hand, one can remember telephone numbers for many years through repetition; this information is said to be stored in long-term memory.

While short-term memory encodes information acoustically, long-term memory encodes it semantically: Baddeley (1966)^[31] discovered that, after 20 minutes, test subjects had the most difficulty recalling a collection of words that had similar meanings (e.g. big, large, great, huge) long-term. Another part of long-term memory is episodic memory, "which attempts to capture information such as 'what', 'when' and 'where'".^[32] With episodic memory, individuals are able to recall specific events such as birthday parties and weddings.

Short-term memory is supported by transient patterns of neuronal communication, dependent on regions of the frontal lobe (especially dorsolateral prefrontal cortex) and the parietal lobe. Long-term memory, on the other hand, is maintained by more stable and permanent changes in neural connections widely spread throughout the brain. The hippocampus is essential (for learning new information) to the consolidation of information from short-term to long-term memory, although it does not seem to store information itself. It was thought that without the hippocampus new memories were unable to be stored into long-term memory and that there would be a very short attention span, as first gleaned from patient Henry Molaison^[33][34] after what was thought to be the full removal of both his hippocampi. More recent examination of his brain, post-mortem, shows that the hippocampus was more intact than first thought, throwing theories drawn from the initial data into question. The hippocampus may be involved in changing neural connections for a period of three months or more after the initial learning.

Research has suggested that long-term memory storage in humans may be maintained by DNA methylation,^[35] and the 'prion' gene.^[36][37]

Further research investigated the molecular basis for long-term memory. By 2015 it had become clear that long-term memory requires gene transcription activation and de novo protein synthesis.^[38] Long-term memory formation depends on both the activation of memory promoting genes and the inhibition of memory suppressor genes, and DNA methylation/DNA demethylation was found to be a major mechanism for achieving this dual regulation.^[39]

Rats with a new, strong long-term memory due to contextual fear conditioning have reduced expression of about 1,000 genes and increased expression of about 500 genes in the hippocampus 24 hours after training, thus exhibiting modified expression of 9.17% of the rat hippocampal genome. Reduced gene expressions were associated with methylations of those genes.^[40]

Considerable further research into long-term memory has illuminated the molecular mechanisms by which methylations are established or removed, as reviewed in 2022.^[41] These mechanisms include, for instance, signal-responsive TOP2B-induced double-strand breaks in immediate early genes. Also the messenger RNAs of many genes that had been subjected to methylation-controlled increases or decreases are transported by neural granules (messenger RNP) to the dendritic spines. At these locations the messenger RNAs can be translated into the proteins that control signaling at neuronal synapses.^[41]

The transition of a memory from short term to long term is called memory consolidation. Little is known about the physiological processes involved. Two propositions of how the brain achieves this task are backpropagation or backprop and positive feedback from the endocrine system. Backprop has been proposed as a mechanism the brain uses to achieve memory consolidation and has been used, for example by Geoffrey E. Hinton, Nobel Prize for Physics in 2024, to build AI software. It implies a feedback to neurons consolidating a given memory to erase that information when the brain learns that that information is misleading or wrong. However, empirical evidence of its existence is not available.^[42]

On the contrary, positive feedback for consolidating a certain short term memory registered in neurons, and considered by the neuro-endocrine systems to be useful, will make that short term memory to consolidate into a permanent one. This has been shown to be true experimentally first in insects,^{[43][44][45][46][47]} which use arginine and nitric oxide levels in their brains and endorphin receptors for this task. The involvemnt of arginine and nitric oxide in memory consolidation has been confirmed in birds, mammals and other creatures, including humans.^[48]

Glial cells have also an important role in memory formation, although how they do their work remains to be unveiled.^[49][50]

Other mechanisms for memory consolidation can not be discarded.

Multi-store model

The multi-store model (also known as Atkinson–Shiffrin memory model) was first described in 1968 by Atkinson and Shiffrin.

The multi-store model has been criticised for being too simplistic. For instance, long-term memory is believed to be actually made up of multiple subcomponents, such as episodic and procedural memory. It also proposes that rehearsal is the only mechanism by which information eventually reaches long-term storage, but evidence shows us capable of remembering things without rehearsal.

The model also shows all the memory stores as being a single unit whereas research into this shows differently. For example, short-term memory can be broken up into different units such as visual information and acoustic information. In a study by Zlonoga and Gerber (1986), patient 'KF' demonstrated certain deviations from the Atkinson–Shiffrin model. Patient KF was brain damaged, displaying difficulties regarding short-term memory. Recognition of sounds such as spoken numbers, letters, words, and easily identifiable noises (such as doorbells and cats meowing) were all impacted. Visual short-term memory was unaffected, suggesting a dichotomy between visual and audial memory.^[51]

Working memory

Main article: Working memory

In 1974 Baddeley and Hitch proposed a "working memory model" that replaced the general concept of short-term memory with active maintenance of information in short-term storage. In this model, working memory consists of three basic stores: the central executive, the phonological loop, and the visuo-spatial sketchpad. In 2000 this model was expanded with the multimodal episodic buffer (Baddeley's model of working memory).^[52]

The central executive essentially acts as an attention sensory store. It channels information to the three component processes: the phonological loop, the visuospatial sketchpad, and the episodic buffer.

The phonological loop stores auditory information by silently rehearsing sounds or words in a continuous loop: the articulatory process (for example the repetition of a telephone number over and over again). A short list of data is easier to remember. The phonological loop is occasionally disrupted. Irrelevant speech or background noise can impede the phonological loop. Articulatory suppression can also confuse encoding and words that sound similar can be switched or misremembered through the phonological similarity effect. the phonological loop also has a limit to how much it can hold at once which means that it is easier to remember a lot of short words rather than a lot of long words, according to the word length effect.

The visuospatial sketchpad stores visual and spatial information. It is engaged when performing spatial tasks (such as judging distances) or visual ones (such as counting the windows on a house or imagining images). Those with aphantasia will not be able to engage the visuospatial sketchpad.

The episodic buffer is dedicated to linking information across domains to form integrated units of visual, spatial, and verbal information and chronological ordering (e.g., the memory of a story or a movie scene). The episodic buffer is also assumed to have links to long-term memory and semantic meaning.

The working memory model explains many practical observations, such as why it is easier to do two different tasks, one verbal and one visual, than two similar tasks, and the aforementioned word-length effect. Working memory is also the premise for what allows us to do everyday activities involving thought. It is the section of memory where we carry out thought processes and use them to learn and reason about topics.^[52]

Researchers distinguish between recognition and recall memory. Recognition memory tasks require individuals to indicate whether they have encountered a stimulus (such as a picture or a word) before. Recall memory tasks require participants to retrieve previously learned information. For example, individuals might be asked to produce a series of actions they have seen before or to say a list of words they have heard before.

• Transience – memories degrade with the passing of time. This occurs in the storage stage of memory, after the information has been stored and before it is retrieved. This can happen in sensory, short-term, and long-term storage. It follows a general pattern where the information is rapidly forgotten during the first couple of days or years, followed by small losses in later days or years.
• Absent-mindedness – Memory failure due to the lack of attention. Attention plays a key role in storing information into long-term memory; without proper attention, the information might not be stored, making it impossible to be retrieved later.

Brain areas involved in the neuroanatomy of memory such as the hippocampus, the amygdala, the striatum, or the mammillary bodies are thought to be involved in specific types of memory. For example, the hippocampus is believed to be involved in spatial learning and declarative learning, while the amygdala is thought to be involved in emotional memory.^[77]

Damage to certain areas in patients and animal models and subsequent memory deficits is a primary source of information. However, rather than implicating a specific area, it could be that damage to adjacent areas, or to a pathway traveling through the area is actually responsible for the observed deficit. Further, it is not sufficient to describe memory, and its counterpart, learning, as solely dependent on specific brain regions. Learning and memory are usually attributed to changes in neuronal synapses, thought to be mediated by long-term potentiation and long-term depression.

In general, the more emotionally charged an event or experience is, the better it is remembered; this phenomenon is known as the memory enhancement effect. Patients with amygdala damage, however, do not show a memory enhancement effect.^[78][79]

Hebb distinguished between short-term and long-term memory. He postulated that any memory that stayed in short-term storage for a long enough time would be consolidated into a long-term memory. Later research showed this to be false. Research has shown that direct injections of cortisol or epinephrine help the storage of recent experiences. This is also true for stimulation of the amygdala. This proves that excitement enhances memory by the stimulation of hormones that affect the amygdala. Excessive or prolonged stress (with prolonged cortisol) may hurt memory storage. Patients with amygdalar damage are no more likely to remember emotionally charged words than nonemotionally charged ones. The hippocampus is important for explicit memory. The hippocampus is also important for memory consolidation. The hippocampus receives input from different parts of the cortex and sends its output out to different parts of the brain also. The input comes from secondary and tertiary sensory areas that have processed the information a lot already. Hippocampal damage may also cause memory loss and problems with memory storage.^[80] This memory loss includes retrograde amnesia which is the loss of memory for events that occurred shortly before the time of brain damage.^[76]

Cognitive neuroscientists consider memory as the retention, reactivation, and reconstruction of the experience-independent internal representation. The term of internal representation implies that such a definition of memory contains two components: the expression of memory at the behavioral or conscious level, and the underpinning physical neural changes (Dudai 2007). The latter component is also called engram or memory traces (Semon 1904). Some neuroscientists and psychologists mistakenly equate the concept of engram and memory, broadly conceiving all persisting after-effects of experiences as memory; others argue against this notion that memory does not exist until it is revealed in behavior or thought (Moscovitch 2007).

One question that is crucial in cognitive neuroscience is how information and mental experiences are coded and represented in the brain. Scientists have gained much knowledge about the neuronal codes from the studies of plasticity, but most of such research has been focused on simple learning in simple neuronal circuits; it is considerably less clear about the neuronal changes involved in more complex examples of memory, particularly declarative memory that requires the storage of facts and events (Byrne 2007). Convergence-divergence zones might be the neural networks where memories are stored and retrieved. Considering that there are several kinds of memory, depending on types of represented knowledge, underlying mechanisms, processes functions and modes of acquisition, it is likely that different brain areas support different memory systems and that they are in mutual relationships in neuronal networks: "components of memory representation are distributed widely across different parts of the brain as mediated by multiple neocortical circuits".^[81]

• Encoding. Encoding of working memory involves the spiking of individual neurons induced by sensory input, which persists even after the sensory input disappears (Jensen and Lisman 2005; Fransen et al. 2002). Encoding of episodic memory involves persistent changes in molecular structures that alter synaptic transmission between neurons. Examples of such structural changes include long-term potentiation (LTP) or spike-timing-dependent plasticity (STDP). The persistent spiking in working memory can enhance the synaptic and cellular changes in the encoding of episodic memory (Jensen and Lisman 2005).
• Working memory. Recent functional imaging studies detected working memory signals in both medial temporal lobe (MTL), a brain area strongly associated with long-term memory, and prefrontal cortex (Ranganath et al. 2005), suggesting a strong relationship between working memory and long-term memory. However, the substantially more working memory signals seen in the prefrontal lobe suggest that this area plays a more important role in working memory than MTL (Suzuki 2007).
• Consolidation and reconsolidation. Short-term memory (STM) is temporary and subject to disruption, while long-term memory (LTM), once consolidated, is persistent and stable. Consolidation of STM into LTM at the molecular level presumably involves two processes: synaptic consolidation and system consolidation. The former involves a protein synthesis process in the medial temporal lobe (MTL), whereas the latter transforms the MTL-dependent memory into an MTL-independent memory over months to years (Ledoux 2007). In recent years, such traditional consolidation dogma has been re-evaluated as a result of the studies on reconsolidation. These studies showed that prevention after retrieval affects subsequent retrieval of the memory (Sara 2000). New studies have shown that post-retrieval treatment with protein synthesis inhibitors and many other compounds can lead to an amnestic state (Nadel et al. 2000b; Alberini 2005; Dudai 2006). These findings on reconsolidation fit with the behavioral evidence that retrieved memory is not a carbon copy of the initial experiences, and memories are updated during retrieval.

Study of the genetics of human memory is in its infancy though many genes have been investigated for their association to memory in humans and non-human animals. A notable initial success was the association of APOE with memory dysfunction in Alzheimer's disease. The search for genes associated with normally varying memory continues. One of the first candidates for normal variation in memory is the protein KIBRA,^{[82][medical citation needed]} which appears to be associated with the rate at which material is forgotten over a delay period. There has been some evidence that memories are stored in the nucleus of neurons.^[83][84]

DNA topoisomerase 2-beta in learning and memory

During a new learning experience, a set of genes is rapidly expressed in the brain. This induced gene expression is considered to be essential for processing the information being learned. Such genes are referred to as immediate early genes (IEGs). DNA topoisomerase 2-beta (TOP2B) activity is essential for the expression of IEGs in a type of learning experience in mice termed associative fear memory.^[93] Such a learning experience appears to rapidly trigger TOP2B to induce double-strand breaks in the promoter DNA of IEG genes that function in neuroplasticity. Repair of these induced breaks is associated with DNA demethylation of IEG gene promoters allowing immediate expression of these IEG genes.^[93]

The double-strand breaks that are induced during a learning experience are not immediately repaired. About 600 regulatory sequences in promoters and about 800 regulatory sequences in enhancers appear to depend on double strand breaks initiated by topoisomerase 2-beta (TOP2B) for activation.^[94][95] The induction of particular double-strand breaks are specific with respect to their inducing signal. When neurons are activated in vitro, just 22 of TOP2B-induced double-strand breaks occur in their genomes.^[96]

Such TOP2B-induced double-strand breaks are accompanied by at least four enzymes of the non-homologous end joining (NHEJ) DNA repair pathway (DNA-PKcs, KU70, KU80, and DNA LIGASE IV) (see Figure). These enzymes repair the double-strand breaks within about 15 minutes to two hours.^[96][97] The double-strand breaks in the promoter are thus associated with TOP2B and at least these four repair enzymes. These proteins are present simultaneously on a single promoter nucleosome (there are about 147 nucleotides in the DNA sequence wrapped around a single nucleosome) located near the transcription start site of their target gene.^[97]

The double-strand break introduced by TOP2B apparently frees the part of the promoter at an RNA polymerase-bound transcription start site to physically move to its associated enhancer (see regulatory sequence). This allows the enhancer, with its bound transcription factors and mediator proteins, to directly interact with the RNA polymerase paused at the transcription start site to start transcription.^[96][98]

Contextual fear conditioning in the mouse causes the mouse to have a long-term memory and fear of the location in which it occurred. Contextual fear conditioning causes hundreds of DSBs in mouse brain medial prefrontal cortex (mPFC) and hippocampus neurons (see Figure: Brain regions involved in memory formation). These DSBs predominately activate genes involved in synaptic processes, that are important for learning and memory.^[99]

Up until the mid-1980s it was assumed that infants could not encode, retain, and retrieve information.^[100] A growing body of research now indicates that infants as young as 6-months can recall information after a 24-hour delay.^[101] Furthermore, research has revealed that as infants grow older they can store information for longer periods of time; 6-month-olds can recall information after a 24-hour period, 9-month-olds after up to five weeks, and 20-month-olds after as long as twelve months.^[102] In addition, studies have shown that with age, infants can store information faster. Whereas 14-month-olds can recall a three-step sequence after being exposed to it once, 6-month-olds need approximately six exposures in order to be able to remember it.^[67][101]

Although 6-month-olds can recall information over the short-term, they have difficulty recalling the temporal order of information. It is only by 9 months of age that infants can recall the actions of a two-step sequence in the correct temporal order – that is, recalling step 1 and then step 2.^[103][104] In other words, when asked to imitate a two-step action sequence (such as putting a toy car in the base and pushing in the plunger to make the toy roll to the other end), 9-month-olds tend to imitate the actions of the sequence in the correct order (step 1 and then step 2). Younger infants (6-month-olds) can only recall one step of a two-step sequence.^[101] Researchers have suggested that these age differences are probably due to the fact that the dentate gyrus of the hippocampus and the frontal components of the neural network are not fully developed at the age of 6-months.^{[68][105][106]}

In fact, the term 'infantile amnesia' refers to the phenomenon of accelerated forgetting during infancy. Importantly, infantile amnesia is not unique to humans, and preclinical research (using rodent models) provides insight into the precise neurobiology of this phenomenon. A review of the literature from behavioral neuroscientist Jee Hyun Kim suggests that accelerated forgetting during early life is at least partly due to rapid growth of the brain during this period.^[107]

One of the key concerns of older adults is the experience of memory loss, especially as it is one of the hallmark symptoms of Alzheimer's disease. However, memory loss is qualitatively different in normal aging from the kind of memory loss associated with a diagnosis of Alzheimer's (Budson & Price, 2005). Research has revealed that individuals' performance on memory tasks that rely on frontal regions declines with age. Older adults tend to exhibit deficits on tasks that involve knowing the temporal order in which they learned information,^[108] source memory tasks that require them to remember the specific circumstances or context in which they learned information,^[109] and prospective memory tasks that involve remembering to perform an act at a future time. Older adults can manage their problems with prospective memory by using appointment books, for example.

Gene transcription profiles were determined for the human frontal cortex of individuals from age 26 to 106 years. Numerous genes were identified with reduced expression after age 40, and especially after age 70.^[110] Genes that play central roles in memory and learning were among those showing the most significant reduction with age. There was also a marked increase in DNA damage, likely oxidative damage, in the promoters of those genes with reduced expression. It was suggested that DNA damage may reduce the expression of selectively vulnerable genes involved in memory and learning.^[110]

Much of the current knowledge of memory has come from studying memory disorders, particularly loss of memory, known as amnesia. Amnesia can result from extensive damage to: (a) the regions of the medial temporal lobe, such as the hippocampus, dentate gyrus, subiculum, amygdala, the parahippocampal, entorhinal, and perirhinal cortices^[111] or the (b) midline diencephalic region, specifically the dorsomedial nucleus of the thalamus and the mammillary bodies of the hypothalamus.^[112] There are many sorts of amnesia, and by studying their different forms, it has become possible to observe apparent defects in individual sub-systems of the brain's memory systems, and thus hypothesize their function in the normally working brain. Other neurological disorders such as Alzheimer's disease and Parkinson's disease^[113][114] can also affect memory and cognition.^[115] Hyperthymesia, or hyperthymesic syndrome, is a disorder that affects an individual's autobiographical memory, essentially meaning that they cannot forget small details that otherwise would not be stored.^{[116][117][118]} Korsakoff's syndrome, also known as Korsakoff's psychosis, amnesic-confabulatory syndrome, is an organic brain disease that adversely affects memory by widespread loss or shrinkage of neurons within the prefrontal cortex.^[76]

While not a disorder, a common temporary failure of word retrieval from memory is the tip-of-the-tongue phenomenon. Those with anomic aphasia (also called nominal aphasia or Anomia), however, do experience the tip-of-the-tongue phenomenon on an ongoing basis due to damage to the frontal and parietal lobes of the brain.

Memory dysfunction can also occur after viral infections.^[119] Many patients recovering from COVID-19 experience memory lapses. Other viruses can also elicit memory dysfunction, including SARS-CoV-1, MERS-CoV, Ebola virus and even influenza virus.^[119][120]

Although people often think that memory operates like recording equipment, this is not the case. The molecular mechanisms underlying the induction and maintenance of memory are very dynamic and comprise distinct phases covering a time window from seconds to even a lifetime.^[133] In fact, research has revealed that our memories are constructed: "current hypotheses suggest that constructive processes allow individuals to simulate and imagine future episodes,^[134] happenings, and scenarios. Since the future is not an exact repetition of the past, simulation of future episodes requires a complex system that can draw on the past in a manner that flexibly extracts and recombines elements of previous experiences – a constructive rather than a reproductive system."^[81] People can construct their memories when they encode them and/or when they recall them. To illustrate, consider a classic study conducted by Elizabeth Loftus and John Palmer (1974)^[135] in which people were instructed to watch a film of a traffic accident and then asked about what they saw. The researchers found that the people who were asked, "How fast were the cars going when they smashed into each other?" gave higher estimates than those who were asked, "How fast were the cars going when they hit each other?" Furthermore, when asked a week later whether they had seen broken glass in the film, those who had been asked the question with smashed were twice more likely to report that they had seen broken glass than those who had been asked the question with hit (there was no broken glass depicted in the film). Thus, the wording of the questions distorted viewers' memories of the event. Importantly, the wording of the question led people to construct different memories of the event – those who were asked the question with smashed recalled a more serious car accident than they had actually seen. The findings of this experiment were replicated around the world, and researchers consistently demonstrated that when people were provided with misleading information they tended to misremember, a phenomenon known as the misinformation effect.^[136]

Research has revealed that asking individuals to repeatedly imagine actions that they have never performed or events that they have never experienced could result in false memories. For instance, Goff and Roediger^[137] (1998) asked participants to imagine that they performed an act (e.g., break a toothpick) and then later asked them whether they had done such a thing. Findings revealed that those participants who repeatedly imagined performing such an act were more likely to think that they had actually performed that act during the first session of the experiment. Similarly, Garry and her colleagues (1996)^[138] asked college students to report how certain they were that they experienced a number of events as children (e.g., broke a window with their hand) and then two weeks later asked them to imagine four of those events. The researchers found that one-fourth of the students asked to imagine the four events reported that they had actually experienced such events as children. That is, when asked to imagine the events they were more confident that they experienced the events.

Research reported in 2013 revealed that it is possible to artificially stimulate prior memories and artificially implant false memories in mice. Using optogenetics, a team of RIKEN-MIT scientists caused the mice to incorrectly associate a benign environment with a prior unpleasant experience from different surroundings. Some scientists believe that the study may have implications in studying false memory formation in humans, and in treating PTSD and schizophrenia.^{[139][140][medical citation needed]}

Memory reconsolidation is when previously consolidated memories are recalled or retrieved from long-term memory to your active consciousness. During this process, memories can be further strengthened and added to but there is also risk of manipulation involved. We like to think of our memories as something stable and constant when they are stored in long-term memory but this is not the case. There are a large number of studies that found that consolidation of memories is not a singular event but are put through the process again, known as reconsolidation.^[141] This is when a memory is recalled or retrieved and placed back into your working memory. The memory is now open to manipulation from outside sources and the misinformation effect which could be due to misattributing the source of the inconsistent information, with or without an intact original memory trace (Lindsay and Johnson, 1989).^[142] One thing that can be sure is that memory is malleable.

This new research into the concept of reconsolidation has opened the door to methods to help those with unpleasant memories or those that struggle with memories. An example of this is if you had a truly frightening experience and recall that memory in a less arousing environment, the memory will be weaken the next time it is retrieved.^[141] "Some studies suggest that over-trained or strongly reinforced memories do not undergo reconsolidation if reactivated the first few days after training, but do become sensitive to reconsolidation interference with time."^[141] This, however does not mean that all memory is susceptible to reconsolidation. There is evidence to suggest that memory that has undergone strong training and whether or not is it intentional is less likely to undergo reconsolidation.^[143] There was further testing done with rats and mazes that showed that reactivated memories were more susceptible to manipulation, in both good and bad ways, than newly formed memories.^[144] It is still not known whether or not these are new memories formed and it is an inability to retrieve the proper one for the situation or if it is a reconsolidated memory. Because the study of reconsolidation is still a newer concept, there is still debate on whether it should be considered scientifically sound.

A UCLA research study published in the June 2008 issue of the American Journal of Geriatric Psychiatry found that people can improve cognitive function and brain efficiency through simple lifestyle changes such as incorporating memory exercises, healthy eating, physical fitness and stress reduction into their daily lives. This study examined 17 subjects, (average age 53) with normal memory performance. Eight subjects were asked to follow a "brain healthy" diet, relaxation, physical, and mental exercise (brain teasers and verbal memory training techniques). After 14 days, they showed greater word fluency (not memory) compared to their baseline performance. No long-term follow-up was conducted; it is therefore unclear if this intervention has lasting effects on memory.^[145]

There are a loosely associated group of mnemonic principles and techniques that can be used to vastly improve memory known as the art of memory.

The International Longevity Center released in 2001 a report^[146] which includes in pages 14–16 recommendations for keeping the mind in good functionality until advanced age. Some of the recommendations are:

• to stay intellectually active through learning, training or reading
• to keep physically active so to promote blood circulation to the brain
• to socialize
• to reduce stress
• to keep sleep time regular
• to avoid depression or emotional instability
• to observe good nutrition.

Memorization is a method of learning that allows an individual to recall information verbatim. Rote learning is the method most often used. Methods of memorizing things have been the subject of much discussion over the years with some writers, such as Cosmos Rossellius using visual alphabets. The spacing effect shows that an individual is more likely to remember a list of items when rehearsal is spaced over an extended period of time. In contrast to this is cramming: an intensive memorization in a short period of time. The spacing effect is exploited to improve memory in spaced repetition flashcard training. Also relevant is the Zeigarnik effect, which states that people remember uncompleted or interrupted tasks better than completed ones. The so-called Method of loci uses spatial memory to memorize non-spatial information.^[147]

Plants lack a specialized organ devoted to memory retention, so plant memory has been a controversial topic in recent years. New advances in the field have identified the presence of neurotransmitters in plants, adding to the hypothesis that plants are capable of remembering.^[148] Action potentials, a physiological response characteristic of neurons, have been shown to have an influence on plants as well, including in wound responses and photosynthesis.^[148] In addition to these homologous features of memory systems in both plants and animals, plants have also been observed to encode, store and retrieve basic short-term memories.

One of the most well-studied plants to show rudimentary memory is the Venus flytrap. Native to the subtropical wetlands of the eastern United States, Venus flytraps have evolved the ability to obtain meat for sustenance, likely due to the lack of nitrogen in the soil.^[149] This is done by two trap-forming leaf tips that snap shut once triggered by a potential prey. On each lobe, three trigger hairs await stimulation. In order to maximize the benefit-to-cost ratio, the plant enables a rudimentary form of memory in which two trigger hairs must be stimulated within thirty seconds in order to result in trap closure.^[149] This system ensures that the trap only closes when potential prey is within grasp.

The time lapse between trigger hair stimulations suggests that the plant can remember an initial stimulus long enough for a second stimulus to initiate trap closure. This memory is not encoded in a brain, as plants lack this specialized organ. Rather, information is stored in the form of cytoplasmic calcium levels. The first trigger causes a subthreshold cytoplasmic calcium influx.^[149] This initial trigger is not enough to activate trap closure, so a subsequent stimulus allows for a secondary influx of calcium. The latter calcium rise superimposes on the initial one, creating an action potential that passes threshold, resulting in trap closure.^[149] Researchers, to prove that an electrical threshold must be met to stimulate trap closure, excited a single trigger hair with a constant mechanical stimulus using Ag/AgCl electrodes.^[150] The trap closed after only a few seconds. This experiment demonstrated that the electrical threshold, not necessarily the number of trigger hair stimulations, was the contributing factor in Venus flytrap memory.

It has been shown that trap closure can be blocked using uncouplers and inhibitors of voltage-gated channels.^[150] After trap closure, these electrical signals stimulate glandular production of jasmonic acid and hydrolases, allowing for digestion of prey.^[151]

Many other plants exhibit the capacity to remember, including Mimosa pudica.^[152] An experimental apparatus was designed to drop potted mimosa plants repeatedly from the same distance and at the same speed. It was observed that the plants' defensive response of curling up their leaves decreased over the sixty times the experiment was repeated. To confirm that this was a mechanism of memory rather than exhaustion, some of the plants were shaken post experiment and displayed normal defensive responses of leaf curling. This experiment demonstrated long-term memory in the plants, as it was repeated a month later, and the plants were observed to remain unfazed by the dropping.^[152]