Democide, or populicide, is "the intentional killing of an unarmed or disarmed person by government agents acting in their authoritative capacity and pursuant to government policy or high command". The term democide, coined by Holocaust historian and statistics expert R. J. Rummel in his book Death by Government, has been described by Holocaust historian Yehuda Bauer as a better term than genocide to refer to certain types of mass killing. According to Rummel, this definition covers a wide range of deaths, including forced labor and concentration camp victims, extrajudicialsummary killings, and mass deaths due to governmental acts of criminal omission and neglect, such as in deliberate famines like the Holodomor, as well as killings by de facto governments, such as killings during a civil war. This definition covers any murder of any number of persons by any government.
Rummel coined democide as an extended term to include forms of government murder not covered by genocide. According to Rummel, democide surpassed war as the leading cause of non-natural death in the 20th century.
Definition
Democide is the murder of any person or people by their
government (normally the one under whose jurisdiction they live),
including genocide, politicide, and mass murder.
Democide is not necessarily the elimination of entire cultural groups
but rather groups within the country that the government feels need to
be eradicated for political reasons and due to claimed future threats.
According to Rummel, genocide has three different meanings.
The ordinary meaning is murder by government of people due to their
national, ethnic, racial or religious group membership. The legal
meaning of genocide refers to the international treaty on genocide, the Convention on the Prevention and Punishment of the Crime of Genocide.
This also includes nonlethal acts that in the end eliminate or greatly
hinder the group. Looking back on history, one can see the different
variations of democides that have occurred, but it still consists of
acts of killing or mass murder. The generalized meaning of genocide is
similar to the ordinary meaning but also includes government killings of
political opponents or otherwise intentional murder. In order to avoid
confusion over which meaning is intended, Rummel created democide for this third meaning.
In "How Many Did Communist Regimes Murder?", Rummel wrote:
First, however, I should clarify the term democide. It means for governments what murder means for an individual under municipal law. It is the premeditated killing of a person in cold blood, or causing the death of a person through reckless and wanton disregard for their life.
Thus, a government incarcerating people in a prison under such deadly
conditions that they die in a few years is murder by the
state—democide—as would parents letting a child die from malnutrition
and exposure be murder. So would government forced labor that kills a
person within months or a couple of years be murder. So would government
created famines that then are ignored or knowingly aggravated by
government action be murder of those who starve to death. And obviously,
extrajudicial executions,
death by torture, government massacres, and all genocidal killing be
murder. However, judicial executions for crimes that internationally
would be considered capital offenses, such as for murder or treason (as
long as it is clear that these are not fabricated for the purpose of
executing the accused, as in communist show trials), are not democide.
Nor is democide the killing of enemy soldiers in combat or of armed
rebels, nor of noncombatants as a result of military action against
military targets.
There is much confusion about what is
meant by totalitarian in the literature, including the denial that such
systems even exist. I define a totalitarian state as one with a system
of government that is unlimited constitutionally
or by countervailing powers in society (such as by a church, rural
gentry, labor unions, or regional powers); is not held responsible to
the public by periodic secret
and competitive elections; and employs its unlimited power to control
all aspects of society, including the family, religion, education,
business, private property, and social relationships. Under Stalin, the Soviet Union was thus totalitarian, as was Mao's China, Pol Pot's Cambodia, Hitler's Germany, and U Ne Win's Burma.
Totalitarianism is then a political ideology for which a totalitarian
government is the agency for realizing its ends. Thus, totalitarianism
characterizes such ideologies as state socialism (as in Burma), Marxism-Leninism as in former East Germany, and Nazism. Even revolutionary Moslem Iran since the overthrow of the Shah in 1978–79 has been totalitarian—here totalitarianism was married to Moslem fundamentalism. In short, totalitarianism is the ideology of absolute power. State socialism, communism, Nazism, fascism,
and Moslem fundamentalism have been some of its recent raiments.
Totalitarian governments have been its agency. The state, with its
international legal sovereignty and independence, has been its base. As
will be pointed out, mortacracy is the result.
Estimates
In his estimates, Rudolph Rummel
relied mostly on historical accounts, an approach that rarely provides
accuracy compared with contemporary academic opinion. In the case of
Mexican democide, Rummel wrote that while "these figures amount to
little more than informed guesses", he thought "there is enough evidence
to at least indict these authoritarian regimes for megamurder." According to Rummel, his research showed that the death toll from
democide is far greater than the death toll from war. After studying
over 8,000 reports of government-caused deaths, Rummel estimated that
there have been 262 million victims of democide in the last century.
According to his figures, six times as many people have died from the
actions of people working for governments than have died in battle. One
of his main findings was that democracies have much less democide than
authoritarian regimes. Rummel argued that there is a relation between political power and
democide. Political mass murder grows increasingly common as political
power becomes unconstrained. At the other end of the scale, where power
is diffuse, checked, and balanced, political violence
is a rarity. According to Rummel, "[t]he more power a regime has, the
more likely people will be killed. This is a major reason for promoting
freedom." Rummel argued that "concentrated political power is the most dangerous thing on earth."
Rummel's estimates, especially about Communist democide, typically included a wide range and cannot be considered determinative. Rummel calculated nearly 43 million deaths due to democide inside and outside the Soviet Union during Stalin's regime. This is much higher than an often quoted figure in the popular press of 20 million, or a 2010s scholarly figure of 9 million. Rummel responded that the 20 million estimate is based on a figure from Robert Conquest's The Great Terror
and that Conquest's qualifier "almost certainly too low" is usually
forgotten. For Rummell, Conquest's calculations excluded camp deaths
before 1936 and after 1950, executions (1939–1953), the forced population transfer in the Soviet Union (1939–1953), the deportation within the Soviet Union of minorities (1941–1944), and those the Soviet Red Army and Cheka (the secret police) executed throughout Eastern Europe after their conquest during the 1944–1945 period. Moreover, the Holodomor that killed 5 million in 1932–1934 (according to Rummel) is also not included. After decades of research in the state archives, most scholars say that
Stalin's regime killed between 6 and 9 million, which is considerably
less than originally thought, while Nazi Germany killed at least 11 million, which is in line with previous estimates.
Criticism of specific estimates
Edward J. M. Rhoads cited as inaccurate Rummel's description of the 1911 Revolution in China as a "very minor affair... no more than 1,000 to 2,000 died," citing a death toll multiple times the number 2,000 among the Manchu ethnic minority. According to Sara M. Butler: "Rummel claims that 350,000 Jews were killed in the Spanish Inquisition, which is 1.7 times higher than the actual Jewish population of Spain at that time."
In historian William Rubinstein's opinion, almost all of Rummel's estimated numbers were false.
Application
Authoritarian and totalitarian regimes
Communist regimes
Rummel applied the concept of democide to Communist regimes. In 1987, Rudolph Rummel's book Death by Government Rummel estimated that 148 million were killed by Communist governments from 1917 to 1987. The list of Communist countries with more than 1 million estimated victims included:
In 1993, Rummel wrote: "Even were we to have total access
to all communist archives we still would not be able to calculate
precisely how many the communists murdered. Consider that even in spite
of the archival statistics and detailed reports of survivors, the best
experts still disagree by over 40 percent on the total number of Jews killed by the Nazis. We cannot expect near this accuracy for the victims of communism. We can, however, get a probable order of magnitude and a relative approximation of these deaths within a most likely range." In 1994, Rummel updated his estimates for Communist regimes at about
110 million people, foreign and domestic, killed by Communist democide
from 1900 to 1987. Due to additional information about Mao Zedong's culpability in the Great Chinese Famine according to Mao: The Unknown Story, a 2005 book authored by Jon Halliday and Jung Chang, Rummel revised upward his total for Communist democide to about 148 million, using their estimate of 38 million famine deaths.
Rummel's figures for Communist governments have been
criticized for the methodology which he used to arrive at them, and they
have also been criticized for being higher than the figures which have
been given by most scholars
Right-wing authoritarian, fascist, and feudal regimes
Democide in Communist and Nationalist China, Nazi Germany,
and the Soviet Union are characterized by Rummel as deka-megamurderers
(128,168,000), while those in Cambodia, Japan, Pakistan, Poland, Turkey,
Vietnam, and Yugoslavia are characterized as the lesser megamurderers
(19,178,000), and cases in Mexico, North Korea, and feudal Russia are
characterized as suspected megamurderers (4,145,000). Rummel wrote that "even though the Nazis hardly matched the democide of
the Soviets and Communist Chinese", they "proportionally killed more".
Colonial regimes
In response to David Stannard's figures about what he terms "the American Holocaust", Rummel estimated that over the centuries of European colonization about 2 million to 15 million American indigenous people
were victims of democide, excluding military battles and unintentional
deaths in Rummel's definition. Rummel wrote that "[e]ven if these
figures are remotely true, then this still make this subjugation of the
Americas one of the bloodier, centuries long, democides in world
history."
Rummel stated that his estimate for those
killed by colonialism is 50,000,000 persons in the 20th century (this
was revised upwards from his initial estimate of 815,000 dead).
Democratic regimes
While democratic regimes are considered by Rummel to be the least likely to commit democide and engage in wars per the democratic peace theory, Rummel wrote that
"democracies themselves are responsible
for some of this democide. Detailed estimates have yet to be made, but
preliminarily work suggests that some 2,000,000 foreigners have been
killed in cold blood by democracies."
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. Memory loss is usually described as forgetfulness or a disorder such as amnesia.
Memory is often understood as an information processing system with explicit and implicit functioning that is made up of a sensory processor, short-term (or working) memory, and long-term memory. 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
information through various categorical models or systems.
Declarative, or explicit memory, is the conscious storage and recollection of data. Under declarative memory resides semantic and episodic memory. Semantic memory refers to memory that is encoded with specific meaning. Meanwhile, episodic memory refers to information that is encoded along a spatial and temporal plane. Declarative memory is usually the primary process thought of when referencing memory. Non-declarative, or implicit, memory is the unconscious storage and recollection of information. 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. Priming is the process of subliminally arousing specific responses from memory and shows that not all memory is consciously activated, whereas procedural memory is the slow and gradual learning of skills that often occurs without conscious attention to learning.
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. The amount of attention given new stimuli can diminish the amount of information that becomes encoded for storage. 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. Finally, the retrieval of information from long-term memory can be disrupted because of decay within long-term memory. Normal functioning, decay over time, and brain damage all affect the accuracy and capacity of the memory.
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) 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. Haptic memory is a type of sensory memory that represents a database for touch stimuli.
Retrieval cues
How we encode information has a big impact on how well we
remember it later. Research on levels of processing shows that memory is
better when encoding emphasizes "deep" aspects of a stimulus (such as
meaning) vs. "shallow" aspects of a stimulus (such as a place). "Deep"
encoding leads to a highly distributed representation and "shallow"
encoding leads to a sparse representation. Thinking about meaning
creates a richer, more connected memory, while shallow processing leads
to weaker, less lasting traces. Memory also works best when the cues we use to recall information match
the ones present during learning which connects to the principle called
encoding specificity. Similarly, context dependence shows that remembering is easier when the
environment at study matches the environment at test. For example,
studying in a "wet" lab can help if the test is in the same setting. Overall, these findings show that both the way we think about
information and the context in which we learn it play a major role in
memory.
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, or argue for a more flexible limit based on information instead of items. Memory capacity can be increased through a process called chunking. 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) 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) 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'". 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 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, and the 'prion' gene.
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. 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.
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.
Considerable further research into long-term memory has
illuminated the molecular mechanisms by which methylations are
established or removed, as reviewed in 2022. 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 neuronalsynapses.
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 laureate 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.
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, which use arginine and nitric oxide levels in their brains and
endorphin receptors for this task. The involvement of arginine and
nitric oxide in memory consolidation has been confirmed in birds,
mammals and other creatures, including humans.
Glial cells have also an important role in memory formation, although how they do their work remains to be unveiled.
Other mechanisms for memory consolidation can not be discarded.
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
highlights how we're 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.
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).
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.
Types
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.
By information type
Topographical memory involves the ability to orient oneself in space, to recognize and follow an itinerary, or to recognize familiar places. Getting lost when traveling alone is an example of the failure of topographic memory.
Declarative memory requires conscious recall, in that some conscious process must call back the information. It is sometimes called explicit memory, since it consists of information that is explicitly stored and retrieved. Declarative memory can be further sub-divided into semantic memory, concerning principles and facts taken independent of context; and episodic memory,
concerning information specific to a particular context, such as a time
and place. Semantic memory allows the encoding of abstract knowledge
about the world, such as "Paris is the capital of France". Episodic
memory, on the other hand, is used for more personal memories, such as
the sensations, emotions, and personal associations
of a particular place or time. Episodic memories often reflect the
"firsts" in life such as a first kiss, first day of school or first time
winning a championship. These are key events in one's life that can be
remembered clearly.
Research suggests that declarative memory is supported by
several functions of the medial temporal lobe system which includes the
hippocampus. Autobiographical memory
– memory for particular events within one's own life – is generally
viewed as either equivalent to, or a subset of, episodic memory. Visual memory
is part of memory preserving some characteristics of our senses
pertaining to visual experience. One is able to place in memory
information that resembles objects, places, animals or people in sort of
a mental image. Visual memory can result in priming and it is assumed some kind of perceptual representational system underlies this phenomenon.
Procedural
In contrast, procedural memory (or implicit memory) is not based on the conscious recall of information, but on implicit learning. It can best be summarized as remembering how to do something. Procedural memory is primarily used in learning motor skills
and can be considered a subset of implicit memory. It is revealed when
one does better in a given task due only to repetition – no new explicit
memories have been formed, but one is unconsciously accessing aspects of those previous experiences. Procedural memory involved in motor learning depends on the cerebellum and basal ganglia.
A characteristic of procedural memory is that the things
remembered are automatically translated into actions, and thus sometimes
difficult to describe. Some examples of procedural memory include the
ability to ride a bike or tie shoelaces.
By temporal direction
Another major way to distinguish different memory functions is whether the content to be remembered is in the past, retrospective memory, or in the future, prospective memory. John Meacham introduced this distinction in a paper presented at the 1975 American Psychological Association annual meeting and subsequently included by Ulric Neisser in his 1982 edited volume, Memory Observed: Remembering in Natural Contexts. Thus, retrospective memory as a category includes semantic, episodic
and autobiographical memory. In contrast, prospective memory is memory
for future intentions, or remembering to remember
(Winograd, 1988). Prospective memory can be further broken down into
event- and time-based prospective remembering. Time-based prospective
memories are triggered by a time-cue, such as going to the doctor
(action) at 4pm (cue). Event-based prospective memories are intentions
triggered by cues, such as remembering to post a letter (action) after
seeing a mailbox (cue). Cues do not need to be related to the action (as
the mailbox/letter example), and lists, sticky-notes, knotted
handkerchiefs, or string around the finger all exemplify cues that
people use as strategies to enhance prospective memory.
Study techniques
To assess infants
Infants do not have the language ability to report on
their memories and so verbal reports cannot be used to assess very young
children's memory. Throughout the years, however, researchers have
adapted and developed a number of measures for assessing both infants'
recognition memory and their recall memory. Habituation and operant conditioning
techniques have been used to assess infants' recognition memory and the
deferred and elicited imitation techniques have been used to assess
infants' recall memory.
Techniques used to assess infants' recognition memory include the following:
Visual paired comparison procedure (relies on habituation):
infants are first presented with pairs of visual stimuli, such as two
black-and-white photos of human faces, for a fixed amount of time; then,
after being familiarized with the two photos, they are presented with
the "familiar" photo and a new photo. The time spent looking at each
photo is recorded. Looking longer at the new photo indicates that they
remember the "familiar" one. Studies using this procedure have found
that 5- to 6-month-olds can retain information for as long as fourteen
days.
Operant conditioning technique: infants
are placed in a crib and a ribbon that is connected to a mobile
overhead is tied to one of their feet. Infants notice that when they
kick their foot the mobile moves – the rate of kicking increases
dramatically within minutes. Studies using this technique have revealed
that infants' memory substantially improves over the first 18-months.
Whereas 2- to 3-month-olds can retain an operant response (such as
activating the mobile by kicking their foot) for a week, 6-month-olds
can retain it for two weeks, and 18-month-olds can retain a similar
operant response for as long as 13 weeks.
Techniques used to assess infants' recall memory include the following:
Deferred imitation technique:
an experimenter shows infants a unique sequence of actions (such as
using a stick to push a button on a box) and then, after a delay, asks
the infants to imitate the actions. Studies using deferred imitation
have shown that 14-month-olds' memories for the sequence of actions can
last for as long as four months.
Elicited imitation technique: is very
similar to the deferred imitation technique; the difference is that
infants are allowed to imitate the actions before the delay. Studies
using the elicited imitation technique have shown that 20-month-olds can
recall the action sequences twelve months later.
To assess children and older adults
Researchers use a variety of tasks to assess older children and adults' memory. Some examples are:
Paired associate learning
– when one learns to associate one specific word with another. For
example, when given a word such as "safe" one must learn to say another
specific word, such as "green". This is stimulus and response.
Free recall – during this task a
subject would be asked to study a list of words and then later they will
be asked to recall or write down as many words that they can remember,
similar to free response questions. Earlier items are affected by retroactive interference (RI), which
means the longer the list, the greater the interference, and the less
likelihood that they are recalled. On the other hand, items that have
been presented lastly suffer little RI, but suffer a great deal from
proactive interference (PI), which means the longer the delay in recall,
the more likely that the items will be lost.
Cued recall – one is given a
significant hints to help retrieve information that has been previously
encoded into the person's memory; typically this can involve a word
relating to the information being asked to remember. This is similar to fill in the blank assessments used in classrooms.
Recognition – subjects are asked to
remember a list of words or pictures, after which point they are asked
to identify the previously presented words or pictures from among a list
of alternatives that were not presented in the original list. This is similar to multiple choice assessments.
Detection paradigm – individuals are
shown a number of objects and color samples during a certain period of
time. They are then tested on their visual ability to remember as much
as they can by looking at testers and pointing out whether the testers
are similar to the sample, or if any change is present.
Savings method – compares the speed of originally learning to the speed of relearning it. The amount of time saved measures memory.
Implicit-memory tasks – information is drawn from memory without conscious realization.
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.
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.
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. This memory loss includes retrograde amnesia which is the loss of memory for events that occurred shortly before the time of brain damage.
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).
APP and LTP in Alzheimer disease
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".
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, 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.
Genetic underpinnings
Several genes,
proteins and enzymes have been extensively researched for their
association with memory. Long-term memory, unlike short-term memory, is
dependent upon the synthesis of new proteins. This occurs within the cell,
and concerns the particular transmitters, receptors, and new synapse
pathways that reinforce the communicative strength between neurons. The
production of new proteins devoted to synapse reinforcement is triggered
after the release of certain signaling substances (such as calcium
within hippocampal neurons) in the cell. In the case of hippocampal
cells, this release is dependent upon the expulsion of magnesium (a
binding molecule) that is expelled after significant and repetitive
synaptic signaling. The temporary expulsion of magnesium frees NMDA receptors to release calcium in the cell, a signal that leads to gene transcription and the construction of reinforcing proteins. For more information, see long-term potentiation (LTP).
One of the newly synthesized proteins in LTP is also
critical for maintaining long-term memory. This protein is an
autonomously active form of the enzyme protein kinase C (PKC), known as PKMζ.
PKMζ maintains the activity-dependent enhancement of synaptic strength
and inhibiting PKMζ erases established long-term memories, without
affecting short-term memory or, once the inhibitor is eliminated, the
ability to encode and store new long-term memories is restored. Also, BDNF is important for the persistence of long-term memories.
The long-term stabilization of synaptic changes is also
determined by a parallel increase of pre- and postsynaptic structures
such as axonal bouton, dendritic spine and postsynaptic density. On the molecular level, an increase of the postsynaptic scaffolding proteins PSD-95 and HOMER1c has been shown to correlate with the stabilization of synaptic enlargement. The cAMP response element-binding protein (CREB) is a transcription factor
which is believed to be important in consolidating short-term to
long-term memories, and which is believed to be downregulated in
Alzheimer's disease.
DNA methylation and demethylation
DNA methylation and demethylation molecular mechanisms
Rats exposed to an intense learning
event may retain a life-long memory of the event, even after a single
training session. The long-term memory of such an event appears to be
initially stored in the hippocampus, but this storage is transient. Much of the long-term storage of the memory seems to take place in the anterior cingulate cortex. When such an exposure was experimentally applied, more than 5,000
differently methylated DNA regions appeared in the hippocampus neuronal genome of the rats at one and at 24 hours after training. These alterations in methylation pattern occurred at many genes that were downregulated, often due to the formation of new 5-methylcytosine
sites in CpG rich regions of the genome. Furthermore, many other genes
were upregulated, likely often due to hypomethylation. Hypomethylation
often results from the removal of methyl groups from previously existing
5-methylcytosines in DNA. Demethylation is carried out by several
proteins acting in concert, including the TET enzymes as well as enzymes of the DNA base excision repair pathway (see Epigenetics in learning and memory).
The pattern of induced and repressed genes in brain neurons subsequent
to an intense learning event likely provides the molecular basis for a
long-term memory of the event.
Studies of the molecular basis for memory formation indicate that epigenetic mechanisms operating in neurons in the brain play a central role in determining this capability. Key epigenetic mechanisms involved in memory include the methylation and demethylation of neuronal DNA, as well as modifications of histone proteins including methylations, acetylations and deacetylations.
Stimulation of brain activity in memory formation is often accompanied by the generation of damage in neuronal DNA that is followed by repair associated with persistent epigenetic alterations. In particular the DNA repair processes of non-homologous end joining and base excision repair are employed in memory formation.
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. 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.
Regulatory
sequence in a promoter at a transcription start site with a paused RNA
polymerase and a TOP2B-induced double-strand break
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. 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.
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. 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.
Brain regions involved in memory formation including medial prefrontal cortex (mPFC)
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.
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.
For the inability of adults to retrieve early memories, see Childhood amnesia.
Up until the mid-1980s it was assumed that infants could not encode, retain, and retrieve information. A growing body of research now indicates that infants as young as 6-months can recall information after a 24-hour delay. 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. 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.
Although six-month-olds can recall information over the
short-term, they have difficulty recalling the temporal order of
information. It is only by nine 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. 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. 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.
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.
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, source memory tasks that require them to remember the specific circumstances or context in which they learned information, 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. 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.
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 or the (b) midline diencephalic region, specifically the dorsomedial
nucleus of the thalamus and the mammillary bodies of the hypothalamus. 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 can also affect memory and cognition. 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. 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.
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.
Interference can hamper memorization and retrieval. There is retroactive interference, when learning new information makes it harder to recall old information and proactive interference,
where prior learning disrupts recall of new information. Although
interference can lead to forgetting, it is important to keep in mind
that there are situations when old information can facilitate learning
of new information. Knowing Latin, for instance, can help an individual
learn a related language such as French – this phenomenon is known as
positive transfer.
Stress has a significant effect on memory formation and
learning. In response to stressful situations, the brain releases
hormones and neurotransmitters (ex. glucocorticoids and catecholamines)
which affect memory encoding processes in the hippocampus. Behavioural
research on animals shows that chronic stress produces adrenal hormones
which impact the hippocampal structure in the brains of rats. An experimental study by German cognitive psychologists L. Schwabe and
O. Wolf demonstrates how learning under stress also decreases memory
recall in humans. In this study, 48 healthy female and male university students
participated in either a stress test or a control group. Those randomly
assigned to the stress test group had a hand immersed in ice cold water
(the reputable SECPT or 'Socially Evaluated Cold Pressor Test') for up
to three minutes, while being monitored and videotaped. Both the stress
and control groups were then presented with 32 words to memorize.
Twenty-four hours later, both groups were tested to see how many words
they could remember (free recall) as well as how many they could
recognize from a larger list of words (recognition performance). The
results showed a clear impairment of memory performance in the stress
test group, who recalled 30% fewer words than the control group. The
researchers suggest that stress experienced during learning distracts
people by diverting their attention during the memory encoding process.
However, memory performance can be enhanced when material
is linked to the learning context, even when learning occurs under
stress. A separate study by cognitive psychologists Schwabe and Wolf
shows that when retention testing is done in a context similar to or
congruent with the original learning task (i.e., in the same room),
memory impairment and the detrimental effects of stress on learning can
be attenuated. Seventy-two healthy female and male university students, randomly assigned to the SECPT stress test
or to a control group, were asked to remember the locations of 15 pairs
of picture cards – a computerized version of the card game
"Concentration" or "Memory". The room in which the experiment took place
was infused with the scent of vanilla, as odour is a strong cue for
memory. Retention testing took place the following day, either in the
same room with the vanilla scent again present, or in a different room
without the fragrance. The memory performance of subjects who
experienced stress during the object-location task decreased
significantly when they were tested in an unfamiliar room without the
vanilla scent (an incongruent context); however, the memory performance
of stressed subjects showed no impairment when they were tested in the
original room with the vanilla scent (a congruent context). All
participants in the experiment, both stressed and unstressed, performed
faster when the learning and retrieval contexts were similar.
This research on the effects of stress on memory may have practical implications for education, for eyewitness testimony
and for psychotherapy: students may perform better when tested in their
regular classroom rather than an exam room, eyewitnesses may recall
details better at the scene of an event than in a courtroom, and persons
with post-traumatic stress may improve when helped to situate their memories of a traumatic event in an appropriate context.
Stressful life experiences may be a cause of memory loss as a person ages. Glucocorticoids that are released during stress cause damage to neurons that are located in the hippocampal
region of the brain. Therefore, the more stressful situations that
someone encounters, the more susceptible they are to memory loss later
on. The CA1 neurons found in the hippocampus are destroyed due to glucocorticoids decreasing the release of glucose and the reuptake of glutamate. This high level of extracellular glutamate allows calcium to enter NMDA receptors
which in return kills neurons. Stressful life experiences can also
cause repression of memories where a person moves an unbearable memory
to the unconscious mind. This directly relates to traumatic events in one's past such as kidnappings, being prisoners of war or sexual abuse as a child.
The more long term the exposure to stress is, the more
impact it may have. However, short term exposure to stress also causes
impairment in memory by interfering with the function of the
hippocampus. Research shows that subjects placed in a stressful
situation for a short amount of time still have blood glucocorticoid
levels that have increased drastically when measured after the exposure
is completed. When subjects are asked to complete a learning task after
short term exposure they often have difficulties. Prenatal stress also
hinders the ability to learn and memorize by disrupting the development
of the hippocampus and can lead to unestablished long term potentiation
in the offspring of severely stressed parents. Although the stress is
applied prenatally, the offspring show increased levels of
glucocorticoids when they are subjected to stress later on in life. One explanation for why children from lower socioeconomic backgrounds
tend to display poorer memory performance than their higher-income peers
is the effects of stress accumulated over the course of the lifetime. The effects of low income on the developing hippocampus is also thought
be mediated by chronic stress responses which may explain why children
from lower and higher-income backgrounds differ in terms of memory
performance.
Sleep affects memory consolidation. During sleep, the
neural connections in the brain are strengthened. This enhances the
brain's abilities to stabilize and retain memories. There have been
several studies which show that sleep improves the retention of memory,
as memories are enhanced through active consolidation. System
consolidation takes place during slow-wave sleep (SWS). This process implicates that memories are reactivated during sleep, but
that the process does not enhance every memory. It also implicates that
qualitative changes are made to the memories when they are transferred
to long-term store during sleep. During sleep, the hippocampus replays
the events of the day for the neocortex. The neocortex then reviews and
processes memories, which moves them into long-term memory. When one
does not get enough sleep it makes it more difficult to learn as these
neural connections are not as strong, resulting in a lower retention
rate of memories. Sleep deprivation makes it harder to focus, resulting
in inefficient learning. Furthermore, some studies have shown that sleep deprivation can lead to false memories
as the memories are not properly transferred to long-term memory. One
of the primary functions of sleep is thought to be the improvement of
the consolidation of information, as several studies have demonstrated
that memory depends on getting sufficient sleep between training and
test. Additionally, data obtained from neuroimaging studies have shown
activation patterns in the sleeping brain that mirror those recorded
during the learning of tasks from the previous day, suggesting that new memories may be solidified through such rehearsal.
Construction for general manipulation
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. In fact, research has revealed that our memories are constructed:
"current hypotheses suggest that constructive processes allow
individuals to simulate and imagine future episodes, 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." 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) 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.
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 (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) 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.
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. 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. 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. "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." 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. 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. 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 new 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.
Exercise, even at light intensity, significantly improves
memory across all age groups, with the greatest benefits observed in
children and adolescents. Even low- to moderate-intensity exercise and
shorter interventions (1–3 months) can produce meaningful cognitive
improvements.
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 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.
Sex differences
Research on sex differences in episodic memory has
produced mixed findings. A recent meta-analysis revealed a small overall
female advantage, with task-specific variations. Women outperformed men
on cued recall and free recall, while men showed an advantage in
complex span tasks. No sex differences were observed in serial recall or
simple span tasks. Factors such as recall direction, stimulus type,
presentation format, response format, and age accounted for variance in
results. Importantly, no publication bias was detected, although effect
sizes varied by sample source and study reporting. Neuroimaging studies
using activation likelihood estimation (ALE) indicated male > female
activity in the lateral prefrontal cortex, visual regions,
parahippocampal cortex, and cerebellum during long-term memory
retrieval. These findings suggest meaningful sex differences in both behavior and
brain function, highlighting the need for cautious interpretation and
further controlled research.
In plants
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.[155]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.[155]
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 subtropicalwetlands 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. 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. 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. 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. 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. 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. After trap closure, these electrical signals stimulate glandular production of jasmonic acid and hydrolases, allowing for digestion of prey.
Many other plants exhibit the capacity to remember, including Mimosa pudica. 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.
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