By Abdulrahman Olagunju How does our brain know that “this” follows “that”? Two people meet, fall in love and live happily ever after—or sometimes not. The sequencing of events that takes place in our head—with one thing coming after another—may have something to do with so-called time cells recently discovered in the human hippocampus. The research provides evidence for how our brain knows the start and end of memories despite time gaps in the middle. As these studies continue, the work could lead to strategies for memory restoration or enhancement. The research has focused on “episodic memory,” the ability to remember the “what, where and when” of a past experience, such as the recollection of what you did when you woke up today. It is part of an ongoing effort to identify how the organ creates such memories. A team led by Leila Reddy, a neuroscience researcher at the French National Center for Scientific Research, sought to understand how human neurons in the hippocampus represent temporal information during a sequence of learning steps to demystify the functioning of time cells in the brain. In a study published this summer in the Journal of Neuroscience, Reddy and her colleagues found that, to organize distinct moments of experience, human time cells fire at successive moments during each task. The study provided further confirmation that time cells reside in the hippocampus, a key memory processing center. They switch on as events unfold, providing a record of the flow of time in an experience. “These neurons could play an important role in how memories are represented in the brain,” Reddy says. “Understanding the mechanisms for encoding time and memory will be an important area of research.” © 2021 Scientific American

Keyword: Learning & Memory; Attention
Link ID: 28133 - Posted: 12.31.2021

Sofia Moutinho When Thomas Edison hit a wall with his inventions, he would nap in an armchair while holding a steel ball. As he started to fall asleep and his muscles relaxed, the ball would strike the floor, waking him with insights into his problems. Or so the story goes. Now, more than 100 years later, scientists have repeated the trick in a lab, revealing that the famous inventor was on to something. People following his recipe tripled their chances of solving a math problem. The trick was to wake up in the transition between sleep and wakefulness, just before deep sleep. “It is a wonderful study,” says Ken Paller, a cognitive neuroscientist at Northwestern University who was not part of the research. Prior work has shown that passing through deep sleep stages helps with creativity, he notes, but this is the first to explore in detail the sleep-onset period and its role in problem-solving. In this transitional period, we are not quite awake, but also not deeply asleep. It can be as short as a minute and occurs right when we start to doze off. Our muscles relax, and we have dreamlike visions or thoughts called hypnagogia, generally related to recent experiences. This phase slips by unnoticed most of the time unless it is interrupted by waking. Like Edison, surrealist painter Salvador Dalí believed interrupting sleep’s onset could boost creativity. (He used a heavy key instead of a metal ball.) To see whether Dalí and Edison were right, researchers recruited more than 100 easy sleepers. The team gave them a math test that required them to convert strings of eight digits into new strings of seven by using specific rules in a stepwise manner, such as “repeat the number if the previous and next digit are identical.” The volunteers weren’t told that there was an easier way to get the right answers by following a hidden rule: The second number in their final string was always the same as the last number in the same string. © 2021 American Association for the Advancement of Science.

Keyword: Sleep; Attention
Link ID: 28106 - Posted: 12.11.2021

By Elizabeth Preston A person trying to learn the way around a new neighborhood might spend time studying a map. You would probably not benefit from being carried rapidly through the air, upside-down in the dark. Yet that’s how some baby bats learn to navigate, according to a study published last month in Current Biology. As their mothers tote them on nightly trips between caves and certain trees, the bat pups gain the skills they need to get around when they grow up. Mothers of many bat species carry their young while flying, said Aya Goldshtein, a behavioral ecologist at the Max Planck Institute of Animal Behavior in Konstanz, Germany. Egyptian fruit bats, for example, are attached to their mothers continuously for the first three weeks of life. While a mother searches for food, her pup clings to her body with two feet and its jaw, latching its teeth around her nipple. Mothers can still be seen flying with older pups that weigh 40 percent of what they do. It hadn’t been clear why the moms go to this length, instead of leaving pups in the cave where they roost, as some other species do. Dr. Goldshtein worked with Lee Harten, a behavioral ecologist at Tel Aviv University in Israel, where both she and Dr. Goldshtein were graduate students at the time in the lab of Yossi Yovel, a study co-author, to make sense of this maternal mystery. The researchers captured Egyptian fruit bat mothers and pups from a cave just outside Tel Aviv. They attached a tag holding a radio transmitter and miniature GPS device to each bat’s fur that would drop off after a couple of weeks. Then, the researchers brought the bats back to their cave. To track the bats, Dr. Harten held an antenna while standing on the roof of a 10-story building with a view of the cave. She directed Dr. Goldshtein, who was on foot or in a car with her own antenna, to follow the radio signals of bat pairs as they flew out at night. But again and again, there was a problem: The pup’s movement would suddenly stop, while the mother’s signal disappeared. “At the beginning we thought that we were doing our job wrong, and just losing the bats,” Dr. Harten said. © 2021 The New York Times Company

Keyword: Learning & Memory; Animal Migration
Link ID: 28102 - Posted: 12.08.2021

Alison Abbott There Is Life After the Nobel Prize Eric Kandel Columbia Univ. Press (2021) In 1996, Denise Kandel warned her husband that were he to win the Nobel prize for his pioneering work on memory, then it should be later rather than sooner. Laureates too often turn into socialites, she warned, and stop contributing to the intellectual life of science. Just four years later, Eric Kandel shared the 2000 Nobel Prize in Physiology or Medicine. He was then 71, an age when he could legitimately have rested on his laurels. But resting is not among Kandel’s many strengths. His new book, There Is Life After the Nobel Prize, outlines his achievements of the past couple of decades — numerous enough to dispel Denise’s fears, he writes. It is hard to disagree. The volume adds to Kandel’s respected literary oeuvre, which ranges from neuroscience textbooks to highly original popular science. But it is slight, and feels like a coda. In it, he summarises his post-Nobel research (on learning and memory deficits in addiction, schizophrenia and ageing), writing and public outreach. And he acknowledges colleagues and sponsors of his long career, particularly the Howard Hughes Medical Institute in Chevy Chase, Maryland, and Columbia University in New York City, where he remains a professor and institute director. A fuller and more poignant autobiography can be found in Kandel’s 2006 book In Search of Memory. There, he explains why his traumatic childhood in Austria drew him to study the mechanisms of memory. That book also presents a marvellous history of neuroscience. Making sense Kandel was born in 1929 in Vienna. His family was Jewish and owned a toy shop. When Hitler annexed Austria in 1938, his parents began their year-long effort to emigrate. They finally arrived in New York shortly before the outbreak of World War II, physically unharmed but psychologically traumatized. © 2021 Springer Nature Limited

Keyword: Learning & Memory
Link ID: 28100 - Posted: 12.08.2021

By Pam Belluck AURORA, Ill. — There is sobering evidence of Samantha Lewis’s struggle with long Covid on her bathroom mirror. Above the sink, she has posted a neon pink index card scrawled with nine steps (4. Wet brush 5. Toothpaste) reminding her how to brush and floss her teeth. It is one of many strategies Ms. Lewis, 34, has learned from “cognitive rehab,” an intensive therapy program for Covid-19 survivors whose lives have been upended by problems like brain fog, memory lapses, dizziness and debilitating fatigue. Nearly two years into the pandemic, advances have been made in treating Covid itself, but long Covid — a constellation of lingering health problems that some patients experience — remains little understood. Post-Covid clinics around the country are trying different approaches to help patients desperate for answers, but there is little data on outcomes so far, and doctors say it is too soon to know what might work, and for which patients. While some physical symptoms of long Covid, like shortness of breath or nausea, can be addressed with medication, cognitive issues are more challenging. Few drugs exist, and while some deficits can rebound with time, they can also be exacerbated by resuming activities too soon or intensively. Over several months, The New York Times visited Ms. Lewis, interviewed her doctors, attended her therapy sessions and read her medical records. Before she was infected with the coronavirus in October 2020, experiencing a modest initial illness that did not require hospitalization, she was successfully juggling a demanding, detail-oriented job while raising a child with autism and attention deficit hyperactivity disorder. But this summer, she scored 25 on a 30-point assessment, placing her in a pre-dementia category called mild cognitive impairment. © 2021 The New York Times Company

Keyword: Learning & Memory
Link ID: 28098 - Posted: 12.04.2021

by Charles Q. Choi One injection of a potential new gene therapy for Angelman syndrome forestalls many of the neurodevelopmental condition’s key traits, according to early tests in mice. “While additional pharmacology and safety studies are needed, our viral vector can potentially provide transformative therapeutic relief with a single dose,” says lead investigator Benjamin Philpot, professor of neuroscience at the University of North Carolina at Chapel Hill. Angelman syndrome, which affects about one in 20,000 children, is associated with significant developmental delays and, often, autism. It arises from mutations or deletions in the maternal copy of the UBE3A gene, which encodes a protein that helps regulate the levels of other important proteins. There are no treatments specifically for Angelman syndrome, but several gene therapies are under development. One in clinical trials requires repeat injections in the spine and has shown serious side effects at high doses. These therapies all aim to restore UBE3A function in neurons. One challenge, though, is that neurons produce several variants, or ‘isoforms,’ of the UBE3A protein that vary slightly in length; in mice, for example, neurons make two isoforms in a ratio of about four short forms for every long one. In contrast to other gene therapies, the new one generates short and long forms of the UBE3A protein at nearly the same ratio as is seen in mouse neurons. Such proportions “may be important for therapeutic efficacy,” says Eric Levine, professor of neuroscience at the University of Connecticut in Farmington, who was not involved in this study. © 2021 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 28093 - Posted: 12.01.2021

Anil Ananthaswamy How our brain, a three-pound mass of tissue encased within a bony skull, creates perceptions from sensations is a long-standing mystery. Abundant evidence and decades of sustained research suggest that the brain cannot simply be assembling sensory information, as though it were putting together a jigsaw puzzle, to perceive its surroundings. This is borne out by the fact that the brain can construct a scene based on the light entering our eyes, even when the incoming information is noisy and ambiguous. Consequently, many neuroscientists are pivoting to a view of the brain as a “prediction machine.” Through predictive processing, the brain uses its prior knowledge of the world to make inferences or generate hypotheses about the causes of incoming sensory information. Those hypotheses — and not the sensory inputs themselves — give rise to perceptions in our mind’s eye. The more ambiguous the input, the greater the reliance on prior knowledge. “The beauty of the predictive processing framework [is] that it has a really large — sometimes critics might say too large — capacity to explain a lot of different phenomena in many different systems,” said Floris de Lange, a neuroscientist at the Predictive Brain Lab of Radboud University in the Netherlands. However, the growing neuroscientific evidence for this idea has been mainly circumstantial and is open to alternative explanations. “If you look into cognitive neuroscience and neuro-imaging in humans, [there’s] a lot of evidence — but super-implicit, indirect evidence,” said Tim Kietzmann of Radboud University, whose research lies in the interdisciplinary area of machine learning and neuroscience. All Rights Reserved © 2021

Keyword: Attention; Vision
Link ID: 28080 - Posted: 11.17.2021

Allison Whitten Every time a human or machine learns how to get better at a task, a trail of evidence is left behind. A sequence of physical changes — to cells in a brain or to numerical values in an algorithm — underlie the improved performance. But how the system figures out exactly what changes to make is no small feat. It’s called the credit assignment problem, in which a brain or artificial intelligence system must pinpoint which pieces in its pipeline are responsible for errors and then make the necessary changes. Put more simply: It’s a blame game to find who’s at fault. AI engineers solved the credit assignment problem for machines with a powerful algorithm called backpropagation, popularized in 1986 with the work of Geoffrey Hinton, David Rumelhart and Ronald Williams. It’s now the workhorse that powers learning in the most successful AI systems, known as deep neural networks, which have hidden layers of artificial “neurons” between their input and output layers. And now, in a paper published in Nature Neuroscience in May, scientists may finally have found an equivalent for living brains that could work in real time. A team of researchers led by Richard Naud of the University of Ottawa and Blake Richards of McGill University and the Mila AI Institute in Quebec revealed a new model of the brain’s learning algorithm that can mimic the backpropagation process. It appears so realistic that experimental neuroscientists have taken notice and are now interested in studying real neurons to find out whether the brain is actually doing it. Simons Foundation All Rights Reserved © 2021

Keyword: Learning & Memory
Link ID: 28044 - Posted: 10.20.2021

Jordana Cepelewicz Leaping, scurrying, flying and swimming through their natural habitats, animals compile a mental map of the world around them — one that they use to navigate home, find food and locate other points of vital interest. Neuroscientists have chiseled away at the problem of how animals do this for decades. A crucial piece of the solution is an elegant neural code that researchers uncovered by monitoring the brains of rats in laboratory settings. That landmark discovery was awarded a Nobel Prize in 2014, and many scientists think the code could be a key component of how the brain handles other abstract forms of information. Yet lab animals in a box with a flat floor only need to navigate through two dimensions, and researchers are now finding that extending the lessons of that situation to the real world is full of challenges and pitfalls. In a pair of studies recently published in Nature and Nature Neuroscience, scientists working with bats and rats showed — to their surprise — that the brain encodes 3D spaces very differently from 2D ones, employing a mechanism that they are still struggling to describe and understand. “We expected something else entirely,” said Nachum Ulanovsky, a neurobiologist at the Weizmann Institute of Science in Israel who led the work in Nature and has studied neural representations of 3D spaces for more than 10 years. “We had to reboot our thinking.” The findings suggest that neuroscientists might need to reconsider what they thought they knew about how the brain encodes natural environments and how animals navigate those spaces. The work also hints at the possibility that other cognitive processes, including memory, might operate very differently than researchers have come to believe. Simons Foundation All Rights Reserved © 2021

Keyword: Learning & Memory
Link ID: 28041 - Posted: 10.16.2021

ByRachel Fritts Across North America, hundreds of bird species waste time and energy raising chicks that aren’t their own. They’re the victims of a “brood parasite” called the cowbird, which adds its own egg to their clutch, tricking another species into raising its offspring. One target, the yellow warbler, has a special call to warn egg-warming females when cowbirds are casing the area. Now, researchers have found the females act on that warning 1 day later—suggesting their long-term memories might be much better than thought. “It’s a very sophisticated and subtle behavioral response,” says Erick Greene, a behavioral ecologist at the University of Montana, Missoula, who was not involved in the study. “Am I surprised? I guess I’m more in awe. It’s pretty dang cool.” Birds have been dazzling scientists with their intellects for decades. Western scrub jays, for instance, can remember where they’ve stored food for the winter—and can even keep track of when it will spoil. There’s evidence that other birds might have a similarly impressive ability to remember certain meaningful calls. “Animals are smart in the context in which they need to be smart,” says Mark Hauber, an animal behavior researcher at the University of Illinois, Urbana-Champaign (UIUC), and the Institute of Advanced Studies in Berlin, who co-authored the new study. He wanted to see whether yellow warblers had the capacity to remember their own important warning call known as a seet. Shelby Lawson The birds make the staccato sound of this call only when a cowbird is near. When yellow warbler females hear it, they go back to their nests and sit tight. (It could just as well be called a “seat” call.) But it’s been unclear whether they still remember the warning in the morning. © 2021 American Association for the Advancement of Science.

Keyword: Animal Communication; Learning & Memory
Link ID: 28039 - Posted: 10.16.2021

by Charles Q. Choi Chronic electrical stimulation of the fornix, a bundle of nerve fibers deep in the brain, rescues learning and memory deficits in mice with mutations of the autism-linked gene CDKL5, according to new research. The results support previous work in mice suggesting that electrical jolts to this fiber tract, which links brain regions involved in memory, could help address cognitive problems in multiple models of neurodevelopmental conditions. These animal studies all use deep brain stimulation (DBS), in which electrodes are placed chronically or, in some cases, permanently in specific neuroanatomical regions. In people, severe cognitive impairment, including memory and learning deficits, is a central feature of cyclin-dependent kinase-like 5 (CDKL5) deficiency disorder, which results from mutations that impair production of the CDKL5 protein. Other characteristics include autism traits and epileptic seizures. “Our hope is to help CDKL5 deficiency patients with at least some aspects of their problems — for example, intellectual disability,” says lead investigator Jianrong Tang, associate professor of pediatrics at the Baylor College of Medicine in Houston, Texas. Little is known about how the loss of CDKL5 affects brain circuitry. In the new study, Tang and his colleagues analyzed the brain’s memory center, the hippocampus, in mice with CDKL5 mutations. The connections between neurons there were less flexible, they found, which likely contributed to the animals’ deficits in learning and memory. The mutations also strengthened inhibitory signals in the dentate gyrus, a part of the hippocampus that helps form new memories. © 2021 Simons Foundation

Keyword: Learning & Memory
Link ID: 28038 - Posted: 10.16.2021

Jon Hamilton People who have had a stroke appear to regain more hand and arm function if intensive rehabilitation starts two to three months after the injury to their brain. A study of 72 stroke patients suggests this is a "critical period," when the brain has the greatest capacity to rewire, a team reports in this week's journal PNAS. The finding challenges the current practice of beginning rehabilitation as soon as possible after a stroke and suggests intensive rehabilitation should go on longer than most insurance coverage allows, says Elissa Newport, a co-author of the study and director of the Center for Brain Plasticity and Recovery at Georgetown University Medical Center. Newport was speaking in place of the study's lead author, Dr. Alexander Dromerick, who died after the study was accepted but before it was published. If the results are confirmed with other larger studies, "the clinical protocol for the timing of stroke rehabilitation would be changed," says Li-Ru Zhao, a professor of neurosurgery at Upstate Medical University in Syracuse, N.Y., who was not involved in the research. The study involved patients treated at Medstar National Rehabilitation Hospital in Washington, D.C., most in their 50s and 60s. One of the study participants was Anthony McEachern, who was 45 when he had a stroke in 2017. Just a few hours earlier, McEachern had been imitating Michael Jackson dance moves with his kids. But at home that night he found himself unable stand up. © 2021 npr

Keyword: Stroke; Learning & Memory
Link ID: 28002 - Posted: 09.22.2021

David Kleinfeld My colleagues and I recently found that we were able to train mice to voluntarily increase the size and frequency of seemingly random dopamine impulses in their brains. Conventional wisdom in neuroscience has held that dopamine levels change solely in response to cues from the world outside of the brain. Our new research shows that increases in dopamine can also be driven by internally mediated changes within the brain. Dopamine is a small molecule found in the brains of mammals and is associated with feelings of reward and happiness. In 2014, my colleagues and I invented a new method to measure dopamine in real time in different parts of the brains of mice. Using this new tool, my former thesis student, Conrad Foo, found that neurons in the brains of mice release large bursts of dopamine – called impulses – for no easily apparent reason. This occurs at random times, but on average about once a minute. Pavlov was famously able to train his dogs to salivate at the sound of a bell, not the sight of food. Today, scientists believe that the bell sound caused a release of dopamine to predict the forthcoming reward. If Pavlov’s dogs could control their cue-based dopamine responses with a little training, we wondered if our mice could control their spontaneous dopamine impulses. To test this, our team designed an experiment that rewarded mice if they increased the strength of their spontaneous dopamine impulses. The mice were able to not only increase how strong these dopamine releases were, but also how often they occurred. When we removed the possibility of a reward, the dopamine impulses returned to their original levels. In the 1990s, neuroscientist Wolfram Schultz discovered that an animal’s brain will release dopamine if the animal expects a reward, not just when receiving a reward. This showed that dopamine can be produced in response to the expectation of a reward, not just the reward itself – the aforementioned modern version of Pavlov’s dog. © 2010–2021, The Conversation US, Inc.

Keyword: Drug Abuse; Learning & Memory
Link ID: 27993 - Posted: 09.15.2021

Sophie Fessl The hormone irisin is necessary for the cognitive benefits of exercise in healthy mice and can rescue cognitive decline associated with Alzheimer’s disease, according to a study published August 20 in Nature Metabolism. According to the authors, these results support the hypothesis that irisin undergirds the cognitive benefits of exercise—a link that has been long debated. In addition, this study has “paved the way for thinking whether irisin could be a therapeutic agent against Alzheimer’s disease,” says biologist Steffen Maak with the Leibniz Institute for Farm Animal Biology in Germany, who has been critical of the methods used to study irisin in the past and was not involved in the study. Many studies have found that exercise is good for the brain, but the molecular mechanisms responsible for the cognitive boost have remained elusive. During her postdoctoral studies, neuroscientist Christiane Wrann found that the gene that codes for irisin becomes highly expressed in the brain during exercise—one of the first studies linking irisin with the brain. See “Irisin Skepticism Goes Way Back” When she joined the faculties at Massachusetts General Hospital and Harvard Medical School, she decided to investigate the hormone further. Wrann, who holds a patent related to irisin and is academic cofounder and consultant for Aevum Therapeutics, a company developing drugs that harness the protective molecular mechanisms of exercise to treat neurodegenerative and neuromuscular disorders, began to investigate whether irisin mediates the positive effects of exercise on the brain. © 1986–2021 The Scientist.

Keyword: Learning & Memory; Hormones & Behavior
Link ID: 27985 - Posted: 09.13.2021

By Nicholas Bakalar Many animals are known to use tools, but a bird named Bruce may be one of the most ingenious nonhuman tool inventors of all: He is a disabled parrot who has designed and uses his own prosthetic beak. Bruce is a kea, a species of parrot found only in New Zealand. He is about 9 years old, and when wildlife researchers found him as a baby, he was missing his upper beak, probably because it had been caught in a trap made for rats and other invasive mammals the country was trying to eliminate. This is a severe disability, as kea use their dramatically long and curved upper beaks for preening their feathers to get rid of parasites and to remove dirt and grime. But Bruce found a solution: He has taught himself to pick up pebbles of just the right size, hold them between his tongue and his lower beak, and comb through his plumage with the tip of the stone. Other animals use tools, but Bruce’s invention of his own prosthetic is unique. Researchers published their findings Friday in the journal Scientific Reports. Studies of animal behavior are tricky — the researchers have to make careful, objective observations and always be wary of bias caused by anthropomorphizing, or erroneously attributing human characteristics to animals. “The main criticism we received before publication was, ‘Well, this activity with the pebbles may have been just accidental — you saw him when coincidentally he had a pebble in his mouth,’” said Amalia P.M. Bastos, an animal cognition researcher at the University of Auckland and the study’s lead author. “But no. This was repeated many times. He drops the pebble, he goes and picks it up. He wants that pebble. If he’s not preening, he doesn’t pick up a pebble for anything else.” Dorothy M. Fragaszy, an emerita professor of psychology at the University of Georgia who has published widely on animal behavior but was unacquainted with Bruce’s exploits, praised the study as a model of how to study tool use in animals. © 2021 The New York Times Company

Keyword: Intelligence; Evolution
Link ID: 27984 - Posted: 09.11.2021

Jordana Cepelewicz Faced with a threat, the brain has to act fast, its neurons making new connections to learn what might spell the difference between life and death. But in its response, the brain also raises the stakes: As an unsettling recent discovery shows, to express learning and memory genes more quickly, brain cells snap their DNA into pieces at many key points, and then rebuild their fractured genome later. The finding doesn’t just provide insights into the nature of the brain’s plasticity. It also demonstrates that DNA breakage may be a routine and important part of normal cellular processes — which has implications for how scientists think about aging and disease, and how they approach genomic events they’ve typically written off as merely bad luck. The discovery is all the more surprising because DNA double-strand breaks, in which both rails of the helical ladder get cut at the same position along the genome, are a particularly dangerous kind of genetic damage associated with cancer, neurodegeneration and aging. It’s more difficult for cells to repair double-strand breaks than other kinds of DNA damage because there isn’t an intact “template” left to guide the reattachment of the strands. Yet it’s also long been recognized that DNA breakage sometimes plays a constructive role, too. When cells are dividing, double-strand breaks allow for the normal process of genetic recombination between chromosomes. In the developing immune system, they enable pieces of DNA to recombine and generate a diverse repertoire of antibodies. Double-strand breaks have also been implicated in neuronal development and in helping turn certain genes on. Still, those functions have seemed like exceptions to the rule that double-strand breaks are accidental and unwelcome. All Rights Reserved © 2021

Keyword: Learning & Memory; Epigenetics
Link ID: 27975 - Posted: 09.01.2021

Virginia Morell Goffin’s cockatoos (Cacatua goffiniana) are so smart they’ve been compared to 3-year-old humans. But what 3-year-old has made their own cutlery set? Scientists have observed wild cockatoos, members of the parrot family, crafting the equivalent of a crowbar, an ice pick, and a spoon to pry open one of their favorite fruits. This is the first time any bird species has been seen creating and using a set of tools in a specific order—a cognitively challenging behavior previously known only in humans, chimpanzees, and capuchin monkeys. The work “supports the idea that parrots have a general [type of] intelligence that allows them to innovate creative solutions to the problems they run into in nature,” says Alex Taylor, a biologist who studies New Caledonian crows at the University of Auckland. “[It] establishes this species as one of the avian family’s most proficient wild tool users.” The discovery happened serendipitously when behavioral ecologist Mark O’Hara was working with wild but captive birds in a research aviary on Yamdena Island in Indonesia. “I’d just turned away, and when I looked back, one of the birds was making and using tools,” says O’Hara, of the Messerli Research Institute. “I couldn’t believe my eyes!” The Goffin’s cockatoo is known for being a clever and innovative social learner. In captivity, the birds have solved complex puzzle boxes and invented rakelike tools to retrieve objects. Several other birds, including hyacinth macaws and New Caledonian crows, make and use tools in the wild, often to extract food, but none seems to make a set of tools. For the new study, O’Hara and his colleagues traveled to this cockatoo’s home on Indonesia’s Tanimbar Islands. The birds live high in the tropical forest canopy, making them difficult to observe. The scientists spent almost 900 hours looking up to watch wild cockatoos feed, but didn’t witness tool use.

Keyword: Learning & Memory; Intelligence
Link ID: 27974 - Posted: 09.01.2021

Terry Gross Human beings are programmed to approach pleasure and avoid pain. It's an instinct that dates back millions of years, to a time when people needed to actively seek food, clothing and shelter every day, or risk death. But psychiatrist Anna Lembke says that in today's world, such basic needs are often readily available — which changes the equation. "Living in this modern age is very challenging. ... We're now having to cope with: How do I live in a world in which everything is provided?" Lembke says. "And if I consume too much of it — which my reflexes compel me to do — I'm going to be even more unhappy." Lembke is the medical director of addiction medicine at Stanford University and chief of the Stanford Addiction Medicine Dual Diagnosis Clinic. Her new book, Dopamine Nation, explores the interconnection of pleasure and pain in the brain and helps explain addictive behaviors — not just to drugs and alcohol, but also to food, sex and smart phones. Lembke says that her patients who are struggling with substance abuse often believe their addictions are fueled by depression, anxiety and insomnia. But she maintains that the reverse is often true: Addictions can become the cause of pain — not the relief from it. That's because the behavior triggers, among other things, an initial response of the neurotransmitter dopamine, which floods the brain with pleasure. But once the dopamine wears off, a person is often left feeling worse than before. "They start out using the drug in order to feel good or in order to experience less pain," Lembke says. "Over time, with repeated exposure, that drug works less and less well. But they find themselves unable to stop, because when they're not using, then they're in a state of a dopamine deficit." © 2021 npr

Keyword: Drug Abuse; Learning & Memory
Link ID: 27964 - Posted: 08.28.2021

By Gretchen Reynolds An intriguing new study shows how exercise may bolster brain health. The study was in mice, but it found that a hormone produced by muscles during exercise can cross into the brain and enhance the health and function of neurons, improving thinking and memory in both healthy animals and those with a rodent version of Alzheimer’s disease. Earlier research shows that people produce the same hormone during exercise, and together the findings suggest that moving could alter the trajectory of memory loss in aging and dementia. We have plenty of evidence already that exercise is good for the brain. Studies in both people and animals show that exercise prompts the creation of new neurons in the brain’s memory center and then helps those new cells survive, mature and integrate into the brain’s neural network, where they can aid in thinking and remembering. Large-scale epidemiological studies also indicate that active people tend to be far less likely to develop Alzheimer’s disease and other forms of dementia than people who rarely exercise. But how does working out affect the inner workings of our brains at a molecular level? Scientists have speculated that exercise might directly change the biochemical environment inside the brain, without involving muscles. Alternatively, the muscles and other tissues might release substances during physical activity that travel to the brain and jump-start processes there, leading to the subsequent improvements in brain health. But in that case, the substances would have to be able to pass through the protective and mostly impermeable blood-brain barrier that separates our brains from the rest of our bodies. Those tangled issues were of particular interest a decade ago to a large group of scientists at Harvard Medical School and other institutions. In 2012, some of these researchers, led by Bruce M. Spiegelman, the Stanley J. Korsmeyer Professor of Cell Biology and Medicine at the Dana-Farber Cancer Institute and Harvard Medical School, identified a previously unknown hormone produced in the muscles of lab rodents and people during exercise and then released into the bloodstream. They named the new hormone irisin, after the messenger god Iris in Greek mythology. © 2021 The New York Times Company

Keyword: Learning & Memory; Muscles
Link ID: 27961 - Posted: 08.25.2021

By Paula Span Learning your odds of eventually developing dementia — a pressing concern for many, especially those with a family history of it — requires medical testing and counseling. But what if everyday behavior, like overlooking a couple of credit card payments or habitually braking while driving, could foretell your risk? A spate of experiments is underway to explore that possibility, reflecting the growing awareness that the pathologies underlying dementia can begin years or even decades before symptoms emerge. “Early detection is key for intervention, at the stage when that would be most effective,” said Sayeh Bayat, the lead author of a driving study funded by the National Institutes of Health and conducted at Washington University in St. Louis. Such efforts could help identify potential volunteers for clinical trials, researchers say, and help protect older people against financial abuse and other dangers. In recent years, many once-promising dementia drugs, particularly for Alzheimer’s disease, have failed in trials. One possible reason, researchers say, is that the drugs are administered too late to be helpful. Identifying risks earlier, when the brain has sustained less damage, could create a pool of potential participants with “preclinical” Alzheimer’s disease, who could then test preventive measures or treatments. It could also bring improvements in daily life. “We could support people’s ability to drive longer, and have safer streets for everyone,” Ms. Bayat offered as an example. © 2021 The New York Times Company

Keyword: Alzheimers; Learning & Memory
Link ID: 27959 - Posted: 08.25.2021