Chapter 13. Memory and Learning

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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 Frances Vinall More than two-thirds of young children in Chicago could be exposed to lead-contaminated water, according to an estimate by the Johns Hopkins Bloomberg School of Public Health and the Stanford University School of Medicine. The research, published Monday in the journal JAMA Pediatrics, estimated that 68 percent of children under the age of 6 in Chicago are exposed to lead-contaminated drinking water. Of that group, 19 percent primarily use unfiltered tap water, which was associated with a greater increase in blood lead levels. “The extent of lead contamination of tap water in Chicago is disheartening — it’s not something we should be seeing in 2024,” lead author Benjamin Huynh, assistant professor of environmental health and engineering at the Johns Hopkins Bloomberg School of Public Health, said in a news release. The study suggested that residential blocks with predominantly Black and Hispanic populations were less likely to be tested for lead, but also disproportionately exposed to contaminated water. Gina Ramirez, Midwest regional lead of environmental health for the Natural Resources Defense Council, said she grew up in Chicago drinking bottled water, but now uses filtered water for her own family, because of a generational awareness of “not trusting my tap” to be safe. The study “confirmed my worst fears that children living in vulnerable populations in the city are the most impacted,” she said. “All children deserve to grow up in a healthy city, and to learn that something inside their home is impacting so many kids health and development is a huge wake-up call.”

Keyword: Neurotoxins; Development of the Brain
Link ID: 29207 - 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 Tomasz Nowakowski, Karthik Shekhar Diverse neurons and their equally diverse circuits are the foundation of the brain’s remarkable ability to process information, store memories, regulate behavior and enable conscious thought. High-throughput, single-cell profiling technologies have made it possible to classify these cells more comprehensively than ever before, offering a 360-degree view of the sheer magnitude of neural diversity in the mammalian brain. A recent effort to define the complete set of transcriptomic cell types in the adult whole mouse brain, for example, defined roughly 5,000 distinct cell types distributed across dozens of brain areas. This landmark accomplishment is a critical step toward integrating information about function and connectivity, and extending similar efforts to the adult human brain. But this impressive gestalt conveys little, if any, information about how such diversity arises and develops in the first place. Single-cell atlases developed to date have been limited to a few points in time, focusing largely on the endpoint of neural development. How is this exquisite panoply of neurons generated and organized into precise and orderly circuits that last a lifetime? Providing the answer is the central task of developmental neuroscience. We want to understand the many transitions that unfold — where cells come from, the paths they take, and when terminal cell states emerge. The comprehensive nature of single-cell technologies offers tremendous promise for defining cell types and reconstructing the trajectories of gene expression that underlie their differentiation. Initial efforts to apply these technologies to development, including in the prenatal human brain, hint at the insights these approaches can bring. Single-cell transcriptomics has helped map the diversity of neural progenitor cells, for example, most notably identifying progenitors that are expanded in humans, and their associated molecular adaptations. Further insights into development will require methods that reveal the specific history of every neuron type, including those that can more densely sample brain cells’ trajectories over time and novel approaches for tracking fate transitions in individual cells. These discoveries will in turn help us to understand neurodevelopmental conditions, many of which are associated with genomic variation, and neurological disorders, such as brain tumors. © 2024 Simons Foundation

Keyword: Development of the Brain
Link ID: 29198 - Posted: 03.19.2024

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 Esther Landhuis In January 2023, the US Food and Drug Administration (FDA) approved lecanemab — an antibody medication that decreases β-amyloid protein build-up in the brain — as a treatment for Alzheimer’s disease. Pivotal evidence came from a large, randomized trial of people with early-stage Alzheimer’s, which afflicts around 32 million people worldwide. By the end of that 18-month study1, patients in the placebo group scored on average 1.66 points worse than their performance at baseline on a standard dementia test, which assesses cognitive and functional changes over time through interviews with a patient and their caregiver. The mean score of treated participants, by comparison, worsened by 1.21 points — a 27% slowing of cognitive decline. But is this improvement meaningful for patients and their families? There are two major categories of drugs used to treat Alzheimer’s disease and other progressive conditions: symptomatic drugs, which treat the symptoms, and disease-modifying drugs, which target the root cause. Donepezil and rivastigmine, for example, are symptomatic drugs that boost the activity of chemicals in the brain to compensate for declines in cognitive and memory function caused by Alzheimer’s disease, but they cannot stop its progression. Lecanemab, developed jointly by Japanese pharmaceutical company Eisai and American biotechnology firm Biogen, targets the underlying issue of amyloid build-up in the brain, and in doing so, could fundamentally change the course of the disease. An important feature of disease-modifying drugs is that their benefits are cumulative. Studies of patients with multiple sclerosis, for example, have shown the benefits of starting disease-modifying drugs earlier in the course of the disease compared with later, including improved mortality rates and reduced disability in the long term. Being able to quantify how long a disease-modifying drug can delay or halt the progression of Alzheimer’s disease could change how researchers understand — and communicate — its benefits. © 2024 Springer Nature Limited

Keyword: Alzheimers
Link ID: 29193 - Posted: 03.16.2024

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 Ellen Barry Twins are a bonanza for research psychologists. In a field perpetually seeking to tease out the effects of genetics, environment and life experience, they provide a natural controlled experiment as their paths diverge, subtly or dramatically, through adulthood. Take Dennis and Douglas. In high school, they were so alike that friends told them apart by the cars they drove, they told researchers in a study of twins in Virginia. Most of their childhood experiences were shared — except that Dennis endured an attempted molestation when he was 13. At 18, Douglas married his high school girlfriend. He raised three children and became deeply religious. Dennis cycled through short-term relationships and was twice divorced, plunging into bouts of despair after each split. By their 50s, Dennis had a history of major depression, and his brother did not. Why do twins, who share so many genetic and environmental inputs, diverge as adults in their experience of mental illness? On Wednesday, a team of researchers from the University of Iceland and Karolinska Institutet in Sweden reported new findings on the role played by childhood trauma. Their study of 25,252 adult twins in Sweden, published in JAMA Psychiatry, found that those who reported one or more trauma in childhood — physical or emotional neglect or abuse, rape, sexual abuse, hate crimes or witnessing domestic violence — were 2.4 times as likely to be diagnosed with a psychiatric illness as those who did not. If a person reported one or more of these experiences, the odds of being diagnosed with a mental illness climbed sharply, by 52 percent for each additional adverse experience. Among participants who reported three or more adverse experiences, nearly a quarter had a psychiatric diagnosis of depressive disorder, anxiety disorder, substance abuse disorder or stress disorder. © 2024 The New York Times Company

Keyword: Depression; Genes & Behavior
Link ID: 29184 - Posted: 03.07.2024

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 Veronique Greenwood It can be hard to tell, at first, when a cell is on the verge of self-destruction. It appears to be going about its usual business, transcribing genes and making proteins. The powerhouse organelles called mitochondria are dutifully churning out energy. But then a mitochondrion receives a signal, and its typically placid proteins join forces to form a death machine. They slice through the cell with breathtaking thoroughness. In a matter of hours, all that the cell had built lies in ruins. A few bubbles of membrane are all that remains. “It’s really amazing how fast, how organized it is,” said Aurora Nedelcu, an evolutionary biologist at the University of New Brunswick who has studied the process in algae. Apoptosis, as this process is known, seems as unlikely as it is violent. And yet some cells undergo this devastating but predictable series of steps to kill themselves on purpose. When biologists first observed it, they were shocked to find self-induced death among living, striving organisms. And although it turned out that apoptosis is a vital creative force for many multicellular creatures, to a given cell it is utterly ruinous. How could a behavior that results in a cell’s sudden death evolve, let alone persist? The tools for apoptosis, molecular biologists have found, are curiously widespread. And as they have sought to understand its molecular process and origins, they’ve found something even more surprising: Apoptosis can be traced back to ancient forms of programmed cell death undertaken by single-celled organisms — even bacteria — that seem to have evolved it as a social behavior. © 2024 the Simons Foundation.

Keyword: Apoptosis; Development of the Brain
Link ID: 29181 - 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 Paula Span Determining whether someone has Alzheimer’s disease usually requires an extended diagnostic process. A doctor takes a patient’s medical history, discusses symptoms, administers verbal and visual cognitive tests. The patient may undergo a PET scan, an M.R.I. or a spinal tap — tests that detect the presence of two proteins in the brain, amyloid plaques and tau tangles, both associated with Alzheimer’s. All of that could change dramatically if new criteria proposed by an Alzheimer’s Association working group are widely adopted. Its final recommendations, expected later this year, will accelerate a shift that is already underway: from defining the disease by symptoms and behavior to defining it purely biologically — with biomarkers, substances in the body that indicate disease. The draft guidelines, Revised Criteria for Diagnosis and Staging of Alzheimer’s Disease, call for a simpler approach. That could mean a blood test to indicate the presence of amyloid. Such tests are already available in some clinics and doctors’ offices. “Someone who has biomarker evidence of amyloid in the brain has the disease, whether they’re symptomatic or not,” said Dr. Clifford R. Jack Jr., the chair of the working group and an Alzheimer’s researcher at the Mayo Clinic. “The pathology exists for years before symptom onset,” he added. “That’s the science. It’s irrefutable.” He and his colleagues on the panel do not recommend testing people who have no symptoms of cognitive decline. But skeptics predict that’s likely to happen nonetheless. If so, a sizable proportion would test positive for amyloid and would therefore be diagnosed with Alzheimer’s. A 2015 Dutch study estimated that more than 10 percent of cognitively normal 50-year-olds would test positive, as would almost 16 percent of 60-year-olds and 23 percent of 70-year-olds. Most of those individuals would never develop dementia. © 2024 The New York Times Company

Keyword: Alzheimers
Link ID: 29177 - 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

Fen-Biao Gao Around 55 million people worldwide suffer from dementia such as Alzheimer’s disease. On Feb. 22, 2024, it was revealed that former talk show host Wendy Williams had been diagnosed with frontotemporal dementia, or FTD, a rare type of dementia that typically affects people ages 45 to 64. Bruce Willis is another celebrity who was diagnosed with the syndrome, according to his family. In contrast to Alzheimer’s, in which the major initial symptom is memory loss, FTD typically involves changes in behavior. The initial symptoms of FTD may include changes in personality, behavior and language production. For instance, some FTD patients exhibit inappropriate social behavior, impulsivity and loss of empathy. Others struggle to find words and to express themselves. This insidious disease can be especially hard for families and loved ones to deal with. There is no cure for FTD, and there are no effective treatments. Up to 40% of FTD cases have some family history, which means a genetic cause may run in the family. Since researchers identified the first genetic mutations that cause FTD in 1998, more than a dozen genes have been linked to the disease. These discoveries provide an entry point to determine the mechanisms that underlie the dysfunction of neurons and neural circuits in the brain and to use that knowledge to explore potential approaches to treatment. I am a researcher who studies the development of FTD and related disorders, including the motor neuron disease amyotrophic lateral sclerosis, or ALS. ALS, also known as Lou Gehrig’s disease, results in progressive muscle weakness and death. Uncovering the similarities in pathology and genetics between FTD and ALS could lead to new ways to treat both diseases. Genes contain the instructions cells use to make the proteins that carry out functions essential to life. Mutated genes can result in mutated proteins that lose their normal function or become toxic. © 2010–2024, The Conversation US, Inc.

Keyword: Alzheimers; ALS-Lou Gehrig's Disease
Link ID: 29161 - Posted: 02.25.2024

David Robson Scientific discoveries can emerge from the strangest places. In early 1900s France, the doctor Albert Calmette and the veterinarian Camille Guérin aimed to discover how bovine tuberculosis was transmitted. To do so, they first had to find a way of cultivating the bacteria. Sliced potatoes – cooked with ox bile and glycerine – proved to be the perfect medium. As the bacteria grew, however, Calmette and Guérin were surprised to find that each generation lost some of its virulence. Animals infected with the microbe (grown through many generations of their culture) no longer became sick but were protected from wild TB. In 1921, the pair tested this potential vaccine on their first human patient – a baby whose mother had just died of the disease. It worked, and the result was the Bacille Calmette-Guérin (BCG) vaccine that has saved millions of lives. A black and white image pf Camille Guérin and physician Albert Calmette side by side. French veterinarian Camille Guérin and physician Albert Calmette developed the BCG jab in 1921 using sliced potatoes cooked with ox bile and glycerine. Photograph: Musée Pasteur Calmette and Guérin could have never imagined that their research would inspire scientists investigating an entirely different kind of disease more than a century later. Yet that is exactly what is happening, with a string of intriguing studies suggesting that BCG can protect people from developing Alzheimer’s disease. If these preliminary results bear out in clinical trials, it could be one of the cheapest and most effective weapons in our fight against dementia. According to the World Health Organization, 55 million people now have dementia, with about 10 million new cases each year. Alzheimer’s disease is by far the most common form, accounting for about 60%-70% of cases. It is characterised by clumps of a protein called amyloid beta that accumulate within the brain, killing neurons and destroying the synaptic connections between the cells. © 2024 Guardian News & Media Limited

Keyword: Alzheimers; Neuroimmunology
Link ID: 29160 - Posted: 02.25.2024