Memory (psychology)

B

Biochemistry of Memory

The study of the biochemistry of memory is another exciting scientific enterprise, but one that can only be touched upon here. Scientists estimate that an adult human brain contains about 100 billion neurons. Each of these is connected to hundreds or thousands of other neurons, forming trillions of neural connections. Neurons communicate by chemical messengers called neurotransmitters. An electrical signal travels along the neuron, triggering the release of neurotransmitters at the synapse, the small gap between neurons. The neurotransmitters travel across the synapse and act on the next neuron by binding with protein molecules called receptors. Most scientists believe that memories are somehow stored among the brain’s trillions of synapses, rather than in the neurons themselves.

Scientists who study the biochemistry of learning and memory often focus on the marine snail Aplysia because its simple nervous system allows them to study the effects of various stimuli on specific synapses. A change in the snail’s behavior due to learning can be correlated with a change at the level of the synapse. One exciting scientific frontier is discovering the changes in neurotransmitters that occur at the level of the synapse.

Other researchers have implicated glucose (a sugar) and insulin (a hormone secreted by the pancreas) as important to learning and memory. Humans and other animals given these substances show an improved capacity to learn and remember. Typically, when animals or humans ingest glucose, the pancreas responds by increasing insulin production, so it is difficult to determine which substance contributes to improved performance. Some studies in humans that have systematically varied the amount of glucose and insulin in the blood have shown that insulin may be the more important of the two substances for learning.

Scientists also have examined the influence of genes on learning and memory. In one study, scientists bred strains of mice with extra copies of a gene that helps build a protein called N-methyl-D-aspartate, or NMDA. This protein acts as a receptor for certain neurotransmitters. The genetically altered mice outperformed normal mice on a variety of tests of learning and memory. In addition, other studies have found that chemically blocking NMDA receptors impairs learning in laboratory rats. Future discoveries from genetic and biochemical studies may lead to treatments for memory deficits from Alzheimer’s disease and other conditions that affect memory.

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VIII

Memory Impairment: The Amnesias

Amnesia means loss of memory. There are many different types of amnesias, but they fall into two major classes according to their cause: functional amnesia and organic amnesia. Functional amnesia refers to memory disorders that seem to result from psychological trauma, not an injury to the brain. Organic amnesia involves memory loss caused by specific malfunctions in the brain. Another type of amnesia is infantile amnesia, which refers to the fact that most people lack specific memories of the first few years of their life.

A

Functional Amnesia

Severe psychological trauma can sometimes cause functional amnesia. People with functional amnesia seem to have nothing physically wrong with their brain, even though the traumatic event presumably affects their brain in some way. In dissociative amnesia (sometimes called limited amnesia), a person loses memory of some important past experiences. For example, a person victimized by a crime may lose his or her memory for the event. Soldiers returning from battle sometimes experience similar symptoms.

Another type of functional amnesia is dissociative fugue, also referred to as functional retrograde amnesia. People with this disorder have much more extensive forgetting that may obscure their whole past. They commonly forget their personal identity and personal memories, and they often unexpectedly wander away from home. Typically the fugue state ends by itself within a few days or weeks. Often, after recovery the individual fails to remember anything that occurred during the fugue state.

Dissociative identity disorder, also called multiple personality disorder, is a type of amnesia in which a person appears to have two or more distinct personal identities. These identities alternate in their control of the individual’s conscious experiences, thoughts, and actions. In many cases, the person’s primary identity cannot recall what happened while the individual was controlled by another identity.

Although functional amnesias are a recurrent theme of television shows and movies, relatively few well-documented cases exist in the scientific literature. Most experts believe that these conditions do exist, but that they are exceedingly rare.

B

Organic Amnesia

Organic amnesia refers to any traumatic forgetting that is produced by specific brain damage. Typically, these amnesias occur as part of brain disorders caused by tumors, strokes, head trauma, or degenerative diseases, such as Alzheimer’s disease. However, certain psychoactive drugs (drugs affecting mood or behavior) can cause amnesia, as can certain dietary deficiencies and electroconvulsive therapy for depression. Organic amnesias may be temporary or permanent. Amnesia resulting from a mild concussion or from electroconvulsive therapy is usually temporary, whereas severe head injuries may lead to permanent memory loss.

The case of the patient H.M., described earlier in this article, is an example of organic amnesia. In 1953 brain surgery for epilepsy left H.M. with dramatic anterograde amnesia, meaning he was unable to remember new information and events that occurred after his operation. Somewhat surprisingly, this severe impairment in the ability to learn new information was accompanied by no detectable impairment in his general intellectual ability or in his ability to use or understand language. H.M. also showed some retrograde amnesia, or inability to remember events before the onset of the surgery. For example, he could not recall that his favorite uncle had died three years earlier. Still, most of his general knowledge was intact, and he performed well on a test of famous faces (of people who had become famous prior to 1950).

Studies of H.M. and other amnesic patients have provided surprising insights into the workings of memory. One remarkable finding is that even though H.M. had severe anterograde amnesia, he (and other amnesic patients like him) still performed normally on tests of implicit memory. For example, H.M. could learn new motor skills, even though he would have no conscious memory of doing so. Even in dense, or severe, amnesias, not all memory abilities are impaired. For more information on implicit memory, see the Implicit Memory section of this article.

Korsakoff’s syndrome, also called Korsakoff’s psychosis, is a disorder that produces severe and often permanent amnesia. In this condition, years of chronic alcoholism and thiamine (vitamin B₁) deficiency cause brain damage, particularly to the thalamus, which helps process sensory information, and to the mammillary bodies, which lie beneath the thalamus. Some patients also have damage to the cortex and cerebellum. Korsakoff’s patients show severe anterograde amnesia, or difficulty learning anything new. In addition, most suffer from retrograde amnesia ranging from mild to severe and typically cannot remember recent experiences. The condition is also associated with other intellectual deficits, such as confusion and disorientation. Korsakoff’s syndrome is named after Sergei Korsakov (Korsakoff), the Russian neurologist who first described it in the late 19th century.

Amnesia also occurs in Alzheimer’s disease, a condition in which the neurons in the brain gradually degenerate, hindering brain function. Damage to the hippocampus and frontal lobes impairs memory. Many other types of organic amnesias exist. For example, in large doses, most depressant drugs can cause acute loss of memory. With severe alcohol or marijuana intoxication, people often forget events that occurred while under influence of the drug.

C

Infantile Amnesia

Infantile amnesia, also called childhood amnesia, refers to the fact that people can remember very little about the first few years of their life. Surveys have shown that most people report their earliest memory to be between their third and fourth birthdays. Furthermore, people’s memories of childhood generally do not become a continuous narrative until after about seven years of age.

Psychologists do not know what causes infantile amnesia, but they have several theories. One view is that brain structures critical to memory are too immature during the first few years of life to record long-term memories. Another theory is that children cannot remember events that occurred before they mastered language. In this view, language provides a system of symbolic representation by which people develop narrative stories of their lives. Such a narrative framework may be necessary for people to remember autobiographical events in a coherent context.

The phenomenon of infantile amnesia does not mean that infants and young children cannot learn. After all, babies learn to stand, walk, and talk. Scientific evidence indicates that even young infants can learn and retain information well. For example, one experiment found that three-month-old babies could learn that kicking their legs moves a mobile over their crib. Up to a month later, the babies could still demonstrate their knowledge that kicking moved the mobile. Infants and toddlers seem to retain implicit memories of their experiences.