Chapter 17. Learning and Memory
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By Sharon Begley, STAT For the first time ever, researchers have managed to reduce people’s risk for dementia — not through a medicine, special diet, or exercise, but by having healthy older adults play a computer-based brain-training game. The training nearly halved the incidence of Alzheimer’s disease and other devastating forms of cognitive and memory loss in older adults a decade after they completed it, scientists reported on Sunday. If the surprising finding holds up, the intervention would be the first of any kind — including drugs, diet, and exercise — to do that. “I think these results are highly, highly promising,” said George Rebok of the Johns Hopkins Bloomberg School of Public Health, an expert on cognitive aging who was not involved in the study. “It’s exciting that this intervention pays dividends so far down the line.” The results, presented at the Alzheimer’s Association International Conference in Toronto, come from the government-funded ACTIVE (Advanced Cognitive Training for Independent and Vital Elderly) study. Starting in 1998, ACTIVE’s 2,832 healthy older adults (average age at the start: 74) received one of three forms of cognitive training, or none, and were evaluated periodically in the years after. In actual numbers, 14 percent of ACTIVE participants who received no training had dementia 10 years later, said psychologist Jerri Edwards of the University of South Florida, who led the study. Among those who completed up to 10 60-to-75-minute sessions of computer-based training in speed-of-processing — basically, how quickly and accurately they can pay attention to, process, and remember brief images on a computer screen — 12.1 percent developed dementia. Of those who completed all 10 initial training sessions plus four booster sessions a few years later, 8.2 percent developed dementia. © 2016 Scientific American
By Tim Page When I returned to California, I brought my diaries into the back yard every afternoon and read them through sequentially, with the hope of learning more about the years before my brain injury. I remembered much of what I’d done professionally, and whatever additional information I needed could usually be found on my constantly vandalized Wikipedia page. Here was the story of an awkward, imperious child prodigy who made his own films and became famous much too early; a music explainer who won a Pulitzer Prize; a driven and obsessive loner whose fascinations led to collaborations with Glenn Gould, Philip Glass and Thomas Pynchon. In 2000, at age 45, I was diagnosed with Asperger’s syndrome. In retrospect, the only surprise is that it took so long. But the diaries offered a more intimate view. Reading them was slow going, and I felt as though my nose was pressed up against the windowpane of my own life. The shaggy-dog accretion of material — phone numbers, long-ago concert dates, coded references to secret loves — all seemed to belong to somebody else. My last clear memory was of a muggy, quiet Sunday morning in July, three months earlier, as I waited for a train in New London, Conn. It was 11:13 a.m., and the train was due to arrive two minutes later. I was contented, proud of my punctuality and expecting an easy ride to New York in the designated “quiet car,” with just enough time to finish whatever book I was carrying. There would be dinner in Midtown with a magical friend, followed by overnight family visits in Baltimore and Washington, and then a flight back to Los Angeles and the University of Southern California, at which point a sabbatical semester would be at an end.
By Tanya Lewis Scientists have made significant progress toward understanding how individual memories are formed, but less is known about how multiple memories interact. Researchers from the Hospital for Sick Children in Toronto and colleagues studied how memories are encoded in the amygdalas of mice. Memories formed within six hours of each other activate the same population of neurons, whereas distinct sets of brain cells encode memories formed farther apart, in a process whereby neurons compete with their neighbors, according to the team’s study, published today (July 21) in Science. “Some memories naturally go together,” study coauthor Sheena Josselyn of the Hospital for Sick Children told The Scientist. For example, you may remember walking down the aisle at your wedding ceremony and, later, your friend having a bit too much to drink at the reception. “We’re wondering about how these memories become linked in your mind,” Josselyn said. When the brain forms a memory, a group of neurons called an “engram” stores that information. Neurons in the lateral amygdala—a brain region involved in memory of fearful events—are thought to compete with one another to form an engram. Cells that are more excitable or have higher expression of the transcription factor CREB—which is critical for the formation of long-term memories—at the time the memory is being formed will “win” this competition and become part of a memory. © 1986-2016 The Scientist
Keyword: Learning & Memory
Link ID: 22467 - Posted: 07.23.2016
By TRIP GABRIEL DO you remember June 27, 2015? If you knew you had been on a sailboat, and that the weather was miserable, and that afterward you had a beer with the other sailors, would you expect to recall — even one year later — at least a few details? I was on that boat, on a blustery Saturday on Long Island Sound. But every detail is missing from my memory, as if snipped out by an overzealous movie editor. The earliest moment I recall from the day is lying in an industrial tube with a kind of upturned colander over my face, fighting waves of claustrophobia. My mind was densely fogged, but I understood that I was in an M.R.I. machine. Someone was scanning my brain. Other hazy scenes followed: being wheeled into a hospital room. My wife, Alice, hovering in the background. A wall clock that read minutes to midnight, an astonishing piece of information. What had happened to the day? Late that night, alone in the room, I noticed two yellow Post-its on the bedside table in Alice’s writing: “You have a condition called transient global amnesia. It will last Hours not DAYS. You’re going to be fine. Your CT scan was clear. You sailed today and drove yourself home,” the note read in part. I had never heard of transient global amnesia, a rare condition in which you are suddenly unable to recall recent events. Its causes are unknown. Unlike other triggers of memory loss, like a stroke or epileptic seizures, the condition is considered harmless, and an episode does not last long. “We don’t understand why it happens,” a neurologist would later tell me. “There are a million theories.” © 2016 The New York Times Company
Keyword: Learning & Memory
Link ID: 22456 - Posted: 07.19.2016
Helen Haste The American psychologist and educationist Jerome Bruner, who has died aged 100, repeatedly challenged orthodoxies and generated novel directions. His elegant, accessible writing reached wide audiences. His colleague Rom Harré described his lectures as inspiring: “He darted all over the place, one topic suggested another and so on through a thrilling zigzag.” To the charge that he was always asking impossible questions, Jerry replied: “They are pretty much impossible, but the search for the impossible is part of what intelligence is about.” He was willing to engage with controversy, both on academic issues and in education politics. Blind at birth because of cataracts, Jerry gained his sight after surgery at the age of two. He credited this for his sense that we actively interpret and organise our world rather than passively react to it – a theme that he continued to develop in different ways. His first work lay in perception, when he resumed research at Harvard after the second world war. He found that children’s judgments of the size of coins and coin-like disks varied: poorer children overestimated the size of the coins. This contributed to the emerging “new look” movement in psychology, involving values, intentions and interpretation in contrast to the then dominant behaviourist focus on passive learning, reward and punishment. His professorship at Harvard came in 1952, and by the middle of the decade a computer metaphor began to influence psychology – the “cognitive revolution”. With Jacqueline Goodnow and George Austin, Jerry published A Study of Thinking (1956). © 2016 Guardian News and Media Limited
By Andy Coghlan There once was a brainy duckling. It could remember whether shapes or colours it saw just after hatching were the same as or different to each other. The feat surprised the researchers, who were initially sceptical about whether the ducklings could grasp such complex concepts as “same” and “different”. The fact that they could suggests the ability to think in an abstract way may be far more common in nature than expected, and not just restricted to humans and a handful of animals with big brains. “We were completely surprised,” says Alex Kacelnik at the University of Oxford, who conducted the experiment along with his colleague Antone Martinho III. Kacelnik and Martinho reasoned that ducklings might be able to grasp patterns relating to shape or colour as part of the array of sensory information they absorb soon after hatching. Doing so would allow them to recognise their mothers and siblings and distinguish them from all others – abilities vital for survival. In ducklings, goslings and other species that depend for survival on following their mothers, newborns learn quickly – a process called filial imprinting. Kacelnik wondered whether this would enable them to be tricked soon after hatching into “following” objects or colours instead of their natural mother, and recognising those same patterns in future. © Copyright Reed Business Information Ltd.
By Tanya Lewis In recent years, research on mammalian navigation has focused on the role of the hippocampus, a banana-shaped structure known to be integral to episodic memory and spatial information processing. The hippocampus’s primary output, a region called CA1, is known to be divided into superficial and deep layers. Now, using two-photon imaging in mice, researchers at Columbia University in New York have found these layers have distinct functions: superficial-layer neurons encode more-stable maps, whereas deep-layer brain cells better represent goal-oriented navigation, according to a study published last week (July 7) in Neuron. “There are lots of catalogued differences in sublayers of pyramidal cells” within the hippocampus, study coauthor Nathan Danielson of Columbia told The Scientist. “The question is, are the principle cells in each subregion doing the same thing? Or is there a finer level of granularity?” For that past few decades, scientists have been chipping away at an explanation of the brain’s “inner GPS.” The 2014 Nobel Prize in Physiology or Medicine honored the discovery of so-called place cells and grid cells in the hippocampus, which keep track of an individual’s location and coordinates in space, respectively. Since then, studies have revealed that neurons in different hippocampal regions have distinct genetic, anatomical, and physiological properties, said Attila Losonczy of Columbia, Danielson’s graduate advisor and a coauthor on the study. © 1986-2016 The Scientist
Keyword: Learning & Memory
Link ID: 22437 - Posted: 07.14.2016
Not much is definitively proven about consciousness, the awareness of one’s existence and surroundings, other than that it’s somehow linked to the brain. But theories as to how, exactly, grey matter generates consciousness are challenged when a fully-conscious man is found to be missing most of his brain. Several years ago, a 44-year-old Frenchman went to the hospital complaining of mild weakness in his left leg. It was discovered then that his skull was filled largely by fluid, leaving just a thin perimeter of actual brain tissue. And yet the man was a married father of two and a civil servant with an IQ of 75, below-average in his intelligence but not mentally disabled. Doctors believe the man’s brain slowly eroded over 30 years due to a build up of fluid in the brain’s ventricles, a condition known as “hydrocephalus.” His hydrocephalus was treated with a shunt, which drains the fluid into the bloodstream, when he was an infant. But it was removed when he was 14 years old. Over the following decades, the fluid accumulated, leaving less and less space for his brain. While this may seem medically miraculous, it also poses a major challenge for cognitive psychologists, says Axel Cleeremans of the Université Libre de Bruxelles.
By Gretchen Reynolds To strengthen your mind, you may first want to exert your leg muscles, according to a sophisticated new experiment involving people, mice and monkeys. The study’s results suggest that long-term endurance exercise such as running can alter muscles in ways that then jump-start changes in the brain, helping to fortify learning and memory. I often have written about the benefits of exercise for the brain and, in particular, how, when lab rodents or other animals exercise, they create extra neurons in their brains, a process known as neurogenesis. These new cells then cluster in portions of the brain critical for thinking and recollection. Even more telling, other experiments have found that animals living in cages enlivened with colored toys, flavored varieties of water and other enrichments wind up showing greater neurogenesis than animals in drab, standard cages. But animals given access to running wheels, even if they don’t also have all of the toys and other party-cage extras, develop the most new brain cells of all. These experiments strongly suggest that while mental stimulation is important for brain health, physical stimulation is even more potent. But so far scientists have not teased out precisely how physical movement remakes the brain, although all agree that the process is bogglingly complex. Fascinated by that complexity, researchers at the National Institutes of Health recently began to wonder whether some of the necessary steps might be taking place far from the brain itself, and specifically, in the muscles, which are the body part most affected by exercise. Working muscles contract, burn fuel and pump out a wide variety of proteins and other substances. The N.I.H. researchers suspected that some of those substances migrated from the muscles into the bloodstream and then to the brain, where they most likely contributed to brain health. © 2016 The New York Times Company
Keyword: Learning & Memory
Link ID: 22429 - Posted: 07.13.2016
By Clare Wilson It is one of life’s great enigmas: why do we sleep? Now we have the best evidence yet of what sleep is for – allowing housekeeping processes to take place that stop our brains becoming overloaded with new memories. All animals studied so far have been found to sleep, but the reason for their slumber has eluded us. When lab rats are deprived of sleep, they die within a month, and when people go for a few days without sleeping, they start to hallucinate and may have epileptic seizures. One idea is that sleep helps us consolidate new memories, as people do better in tests if they get a chance to sleep after learning. We know that, while awake, fresh memories are recorded by reinforcing connections between brain cells, but the memory processes that take place while we sleep have remained unclear. Support is growing for a theory that sleep evolved so that connections in the brain can be pruned down during slumber, making room for fresh memories to form the next day. “Sleep is the price we pay for learning,” says Giulio Tononi of the University of Wisconsin-Madison, who developed the idea. Now we have the most direct evidence yet that he’s right. Tononi’s team measured the size of these connections or synapses in brain slices taken from mice. The synapses in samples taken at the end of a period of sleep were 18 per cent smaller than those in samples taken from before sleep, showing that the synapses between neurons are weakened during slumber. © Copyright Reed Business Information Ltd.
By Andy Coghlan It could be that romantic restaurant, or your favourite park bench. A specific part of the brain seems to be responsible for learning and remembering the precise locations of places that are special to us, research in mice has shown for the first time. Place cells are neurons that help us map our surroundings, and both mice and humans have such cells in the hippocampus – a brain region vital for learning, memory and navigation. Nathan Danielson at Columbia University in New York and his colleagues focused on a part of the hippocampus that feeds signals to the rest of the brain, called CA1. They found that in mice, the CA1 layer where general environment maps are learned and stored is different to the one for locations that have an important meaning. Treadmill test They discovered this by recording brain activity in the two distinct layers of CA1, using mice placed on a treadmill. The treadmill rotated between six distinctive surface materials – including silky ribbons, green pom-pom fabric and silver glitter masking tape. At all times, the mice were able to lick a sensor to try to trigger the release of drinking water. During the first phase of the experiment, however, the sensor only worked at random times. The mice formed generalised maps of their experience on the multi-surfaced treadmill, and the team found that these were stored in the superficial layer of CA1. © Copyright Reed Business Information Ltd.
Keyword: Learning & Memory
Link ID: 22414 - Posted: 07.09.2016
By Louise Whiteley It’s an appealing idea: the notion that understanding the learning brain will tell us how to maximise children’s potential, bypassing the knotty complexities of education research. But promises to replace sociological complexity with biological certainty should always be treated with caution. Hilary and Steven Rose are deeply sceptical of claims that neuroscience can inform education and early intervention policy, and deeply concerned about the use of such claims to support neoliberal agendas. They argue that focusing on the brain encourages a focus on the individual divorced from their social context, and that this is easily aligned with a view of poor achievement as a personal moral failing, rather than a practical consequence of poverty and inequality. Whether or not you end up cheerleading for the book’s political agenda, its deconstruction of faulty claims about how neuroscience translates into the classroom is relevant to anyone interested in education. The authors tear apart the scientific logic of policy documents, interrogate brain-based interventions and dismantle prevalent neuro-myths. One of the book’s meatiest chapters deals with government reports advocating early intervention to increase “mental capital”, and thus reduce the future economic burden of deprived, underachieving brains. As we discover, the neuroscientific foundations of these reports are shaky. For instance, they tend to assume that the more synaptic connections between brain cells the better, and that poor environment in a critical early period permanently reduces the number of synapses. This makes early intervention focusing on the individual child and “poor parenting” seem like the obvious solution. But pruning of synapses is just as important to brain development, and learning involves the continual forming and reforming of synaptic connections. More is not necessarily better. And while an initial explosion in synapses can be irreversibly disrupted by extreme neglect, the evidence just isn’t there yet for extrapolating this to the more common kinds of childhood deprivation that such reports address.
Laura Sanders Feeling good may help the body fight germs, experiments on mice suggest. When activated, nerve cells that help signal reward also boost the mice’s immune systems, scientists report July 4 in Nature Medicine. The study links positive feelings to a supercharged immune system, results that may partially explain the placebo effect. Scientists artificially dialed up the activity of nerve cells in the ventral tegmental area — a part of the brain thought to help dole out rewarding feelings. This activation had a big effect on the mice’s immune systems, Tamar Ben-Shaanan of Technion-Israel Institute of Technology in Haifa and colleagues found. A day after the nerve cells in the ventral tegmental area were activated, mice were infected with E. coli bacteria. Later tests revealed that mice with artificially activated nerve cells had less E. coli in their bodies than mice without the nerve cell activation. Certain immune cells seemed to be ramped up, too. Monocytes and macrophages were more powerful E. coli killers after the nerve cell activation. If a similar effect is found in people, the results may offer a biological explanation for how positive thinking can influence health. |© Society for Science & the Public 2000 - 2016
Jon Hamilton Researchers have identified a substance in muscles that helps explain the connection between a fit body and a sharp mind. When muscles work, they release a protein that appears to generate new cells and connections in a part of the brain that is critical to memory, a team reports Thursday in the journal Cell Metabolism. The finding "provides another piece to the puzzle," says Henriette van Praag, an author of the study and an investigator in brain science at the National Institute on Aging. Previous research, she says, had revealed factors in the brain itself that responded to exercise. The discovery came after van Praag and a team of researchers decided to "cast a wide net" in searching for factors that could explain the well-known link between fitness and memory. They began by looking for substances produced by muscle cells in response to exercise. That search turned up cathepsin B, a protein best known for its association with cell death and some diseases. Experiments showed that blood levels of cathepsin B rose in mice that spent a lot of time on their exercise wheels. What's more, as levels of the protein rose, the mice did better on a memory test in which they had to swim to a platform hidden just beneath the surface of a small pool. The team also found evidence that, in mice, cathepsin B was causing the growth of new cells and connections in the hippocampus, an area of the brain that is central to memory. But the researchers needed to know whether the substance worked the same way in other species. So they tested monkeys, and found that exercise did, indeed, raise circulating levels of cathepsin in the blood. © 2016 npr
by Helen Thompson Young zebra finches (Taeniopygia guttata) learn to sing from a teacher, usually dad. Remembering dad’s tunes may even be hardwired into the birds’ brains. Researchers at the Okinawa Institute of Science and Technology in Japan measured activity in the brains of male juvenile birds listening to recordings of singing adult males, including their fathers. The team focused its efforts on neurons in a part of the brain called the caudomedial nidopallium that’s thought to influence song learning and memory. A subset of neurons in the caudomedial nidopallium lit up in response to songs performed by dad but not those of strangers, the team reports June 21 in Nature Communications. The more baby birds heard songs, the more their neurons responded and the clearer their own songs became. Sleep and a neurotransmitter called GABA influenced this selectivity. The researchers suggest that this particular region of the brain stores song memories as finches learn to sing, and GABA may drive the storage of dad’s songs over others. Researchers played a variety of sounds for young zebra finches: their own song, dad’s song and songs and calls from other adult finches. Over time, their songs became more and more similar to that of their father. |© Society for Science & the Public 2000 - 2016
Laura Sanders If you want to lock new information into your brain, try working up a sweat four hours after first encountering it. This precisely timed trick, described June 16 in Current Biology, comes courtesy of 72 people who learned the location of 90 objects on a computer screen. Some of these people then watched relaxing nature videos, while others worked up a sweat on stationary bikes, alternating between hard and easy pedaling for 35 minutes. This workout came either soon after the cram session or four hours later. Compared with both the couch potatoes and the immediate exercisers, the people who worked out four hours after their learning session better remembered the objects’ locations two days later. The delayed exercisers also had more consistent activity in the brain’s hippocampus, an area important for memory, when they remembered correctly. That consistency indicates that the memories were stronger, Eelco van Dongen of the Donders Institute in the Netherlands and colleagues propose. The researchers don’t yet know how exercise works its memory magic, but they have a guess. Molecules sparked by aerobic exercise, including the neural messenger dopamine and the protein BDNF, may help solidify memories by reorganizing brain cell connections. Citations E. van Dongen et al. Physical exercise performed four hours after learning improves memory retention and increases hippocampal pattern similarity during retrieval. Current Biology. Published online June 16, 2016. doi: 10.1016/j.cub.2016.04.071. © Society for Science & the Public 2000 - 2016
Keyword: Learning & Memory
Link ID: 22330 - Posted: 06.18.2016
By Aleszu Bajak Can the various puzzles and quizzes associated with commercial brain-training games really improve cognitive function — or better yet, stave off cognitive decline? To date, the scientific evidence is murky, but that hasn’t kept companies from trying to cash-in on consumers’ native desire for quick fixes to complex health problems. The most famous among such companies is probably Lumosity, a product of San Francisco-based Lumos Labs, which once marketed its suite of web-based games and mobile apps as being “built on proven neuroscience,” and by encouraging users to “harness your brain’s neuroplasticity and train your way to a brighter life.” Exercising your brain with online brain-training games like Lumosity (above) or Smart Brain Aging sounds like a great idea, but the science is still murky. Exercising your brain with online brain-training games like Lumosity (above) or Smart Brain Aging sounds like a great idea, but the science is still murky. Those claims were among several that attracted the attention of the Federal Trade Commission, which earlier this year filed a complaint against the company. Lumosity was ultimately slapped with $50 million in fines for deceiving consumers — although $48 million of that was reportedly suspended by a district court, because the company was financially unable to pay the full amount. “Lumosity preyed on consumers’ fears about age-related cognitive decline, suggesting their games could stave off memory loss, dementia, and even Alzheimer’s disease,” said Jessica Rich, Director of the FTC’s Bureau of Consumer Protection, in a statement accompanying the settlement. “But Lumosity simply did not have the science to back up its ads.” Copyright 2016 Undark
By Ashley P. Taylor Sleep is known to aid memory and learning. For example, people who learn something, sleep on it, and are tested on the material after they wake up tend to perform better than those who remain awake in the interim. Within that general phenomenon, however, there’s a lot of unexplained variation. University of California, Riverside, sleep researcher Sara Mednick wondered “what else might be going during that sleep period that helps people’s memories,” she told The Scientist. As it turns out, activity of the autonomic nervous system (ANS) explains a large part of this variation, Mednick and colleagues show in a paper published today (June 13) in PNAS. The researchers measured not only the electrical activity of the brain during sleep, but also that of the heart, providing an indicator of ANS activity. They found that the beat-to-beat variation in heart rate accounted for much of the previously unexplained variation in how well people performed on memory and creativity tests following a nap. “There is a good possibility that this additional measure [heart-rate variability] may help account for discrepant findings in the sleep-dependent memory consolidation literature,” sleep and cognition researcher Rebecca Spencer of the University of Massachusetts, Amherst, who was not involved in the work, wrote in an email. “Perhaps we put too large of a focus on sleep physiology from the CNS [central nervous system] and ignore a significant role of the ANS.” © 1986-2016 The Scientist
By Julia Shaw Can you trust your memory? Picture this. You are in a room full of strangers and you are going around introducing yourself. You say your name to about a dozen people, and they say their names to you. How many of these names are you going to remember? More importantly, how many of these names are you going to misremember? Perhaps you call a person you just met John instead of Jack. This kind of thing happens all the time. Now magnify the situation. You are talking to a close friend, and you disclose something important to them, perhaps even something traumatic. You might, for example, say you witnessed the Paris attacks in 2015. But, how can you know for sure that your memory is accurate? Like most people, you probably feel that misremembering someone’s name is totally different from misremembering an important and emotional life event. That you could never forget #JeSuisParis, and will always have stable and reliable memories of such atrocities. I’m sure that is what those who witnessed 9/11, the 7/7 bombings in London or the assassination of JFK also thought. However, when experimenters conduct research on the accuracy of these so-called “flashbulb memories,” they find that many people make grave errors in their recollections of important historical and personal events. And these errors are more than just omissions. © 2016 Scientific American
Keyword: Learning & Memory
Link ID: 22320 - Posted: 06.14.2016
By Sandra G. Boodman Richard McGhee and his family believed the worst was behind them. McGhee, a retired case officer at the Defense Intelligence Agency who lives near Annapolis, had spent six months battling leukemia as part of a clinical trial at MD Anderson Cancer Center in Houston. The experimental chemotherapy regimen he was given had worked spectacularly, driving his blood cancer into a complete remission. But less than nine months after his treatment ended, McGhee abruptly fell apart. He became moody, confused and delusional — even childish — a jarring contrast with the even-keeled, highly competent person he had been. He developed tremors in his arms, had trouble walking and became incontinent. “I was really a mess,” he recalled. Doctors suspected he had developed a rapidly progressive and fatal dementia, possibly a particularly aggressive form of Alzheimer’s disease. If that was the case, his family was told, his life span would be measured in months. Luckily, the cause of McGhee’s precipitous decline proved to be much more treatable — and prosaic — than doctors initially feared. “It’s really a pleasure to see somebody get better so rapidly,” said Michael A. Williams, a professor of neurology and neurosurgery at the University of Washington School of Medicine in Seattle. Until recently, Williams was affiliated with Baltimore’s Sinai Hospital, where he treated McGhee in 2010. “This was a diagnosis waiting to be found.”