Chapter 17. Learning and Memory

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By Diana Kwon Overall, people in U.S. live longer than they did a hundred years ago. The growing number of people reaching old age has meant an increased proportion are at risk of developing dementia or Alzheimer’s disease, illnesses that typically strike later in life. However, researchers have found that, in the U.S. and elsewhere, dementia risk may actually be decreasing, at least in a subset of the population. A new study provides a potential explanation for this trend: Human brains may be getting larger—and thus more resilient to degeneration—over time. Several large population studies in countries including the U.S. and Great Britain have found that, in recent decades, the number of new cases, or incidence, of dementia has declined. Among these is the Framingham Heart Study, which has been collecting data from individuals living in Framingham, Massachusetts since 1948. Now accommodating a third generation of participants, the study includes data from more than 15,000 people. In 2016, Sudha Seshadri, a neurologist at UT Health San Antonio and her colleagues published findings revealing that while the prevalence—the total number of people with dementia—had increased, the incidence had declined since the late 1970s. “That was a piece of hopeful news,” Seshadri says. “It suggested that over 30 years, the average age at which somebody became symptomatic had gone up.” These findings left the team wondering: What was the cause of this reduced dementia risk? While the cardiovascular health of the Framingham residents and their descendants—which can influence the chances of developing dementia—had also improved over the decades, this alone could not fully explain the decline. On top of that, the effect only appeared in people who had obtained a high school diploma, which, according to Seshadri, pointed to the possibility that greater resilience against dementia may result from changes that occur in early life. © 2024 SCIENTIFIC AMERICAN,

Keyword: Development of the Brain; Learning & Memory
Link ID: 29265 - Posted: 04.20.2024

By Bob Holmes Like many of the researchers who study how people find their way from place to place, David Uttal is a poor navigator. “When I was 13 years old, I got lost on a Boy Scout hike, and I was lost for two and a half days,” recalls the Northwestern University cognitive scientist. And he’s still bad at finding his way around. The world is full of people like Uttal — and their opposites, the folks who always seem to know exactly where they are and how to get where they want to go. Scientists sometimes measure navigational ability by asking someone to point toward an out-of-sight location — or, more challenging, to imagine they are someplace else and point in the direction of a third location — and it’s immediately obvious that some people are better at it than others. “People are never perfect, but they can be as accurate as single-digit degrees off, which is incredibly accurate,” says Nora Newcombe, a cognitive psychologist at Temple University who coauthored a look at how navigational ability develops in the 2022 Annual Review of Developmental Psychology. But others, when asked to indicate the target’s direction, seem to point at random. “They have literally no idea where it is.” While it’s easy to show that people differ in navigational ability, it has proved much harder for scientists to explain why. There’s new excitement brewing in the navigation research world, though. By leveraging technologies such as virtual reality and GPS tracking, scientists have been able to watch hundreds, sometimes even millions, of people trying to find their way through complex spaces, and to measure how well they do. Though there’s still much to learn, the research suggests that to some extent, navigation skills are shaped by upbringing. Nurturing navigation skills

Keyword: Learning & Memory
Link ID: 29255 - Posted: 04.13.2024

By Nicole Rust We readily (and reasonably) accept that the causes of memory dysfunction, including Alzheimer’s disease, reside in the brain. The same is true for many problems with seeing, hearing and motor control. We acknowledge that understanding how the brain supports these functions is important for developing treatments for their corresponding dysfunctions, including blindness, deafness and Parkinson’s disease. Applying the analogous assertion to mood—that understanding how the brain supports mood is crucial for developing more effective treatments for mood disorders, such as depression—is more controversial. For brain researchers unfamiliar with the controversy, it can be befuddling. You might hear, “Mental disorders are psychological, not biological,” and wonder, what does that mean, exactly? Experts have diverse opinions on the matter, with paper titles ranging from “Brain disorders? Not really,” to “Brain disorders? Precisely.” Even though a remarkable 21 percent of adults in the United States will experience a mood disorder at some point in their lives, we do not fully understand what causes them, and existing treatments do not work for everyone. How can we best move toward an impactful understanding of mood and mood disorders, with the longer-term goal of helping these people? What, if anything, makes mood fundamentally different from, say, memory? The answer turns out to be complex and nuanced—here, I hope to unpack it. I also ask brain and mind researchers with diverse perspectives to chime in. Among contemporary brain and mind researchers, I have yet to find any whose position is driven by the notion that some force in the universe beyond the brain, like a nonmaterial soul, gives rise to mood. Rather, the researchers generally agree that our brains mediate all mental function. If everyone agrees that both memory and mood disorders follow from things that happen in the brain, why would the former but not the latter qualify as “brain disorders”? © 2024 Simons Foundation

Keyword: Depression; Learning & Memory
Link ID: 29251 - Posted: 04.11.2024

By Markham Heid The human hand is a marvel of nature. No other creature on Earth, not even our closest primate relatives, has hands structured quite like ours, capable of such precise grasping and manipulation. But we’re doing less intricate hands-on work than we used to. A lot of modern life involves simple movements, such as tapping screens and pushing buttons, and some experts believe our shift away from more complex hand activities could have consequences for how we think and feel. “When you look at the brain’s real estate — how it’s divided up, and where its resources are invested — a huge portion of it is devoted to movement, and especially to voluntary movement of the hands,” said Kelly Lambert, a professor of behavioral neuroscience at the University of Richmond in Virginia. Dr. Lambert, who studies effort-based rewards, said that she is interested in “the connection between the effort we put into something and the reward we get from it” and that she believes working with our hands might be uniquely gratifying. In some of her research on animals, Dr. Lambert and her colleagues found that rats that used their paws to dig up food had healthier stress hormone profiles and were better at problem solving compared with rats that were given food without having to dig. She sees some similarities in studies on people, which have found that a whole range of hands-on activities — such as knitting, gardening and coloring — are associated with cognitive and emotional benefits, including improvements in memory and attention, as well as reductions in anxiety and depression symptoms. These studies haven’t determined that hand involvement, specifically, deserves the credit. The researchers who looked at coloring, for example, speculated that it might promote mindfulness, which could be beneficial for mental health. Those who have studied knitting said something similar. “The rhythm and repetition of knitting a familiar or established pattern was calming, like meditation,” said Catherine Backman, a professor emeritus of occupational therapy at the University of British Columbia in Canada who has examined the link between knitting and well-being. © 2024 The New York Times Company

Keyword: Learning & Memory; Stress
Link ID: 29231 - Posted: 04.02.2024

By Marta Zaraska The renowned Polish piano duo Marek and Wacek didn’t use sheet music when playing live concerts. And yet onstage the pair appeared perfectly in sync. On adjacent pianos, they playfully picked up various musical themes, blended classical music with jazz and improvised in real time. “We went with the flow,” said Marek Tomaszewski, who performed with Wacek Kisielewski until Wacek’s death in 1986. “It was pure fun.” The pianists seemed to read each other’s minds by exchanging looks. It was, Marek said, as if they were on the same wavelength. A growing body of research suggests that might have been literally true. Dozens of recent experiments studying the brain activity of people performing and working together — duetting pianists, card players, teachers and students, jigsaw puzzlers and others — show that their brain waves can align in a phenomenon known as interpersonal neural synchronization, also known as interbrain synchrony. “There’s now a lot of research that shows that people interacting together display coordinated neural activities,” said Giacomo Novembre, a cognitive neuroscientist at the Italian Institute of Technology in Rome, who published a key paper on interpersonal neural synchronization last summer. The studies have come out at an increasing clip over the past few years — one as recently as last week — as new tools and improved techniques have honed the science and theory. They’re finding that synchrony between brains has benefits. It’s linked to better problem-solving, learning and cooperation, and even with behaviors that help others at a personal cost. What’s more, recent studies in which brains were stimulated with an electric current hint that synchrony itself might cause the improved performance observed by scientists. © 2024 the Simons Foundation.

Keyword: Attention
Link ID: 29229 - Posted: 03.30.2024

By Jake Buehler Much like squirrels, black-capped chickadees hide their food, keeping track of many thousands of little treasures wedged into cracks or holes in tree bark. When a bird returns to one of their many food caches, a particular set of nerve cells in the memory center of their brains gives a brief flash of activity. When the chickadee goes to another stash, a different combination of neurons lights up. These neural combinations act like bar codes, and identifying them may give key insights into how episodic memories — accounts of specific past events, like what you did on your birthday last year or where you’ve left your wallet — are encoded and recalled in the brain, researchers report March 29 in Cell. This kind of memory is challenging to study in animals, says Selmaan Chettih, a neuroscientist at Columbia University. “You can’t just ask a mouse what memories it formed today.” But chickadees’ very precise behavior provides a golden opportunity for researchers. Every time a chickadee makes a cache, it represents a single, well-defined moment logged in the hippocampus, a structure in the vertebrate brain vital for memory. To study the birds’ episodic memory, Chettih and his colleagues built a special arena made of 128 small, artificial storage sites. The team inserted small probes into five chickadees’ brains to track the electrical activity of individual neurons, comparing that activity with detailed recordings of the birds’ body positions and behaviors. A black-capped chickadee stores sunflower seeds in an artificial arena made of 128 different perches and pockets. These birds excel at finding their hidden food stashes. The aim of the setup was to see how their brain stores and retrieves the memory of each hidey-hole. Researchers closely observed five chickadees, comparing their caching behavior with the activity from nerve cells in their hippocampus, the brain’s memory center. © Society for Science & the Public 2000–2024.

Keyword: Learning & Memory
Link ID: 29228 - Posted: 03.30.2024

By Angie Voyles Askham For Christopher Zimmerman, it was oysters: After a bout of nausea on a beach vacation, he could hardly touch the mollusks for months. For others, that gut-lurching trigger is white chocolate, margaritas or spicy cinnamon candy. Whatever the taste, most people know the feeling of not being able to stomach a food after it has caused—or seemed to cause—illness. That response helps us learn which foods are safe, making it essential for survival. But how the brain links an unpleasant gastric event to food consumed hours prior has long posed a mystery, says Zimmerman, who is a postdoctoral fellow in Ilana Witten’s lab at Princeton University. The time scale for this sort of conditioned food aversion is an order of magnitude different from other types of learning, which involve delays of only a few seconds, says Peter Dayan, director of computational neuroscience at the Max Planck Institute for Biological Cybernetics, who was not involved in the work. “You need to have something that bridges that gap in time” between eating and feeling ill, he says. A newly identified neuronal circuit can do just that. Neurons in the mouse brainstem that respond to drug-induced nausea reactivate a specific subset of cells in the animals’ central amygdala that encode information about a recently tasted food. And that reactivation happens with novel—but not familiar—flavors, according to work that Zimmerman presented at the annual COSYNE meeting in Lisbon last month. With new flavors, animals seem primed to recall a recent meal if they get sick, Zimmerman says. As he put it in his talk, “it suggests that the common phrase we associate with unexpected nausea, that ‘it must be something I ate,’ is literally built into the brain in the form of this evolutionarily hard-wired prior.” © 2024 Simons Foundation

Keyword: Learning & Memory; Evolution
Link ID: 29226 - Posted: 03.30.2024

By Max Kozlov Neurons (shown here in a coloured scanning electron micrograph) mend broken DNA during memory formation. Credit: Ted Kinsman/Science Photo Library When a long-term memory forms, some brain cells experience a rush of electrical activity so strong that it snaps their DNA. Then, an inflammatory response kicks in, repairing this damage and helping to cement the memory, a study in mice shows. The findings, published on 27 March in Nature1, are “extremely exciting”, says Li-Huei Tsai, a neurobiologist at the Massachusetts Institute of Technology in Cambridge who was not involved in the work. They contribute to the picture that forming memories is a “risky business”, she says. Normally, breaks in both strands of the double helix DNA molecule are associated with diseases including cancer. But in this case, the DNA damage-and-repair cycle offers one explanation for how memories might form and last. It also suggests a tantalizing possibility: this cycle might be faulty in people with neurodegenerative diseases such as Alzheimer’s, causing a build-up of errors in a neuron’s DNA, says study co-author Jelena Radulovic, a neuroscientist at the Albert Einstein College of Medicine in New York City. This isn’t the first time that DNA damage has been associated with memory. In 2021, Tsai and her colleagues showed that double-stranded DNA breaks are widespread in the brain, and linked them with learning2. To better understand the part these DNA breaks play in memory formation, Radulovic and her colleagues trained mice to associate a small electrical shock with a new environment, so that when the animals were once again put into that environment, they would ‘remember’ the experience and show signs of fear, such as freezing in place. Then the researchers examined gene activity in neurons in a brain area key to memory — the hippocampus. They found that some genes responsible for inflammation were active in a set of neurons four days after training. Three weeks after training, the same genes were much less active. © 2024 Springer Nature Limited

Keyword: Learning & Memory; Genes & Behavior
Link ID: 29223 - Posted: 03.28.2024

By Ingrid Wickelgren You see a woman on the street who looks familiar—but you can’t remember how you know her. Your brain cannot attach any previous experiences to this person. Hours later, you suddenly recall the party at a friend’s house where you met her, and you realize who she is. In a new study in mice, researchers have discovered the place in the brain that is responsible for both types of familiarity—vague recognition and complete recollection. Both, moreover, are represented by two distinct neural codes. The findings, which appeared on February 20 in Neuron, showcase the use of advanced computer algorithms to understand how the brain encodes concepts such as social novelty and individual identity, says study co-author Steven Siegelbaum, a neuroscientist at the Mortimer B. Zuckerman Mind Brain Behavior Institute at Columbia University. The brain’s signature for strangers turns out to be simpler than the one used for old friends—which makes sense, Siegelbaum says, given the vastly different memory requirements for the two relationships. “Where you were, what you were doing, when you were doing it, who else [was there]—the memory of a familiar individual is a much richer memory,” Siegelbaum says. “If you’re meeting a stranger, there’s nothing to recollect.” The action occurs in a small sliver of a brain region called the hippocampus, known for its importance in forming memories. The sliver in question, known as CA2, seems to specialize in a certain kind of memory used to recall relationships. “[The new work] really emphasizes the importance of this brain area to social processing,” at least in mice, says Serena Dudek, a neuroscientist at the National Institute of Environmental Health Sciences, who was not involved in the study. © 2024 SCIENTIFIC AMERICAN,

Keyword: Attention; Learning & Memory
Link ID: 29222 - Posted: 03.28.2024

By Holly Barker Our understanding of memory is often summed up by a well-worn mantra: Neurons that fire together wire together. Put another way, when two brain cells simultaneously send out an impulse, their synapses strengthen, whereas connections between less active neurons slowly diminish. But there may be more to it, a new preprint suggests: To consolidate memories, synapses may also influence neighboring neurons by using a previously unknown means of communication. When synapses strengthen, they release a virus-like particle that weakens the surrounding cells’ connections, the new work shows. This novel form of plasticity may aid memory by helping some synapses to shout above the background neuronal hubbub, the researchers say. The mechanism involves the neuronal gene ARC, which is known to contribute to learning and memory and encodes a protein that assembles into virus-like capsids—protein shells that viruses use to package and spread their genetic material. ARC capsids enclose ARC messenger RNA and transfer it to nearby neurons, according to a 2018 study. This leads to an increase in ARC protein and, in turn, a decrease in the number of excitatory AMPA receptors at those cells’ synapses, the preprint shows. “ARC has this crazy virus-like biology,” says Jason Shepherd, associate professor of neurobiology at the University of Utah, who led the 2018 study and the new work. But how ARC capsids form and eject from neurons was unclear, he says. As it turns out, synaptic strengthening spurs ARC capsid release, according to the preprint. When neuronal connections strengthen, ARC capsids are packaged into vesicles, which then bubble out of neurons through their interactions with a protein called IRSp53. Surrounding cells absorb the vesicles containing ARC, which tamps down their synapses, the new work suggests. © 2024 Simons Foundation

Keyword: Learning & Memory
Link ID: 29209 - Posted: 03.23.2024

By Shaena Montanari When Nacho Sanguinetti-Scheck came across a seal study in Science in 2023, he saw it as confirmation of the “wild” research he had recently been doing himself. In the experiment, the researchers had attached portable, noninvasive electroencephalogram caps, custom calibrated to sense brain waves through blubber, to juvenile northern elephant seals. After testing the caps on five seals in an outdoor pool, the team attached the caps to eight seals free-swimming in the ocean. The results were striking: In the pool, the seals slept for six hours a day, but in the open ocean, they slept for just about two. And when seals were in REM sleep in the ocean, they flipped belly up and slowly spiraled downward, hundreds of meters below the surface. It was “one of my favorite papers of the past years,” says Sanguinetti-Scheck, a Harvard University neuroscience postdoctoral researcher who studies rodent behavior in the wild. “It’s just beautiful.” It was also the kind of experiment that needed to be done beyond the confines of a lab setting, he says. “You cannot see that in a pool.” Sanguinetti-Scheck is part of a growing cadre of researchers who champion the importance of studying animal behavior in the wild. Studying animals in the environment in which they evolved, these researchers say, can provide neuroscientific insight that is truly correlated with natural behavior. But not everyone agrees. In February, a group of about two dozen scientists and philosophers gathered in snowy, mountainous Terzolas, Italy, to wrestle with what, exactly, “natural behavior” means. “People don’t really think, ‘Well, what does it mean?’” says Mateusz Kostecki, a doctoral student at Nencki Institute of Experimental Biology in Poland. He helped organize the four-day workshop as “a good occasion to think critically about this trend.” © 2024 Simons Foundation

Keyword: Evolution; Sleep
Link ID: 29205 - Posted: 03.21.2024

By Claudia López Lloreda Loss of smell, headaches, memory problems: COVID-19 can bring about a troubling storm of neurological symptoms that make everyday tasks difficult. Now new research adds to the evidence that inflammation in the brain might underlie these symptoms. Not all data point in the same direction. Some new studies suggest that SARS-CoV-2, the virus that causes COVID-19, directly infects brain cells. Those findings bolster the hypothesis that direct infection contributes to COVID-19-related brain problems. But the idea that brain inflammation is key has gotten fresh support: one study, for example, has identified specific brain areas prone to inflammation in people with COVID-191. “The whole body of literature is starting to come together a little bit more now and give us some more concrete answers,” says Nicola Fletcher, a neurovirologist at University College Dublin. Immunological storm When researchers started looking for a culprit for the brain problems caused by COVID-19, inflammation quickly became a key suspect. That’s because inflammation — the flood of immune cells and chemicals that the body releases against intruders — has been linked to the cognitive symptoms caused by other viruses, such as HIV. SARS-CoV-2 stimulates a strong immune response throughout the body, but it was unclear whether brain cells themselves contributed to this response and, if so, how. Helena Radbruch, a neuropathologist at the Charité – Berlin University Medicine, and her colleagues looked at brain samples from people who’d died of COVID-19. They didn’t find any cells infected with SARS-CoV-2. But they did find these people had more immune activity in certain brain areas than did people who died from other causes. This unusual activity was noticeable in regions such as the olfactory bulb, which is involved in smell, and the brainstem, which controls some bodily functions, such as breathing. It was seen only in the brains of people who had died soon after catching the virus. © 2024 Springer Nature Limited

Keyword: Learning & Memory; Attention
Link ID: 29202 - Posted: 03.21.2024

By Julian E. Barnes New studies by the National Institutes of Health failed to find evidence of brain injury in scans or blood markers of the diplomats and spies who suffered symptoms of Havana syndrome, bolstering the conclusions of U.S. intelligence agencies about the strange health incidents. Spy agencies have concluded that the debilitating symptoms associated with Havana syndrome, including dizziness and migraines, are not the work of a hostile foreign power. They have not identified a weapon or device that caused the injuries, and intelligence analysts now believe the symptoms are most likely explained by environmental factors, existing medical conditions or stress. The lead scientist on one of the two new studies said that while the study was not designed to find a cause, the findings were consistent with those determinations. The authors said the studies are at odds with findings from researchers at the University of Pennsylvania, who found differences in brain scans of people with Havana syndrome symptoms and a control group Dr. David Relman, a prominent scientist who has had access to the classified files involving the cases and representatives of people suffering from Havana syndrome, said the new studies were flawed. Many brain injuries are difficult to detect with scans or blood markers, he said. He added that the findings do not dispute that an external force, like a directed energy device, could have injured the current and former government workers. The studies were published in The Journal of the American Medical Association on Monday alongside an editorial by Dr. Relman that was critical of the findings. © 2024 The New York Times Company

Keyword: Learning & Memory; Depression
Link ID: 29196 - Posted: 03.19.2024

By Meghan Rosen Leakiness in the brain could explain the memory and concentration problems linked to long COVID. In patients with brain fog, MRI scans revealed signs of damaged blood vessels in their brains, researchers reported February 22 in Nature Neuroscience. In these people, dye injected into the bloodstream leaked into their brains and pooled in regions that play roles in language, memory, mood and vision. It’s the first time anyone’s shown that long COVID patients can have leaky blood brain barriers, says study coauthor Matthew Campbell, a geneticist at Trinity College Dublin in Ireland. That barrier, tightly knit cells lining blood vessels, typically keeps riffraff out of the brain, like bouncers guarding a nightclub. If the barrier breaks down, bloodborne viruses, cells and other interlopers can sneak into the brain’s tissues and wreak havoc, says Avindra Nath, a neurologist at the National Institutes of Health in Bethesda, Md. It’s too early to say definitively whether that’s happening in people with long COVID, but the new study provides evidence that “brain fog has a biological basis,” says Nath, who wasn’t involved with the work. That alone is important for patients, he says, because their symptoms may be otherwise discounted by physicians. For some people, brain fog can feel like a slowdown in thinking or difficulty recalling short-term memories, Campbell says. For example, “patients will go for a drive, and forget where they’re driving to.” That might sound trivial, he says, but it actually pushes people into panic mode. © Society for Science & the Public 2000–2024.

Keyword: Attention; Learning & Memory
Link ID: 29192 - Posted: 03.16.2024

By Laura Dattaro Steven McCarroll just wanted to compare how different cell types express genes in people with and without schizophrenia. But when he sequenced the transcriptomes of more than 1 million cortical cells from 191 postmortem brains, what leapt out from the data went far beyond his simple case-control comparison: Astrocytes and neurons from all of the brains coordinate their expression of certain genes needed for healthy synapses, a relationship the team dubbed the Synaptic Neuron-and-Astrocyte Program (SNAP) and described in a paper published in Nature today. “The data led us to something much more exciting and surprising than what we set out to do,” says McCarroll, professor of biomedical science and genetics at Harvard Medical School. SNAP is an intricate dance, McCarroll and his colleagues found: The more a person’s neurons express synaptic genes, so too do their astrocytes, but this coordination wanes in older people and those with schizophrenia. Because astrocytes — a type of glial cell — and neurons are in constant communication and the findings are correlational, it’s unclear which cell type choreographs this dance. But other evidence suggests that astrocytes take the lead, says Stephen Quake, professor of bioengineering at Stanford University, who was not involved in McCarroll’s work. In mice trained to fear a foot shock, for example, neurons involved in memory formation express neurotensin, whereas astrocytes express a receptor for it, Quake and his colleagues reported last month in Nature. But when they inhibited the animals’ astrocytes during fear training, the mice performed worse on memory tests, suggesting those cells play an active role in long-term memory formation, Quake says — and govern the relationship McCarroll found. © 2024 Simons Foundation

Keyword: Learning & Memory; Glia
Link ID: 29183 - Posted: 03.07.2024

By Katherine Ellison Jonel Dershem first noticed problems with her memory in 2016 after her breast cancer surgery. She was only 50 and at first blamed the lapses on chemotherapy, and then on her busy, stressful life. So did her husband and friends — and doctor. “I kept blowing it off,” said Dershem, an obstetrician from Voorhees, N.J., whose challenges began with little things like leaving a faucet running and progressed to trouble finishing routine tasks. “I was our family’s primary breadwinner. I didn’t want there to be any serious problems.” In December 2022, nearly seven years after her memory loss began, Dershem was diagnosed with mild cognitive impairment (MCI). Her delayed diagnosis wasn’t unusual, but experts say that needs to change. More than occasional forgetfulness, MCI causes problems that disrupt daily life but don’t make it impossible to function, said Ronald Petersen, director of the Mayo Clinic Alzheimer’s Disease Research Center and the Mayo Clinic Study of Aging. It is often but not always a precursor to dementia, he added. “It’s a subtle condition,” said Petersen, who in 1999 led the first study differentiating patients with MCI from healthy subjects and those with dementia. If you miss a golf date once, no worries, he said, but if “that happened a couple of times last week and people in your family are starting to worry about you — well, that may be MCI.” “With MCI, people can still drive, pay their bills and do their taxes — they just do so less efficiently,” Petersen said. A 2022 study in the journal Alzheimer’s & Dementia projected that 14.4 million people in the United States would have MCI in 2025, and 19.3 million in 2050. An American Academy of Neurology subcommittee estimated that about 1 in 10 people ages 70 to 74 had MCI, and 1 in 4 ages 80 to 84 in 2018.

Keyword: Alzheimers; Learning & Memory
Link ID: 29178 - Posted: 03.05.2024

By Erica Goode Authors don’t get to choose what’s going on in the world when their books are published. More than a few luckless writers ended up with a publication date of Sept. 11, 2001, or perhaps Nov. 8, 2016, the day Donald Trump was elected. But Charan Ranganath, the author of “Why We Remember: Unlocking Memory’s Power to Hold on to What Matters,”was more fortunate. His book went on sale last month, not long after the Department of Justice released a report describing President Joe Biden as an “elderly man with a poor memory” who, in interviews, was “struggling to remember events,” including the year that his son Beau died. BOOK REVIEW — “Why We Remember: Unlocking Memory’s Power to Hold on to What Matters,” by Charan Ranganath (Doubleday, 304 pages). The special counsel’s report immediately became a topic of intense discussion — disputed by the White House, seized on by many Republicans, analyzed by media commentators, and satirized by late-night television hosts. But for Ranganath, a psychologist and neuroscientist at the University of California, Davis, who for decades has been studying the workings of memory, the report’s release was a stroke of luck. His book, which dispels many widespread but wrongheaded assumptions about memory — including some to which that special counsel Robert K. Hur appears to subscribe — could easily have been written as a corrective response. If Ranganath has a central message, it is that we are far too concerned about forgetting. Memory does not work like a recording device, preserving everything we have heard, seen, said, and done. Not remembering names or exact dates; having no recollection of the details of a conversation; being unable to recall where you left your glasses or your keys; or watching movies you saw in the past as if you are seeing them for the first time — these are not the symptoms of a failing brain.

Keyword: Learning & Memory
Link ID: 29172 - Posted: 03.02.2024

By Pam Belluck Long Covid may lead to measurable cognitive decline, especially in the ability to remember, reason and plan, a large new study suggests. Cognitive testing of nearly 113,000 people in England found that those with persistent post-Covid symptoms scored the equivalent of 6 I.Q. points lower than people who had never been infected with the coronavirus, according to the study, published Wednesday in The New England Journal of Medicine. People who had been infected and no longer had symptoms also scored slightly lower than people who had never been infected, by the equivalent of 3 I.Q. points, even if they were ill for only a short time. The differences in cognitive scores were relatively small, and neurological experts cautioned that the results did not imply that being infected with the coronavirus or developing long Covid caused profound deficits in thinking and function. But the experts said the findings are important because they provide numerical evidence for the brain fog, focus and memory problems that afflict many people with long Covid. “These emerging and coalescing findings are generally highlighting that yes, there is cognitive impairment in long Covid survivors — it’s a real phenomenon,” said James C. Jackson, a neuropsychologist at Vanderbilt Medical Center, who was not involved in the study. He and other experts noted that the results were consistent with smaller studies that have found signals of cognitive impairment. The new study also found reasons for optimism, suggesting that if people’s long Covid symptoms ease, the related cognitive impairment might, too: People who had experienced long Covid symptoms for months and eventually recovered had cognitive scores similar to those who had experienced a quick recovery, the study found. © 2024 The New York Times Company

Keyword: Attention; Learning & Memory
Link ID: 29171 - Posted: 02.29.2024

Terry Gross When cognitive neuroscientist Charan Ranganath meets someone for the first time, he's often asked, "Why am I so forgetful?" But Ranganath says he's more interested in what we remember, rather than the things we forget. "We're not designed to carry tons and tons of junk with us. I don't know that anyone would want to remember every temporary password that they've ever had," he says. "I think what [the human brain is] designed for is to carry what we need and to deploy it rapidly when we need it." Ranganath directs the Dynamic Memory Lab at the University of California, Davis, where he's a professor of psychology and neuroscience. In the new book, Why We Remember, he writes about the fundamental mechanisms of memory — and why memories often change over time. Sponsor Message Ranganath recently wrote an op-ed for The New York Times in which he reflected on President Biden's memory gaffes — and the role that memory plays in the current election cycle. "I'm just not in the position to say anything about the specifics of [either Biden or Trump's] memory problems," he says. "This is really more of an issue of people understanding what happens with aging. And, one of the nice things about writing this editorial is I got a lot of feedback from people who felt personally relieved by this because they're worried about their own memories." I think it would be a good idea to have a comprehensive physical and mental health evaluation that's fairly transparent. We certainly have transparency or seek transparency about other things like a candidate's finances, for instance. And obviously health is a very important factor. And I think at the end of the day, we'll still be in a position of saying, "OK, what's enough? What's the line between healthy and unhealthy?" But I think it's important to do because yes, as we get older we do have memory problems. ... © 2024 npr

Keyword: Learning & Memory; Development of the Brain
Link ID: 29166 - Posted: 02.27.2024

Nancy S. Jecker & Andrew Ko Putting a computer inside someone’s brain used to feel like the edge of science fiction. Today, it’s a reality. Academic and commercial groups are testing “brain-computer interface” devices to enable people with disabilities to function more independently. Yet Elon Musk’s company, Neuralink, has put this technology front and center in debates about safety, ethics and neuroscience. In January 2024, Musk announced that Neuralink implanted its first chip in a human subject’s brain. The Conversation reached out to two scholars at the University of Washington School of Medicine – Nancy Jecker, a bioethicst, and Andrew Ko, a neurosurgeon who implants brain chip devices – for their thoughts on the ethics of this new horizon in neuroscience. How does a brain chip work? Neuralink’s coin-size device, called N1, is designed to enable patients to carry out actions just by concentrating on them, without moving their bodies. Subjects in the company’s PRIME study – short for Precise Robotically Implanted Brain-Computer Interface – undergo surgery to place the device in a part of the brain that controls movement. The chip records and processes the brain’s electrical activity, then transmits this data to an external device, such as a phone or computer. The external device “decodes” the patient’s brain activity, learning to associate certain patterns with the patient’s goal: moving a computer cursor up a screen, for example. Over time, the software can recognize a pattern of neural firing that consistently occurs while the participant is imagining that task, and then execute the task for the person. © 2010–2024, The Conversation US, Inc.

Keyword: Robotics; Learning & Memory
Link ID: 29151 - Posted: 02.20.2024