Most Recent Links

Follow us on Facebook or subscribe to our mailing list, to receive news updates. Learn more.


Links 101 - 120 of 28621

By Laurie McGinley ABINGTON, Pa. — Wrapped in a purple blanket, Robert Williford settles into a quiet corner of a bustling neurology clinic, an IV line delivering a colorless liquid into his left arm. The 67-year-old, who has early Alzheimer’s disease, is getting his initial dose of Leqembi. The drug is the first to clearly slow the fatal neurodegenerative ailment that afflicts 6.7 million older Americans, though the benefits may be modest. The retired social worker, one of the first African Americans to receive the treatment, hopes it will ease his forgetfulness so “I drive my wife less crazy.” But as Williford and his doctors embark on this treatment, they are doing so with scant scientific data about how the medication might work in people of color. In the pivotal clinical trial for the drug, Black patients globally accounted for only 47 of the 1,795 participants — about 2.6 percent. For U.S. trial sites, the percentage was 4.5 percent. The proportion of Black enrollees was similarly low for Eli Lilly Alzheimer’s drug, called donanemab, expected to be cleared by the Food and Drug Administration in coming months. Black people make up more than 13 percent of the U.S. population. The paltry data for the new class of groundbreaking drugs, which strip a sticky substance called amyloid beta from the brain, has ignited an intense debate among researchers and clinicians. Will the medications — the first glimmer of hope after years of failure — be as beneficial for African Americans as for White patients? “Are these drugs going to work in non-Whites? And particularly in Blacks? We just don’t have enough data, I don’t think,” said Suzanne E. Schindler, a clinical neurologist and dementia specialist at Washington University in St. Louis.

Keyword: Alzheimers
Link ID: 29122 - Posted: 01.31.2024

By Jyoti Madhusoodanan On July 12, 2015, Elena Daly was packing for a family vacation when she walked into her 16-year-old son’s room and found him unconscious. Her son, Max, had overdosed on opioids, aspirated vomit, and fallen into a coma. By that point, Max had struggled with addiction for about three years. He had tried medication, therapy, and residential treatment programs in France, where the family lives, as well as in the United States and the United Kingdom. In fact, his July relapse occurred just days after returning home from a six-month stint in an in-patient rehab program. The coma lasted three days and worsened a pre-existing movement disorder to a degree where Max was unable to attend high school. “I couldn’t hold a pen without throwing it across the room or hold a cup of coffee without spilling it on myself,” he recently recalled. Max’s struggles with opioid use are not unusual: An estimated 40 to 60 percent of people who have an addiction experience relapse after treatment. Some researchers have suggested that a substantial portion of those who relapse suffer from what might be considered a “treatment-resistant” form of the disorder, though that condition is not formally recognized as a medical diagnosis. In recent years, scientists have explored treating these intractable cases of opioid dependence with deep brain stimulation, an intervention that entails surgically implanting an electrode into a precisely determined region of the brain, where it delivers regular pulses to control problematic electric signals. The surgery has proven effective for neurological conditions such as Parkinson’s disease and essential tremor, a disorder that can cause a person’s limbs, head, trunk, and voice to quake. But for researchers attempting to study its efficacy for addiction, the procedure’s invasiveness and cost — typically in the hundreds of thousands of dollars — have raised steep hurdles. Work in the field has largely been limited to one-off treatments and small studies with one or a few participants, making it tough to ascertain how many people globally have received the treatment or how successful it has been for them.

Keyword: Drug Abuse
Link ID: 29121 - Posted: 01.31.2024

Ashley Montgomery In December 1963, a military family named the Gardners had just moved to San Diego, Calif. The oldest son, 17-year-old Randy Gardner, was a self-proclaimed "science nerd." His family had moved every two years, and in every town they lived in, Gardner made sure to enter the science fair. He was determined to make a splash in the 10th Annual Greater San Diego Science Fair. When researching potential topics, Gardner heard about a radio deejay in Honolulu, Hawaii, who avoided sleep for 260 hours. So Gardner and his two friends, Bruce McAllister and Joe Marciano, set out to beat this record. Randy Gardner spoke to NPR's Hidden Brain host Shankar Vedantam in 2017. When asked about his interest in breaking a sleep deprivation record, Gardner said, "I'm a very determined person, and when I get things under my craw, I can't let it go until there's some kind of a solution." Of his scientific trio, Randy lost the coin toss: He would be the test subject who would deprive himself of sleep. His two friends would take turns monitoring his mental and physical reaction times as well as making sure Gardner didn't fall asleep. The experiment began during their school's winter break on Dec. 28, 1963. Three days into sleeplessness, Gardner said, he experienced nausea and had trouble remembering things. Speaking to NPR in 2017, Gardner said: "I was really nauseous. And this went on for just about the entire rest of the experiment. And it just kept going downhill. I mean, it was crazy where you couldn't remember things. It was almost like an early Alzheimer's thing brought on by lack of sleep." But Gardner stayed awake. The experiment gained the attention of local reporters, which, in Gardner's opinion, was good for the experiment "because that kept me awake," he said. "You know, you're dealing with these people and their cameras and their questions." The news made its way to Stanford, Calif., where a young Stanford sleep researcher named William C. Dement was so intrigued that he drove to San Diego to meet Gardner. © 2024 npr

Keyword: Sleep
Link ID: 29120 - Posted: 01.31.2024

By Gina Kolata Aissam Dam, an 11-year-old boy, grew up in a world of profound silence. He was born deaf and had never heard anything. While living in a poor community in Morocco, he expressed himself with a sign language he invented and had no schooling. Last year, after moving to Spain, his family took him to a hearing specialist, who made a surprising suggestion: Aissam might be eligible for a clinical trial using gene therapy. On Oct. 4, Aissam was treated at the Children’s Hospital of Philadelphia, becoming the first person to get gene therapy in the United States for congenital deafness. The goal was to provide him with hearing, but the researchers had no idea if the treatment would work or, if it did, how much he would hear. The treatment was a success, introducing a child who had known nothing of sound to a new world. “There’s no sound I don’t like,” Aissam said, with the help of interpreters during an interview last week. “They’re all good.” While hundreds of millions of people in the world live with hearing loss that is defined as disabling, Aissam is among those whose deafness is congenital. His is an extremely rare form, caused by a mutation in a single gene, otoferlin. Otoferlin deafness affects about 200,000 people worldwide. The goal of the gene therapy is to replace the mutated otoferlin gene in patients’ ears with a functional gene. Although it will take years for doctors to sign up many more patients — and younger ones — to further test the therapy, researchers said that success for patients like Aissam could lead to gene therapies that target other forms of congenital deafness. © 2024 The New York Times Company

Keyword: Hearing
Link ID: 29119 - Posted: 01.27.2024

James O’Brien for Quanta Magazine In recent decades, neuroscience has seen some stunning advances, and yet a critical part of the brain remains a mystery. I am referring to the cerebellum, so named for the Latin for “little brain,” which is situated like a bun at the back of the brain. This is no small oversight: The cerebellum contains three-quarters of all the brain’s neurons, which are organized in an almost crystalline arrangement, in contrast to the tangled thicket of neurons found elsewhere. Encyclopedia articles and textbooks underscore the fact that the cerebellum’s function is to control body movement. There is no question that the cerebellum has this function. But scientists now suspect that this long-standing view is myopic. Or so I learned in November in Washington, D.C., while attending the Society for Neuroscience annual meeting, the largest meeting of neuroscientists in the world. There, a pair of neuroscientists organized a symposium on newly discovered functions of the cerebellum unrelated to motor control. New experimental techniques are showing that in addition to controlling movement, the cerebellum regulates complex behaviors, social interactions, aggression, working memory, learning, emotion and more. The connection between the cerebellum and movement has been known since the 19th century. Patients suffering trauma to the brain region had obvious difficulties with balance and movement, leaving no doubt that it was critical for coordinating motion. Over the decades, neuroscientists developed a detailed understanding of how the cerebellum’s unique neural circuitry controls motor function. The explanation of how the cerebellum worked seemed watertight. Then, in 1998, in the journal Brain, neurologists reported on wide-ranging emotional and cognitive disabilities in patients with damage to the cerebellum. For example, in 1991, a 22-year-old female college student had fallen while ice skating; a CT scan revealed a tumor in her cerebellum. After it was removed surgically, she was a completely different person. The bright college student had lost her ability to write with proficiency, do mental arithmetic, name common objects or copy a simple diagram. Her mood flattened. She hid under covers and behaved inappropriately, undressing in the corridors and speaking in baby talk. Her social interactions, including recognizing familiar faces, were also impaired.

Keyword: Emotions; Movement Disorders
Link ID: 29118 - Posted: 01.27.2024

By Erin Garcia de Jesús Bruce the kea is missing his upper beak, giving the olive green parrot a look of perpetual surprise. But scientists are the astonished ones. The typical kea (Nestor notabilis) sports a long, sharp beak, perfect for digging insects out of rotten logs or ripping roots from the ground in New Zealand’s alpine forests. Bruce has been missing the upper part of his beak since at least 2012, when he was rescued as a fledgling and sent to live at the Willowbank Wildlife Reserve in Christchurch. The defect prevents Bruce from foraging on his own. Keeping his feathers clean should also be an impossible task. In 2021, when comparative psychologist Amalia Bastos arrived at the reserve with colleagues to study keas, the zookeepers reported something odd: Bruce had seemingly figured out how to use small stones to preen. “We were like, ‘Well that’s weird,’ ” says Bastos, of Johns Hopkins University. Over nine days, the team kept a close eye on Bruce, quickly taking videos if he started cleaning his feathers. Bruce, it turned out, had indeed invented his own work-around to preen, the researchers reported in 2021 in Scientific Reports. First, Bruce selects the proper tool, rolling pebbles around in his mouth with his tongue and spitting out candidates until he finds one that he likes, usually something pointy. Next, he holds the pebble between his tongue and lower beak. Then, he picks through his feathers. “It’s crazy because the behavior was not there from the wild,” Bastos says. When Bruce arrived at Willowbank, he was too young to have learned how to preen. And no other bird in the aviary uses pebbles in this way. “It seems like he just innovated this tool use for himself,” she says. © Society for Science & the Public 2000–2024.

Keyword: Intelligence; Evolution
Link ID: 29117 - Posted: 01.27.2024

By Christian Guay & Emery Brown What does it mean to be conscious? People have been thinking and writing about this question for millennia. Yet many things about the conscious mind remain a mystery, including how to measure and assess it. What is a unit of consciousness? Are there different levels of consciousness? What happens to consciousness during sleep, coma and general anesthesia? As anesthesiologists, we think about these questions often. We make a promise to patients every day that they will be disconnected from the outside world and their inner thoughts during surgery, retain no memories of the experience and feel no pain. In this way, general anesthesia has enabled tremendous medical advances, from microscopic vascular repairs to solid organ transplants. In addition to their tremendous impact on clinical care, anesthetics have emerged as powerful scientific tools to probe questions about consciousness. They allow us to induce profound and reversible changes in conscious states—and study brain responses during these transitions. But one of the challenges that anesthesiologists face is measuring the transition from one state to another. That’s because many of the approaches that exist interrupt or disrupt what we are trying to study. Essentially, assessing the system affects the system. In studies of human consciousness, determining whether someone is conscious can arouse the person being studied—confounding that very assessment. To address this challenge, we adapted a simple approach we call the breathe-squeeze method. It offers us a way to study changes in conscious state without interrupting those shifts. To understand this approach, it helps to consider some insights from studies of consciousness that have used anesthetics. For decades researchers have used electroencephalography (EEG) to observe electrical activity in the brains of people receiving various anesthetics. They can then analyze that activity with EEG readings to characterize patterns that are specific to various anesthetics, so-called anesthetic signatures. © 2024 SCIENTIFIC AMERICAN

Keyword: Consciousness; Sleep
Link ID: 29116 - Posted: 01.27.2024

By Shaena Montanari Around 2012, Jennifer Groh and her colleagues began a series of experiments investigating the effect of eye movements on auditory signals in the brain. It wasn’t until years later that they noticed something curious in their data: In both an animal model and in people, eye movements coincide with ripples across the eardrum. The finding, published in 2018, seemed “weird,” says Groh, professor of psychology and neuroscience at Duke University — and ripe for further investigation. “You can go your whole career never studying something that is anywhere near as beautifully regular and reproducible,” she says. “Signals that are really robust are unlikely to be just random.” A new experiment from Groh’s lab has now taken her observation a step further and suggests the faint sounds — dubbed “eye movement-related eardrum oscillations,” or EMREOs for short — serve to link two sensory systems. The eardrum oscillations contain “clean and precise” information about the direction of eye movements and, according to Groh’s working hypothesis, help animals connect sound with a visual scene. “The basic problem is that the way we localize visual information and the way we localize sounds leads to two different reference frames,” Groh says. EMREOs, she adds, play a part in relating those frames. The brain, and not the eyes, must generate the oscillations, Groh and her colleagues say, because they happen at the same time as eye movements, or sometimes even before. To learn more about the oscillations, the team placed small microphones in the ears of 10 volunteers, who then performed visual tasks while the researchers tracked their eye movements. The group published their results in Proceedings of the National Academy of Sciences in November. © 2024 Simons Foundation

Keyword: Hearing
Link ID: 29115 - Posted: 01.27.2024

Jon Hamilton Scientists know that Black people are at a greater risk for health problems like heart disease, diabetes and Alzheimer's disease than white people. A growing body of research shows that racism in health care and in daily life contributes to these long-standing health disparities for Black communities. Now, some researchers are asking whether part of the explanation involves how racism, across individual interactions and systems, may physically alter the brain. "That could be behaviors like, let's say, a woman clutching her purse as a black man is walking next to her. Or they could be verbal, like someone saying, like... 'I didn't expect you to be so articulate,'" says Negar Fani, a clinical neuroscientist at Emory University who studies people experiencing Posttraumatic Stress Disorder, or PTSD. Recently, Fani has collaborated with Nate Harnett, an assistant professor of psychiatry at Harvard Medical School, to study how the brain responds to traumatic events and extreme stress, including the events and stress related to racism. So how does one go about measuring the impact of zoomed out, societal-scale issues on the individual? Harnett is the first to admit, it's not the simplest task. "It's very difficult for neuroimaging to look specifically at redlining," notes Harnett. But he can—indirectly. For example, Harnett has used inequities in neighborhood resources as a way of tracking or measuring structural racism. "We're able to look at these sort of proxy measures in these outcomes of structural racism and then correlate those with both brain and behavioral responses to stress or trauma and see how they tie with different psychiatric disorders like PTSD," Harnett says. In other research, Harnett and Fani have looked at correlations between racial discrimination and the response to threat in Black women who had experienced trauma. Fani says patients who experience PTSD tend to be more vigilant or show hyperarousal and be startled easily. Fani says their bodies are in a constant state of fight or flight—even when they're in a safe situation. But in patients who've also experienced racial discrimination, Fani says she sees the opposite effect: They show an increased activation in areas related to emotion regulation. In some ways, Fani says this activation can be adaptive. For example, people may experience microaggressions or discrimination at work and need to regulate their emotional response in order to get through the moment. But when people have to utilize this strategy over long periods of time, Fani and Harnett think it may contribute to the degradation they've seen in other areas in the brain. © 2024 npr

Keyword: Stress; Aggression
Link ID: 29114 - Posted: 01.27.2024

By Sara Reardon Lustful male marsupials sacrifice their sleep for weeks to make more time for mating1. The antechinus, an Australian marsupial roughly the size of a gerbil, is a rare example of a mammal that mates during a certain season and never again. Roughly every August, male antechinus enter a three-week breeding frenzy in which they mate with every female they can and then die en masse. “It’s very short, very intense,” says zoologist Erika Zaid at La Trobe University in Melbourne, Australia. Males generally live for only one year; females can live for at least a year longer and produce more than one litter. To find out how males make enough time for sex in their short lives, Zaid and her colleagues trapped ten male and five female dusky antechinus (Antechinus swainsonii) and kept them in separate enclosures so they couldn’t mate. They attached activity monitors to the animals’ collars and collected blood samples to measure biomarkers. The researchers found that captive males, but not females, moved around much more and slept less during breeding season than they did the rest of the year. On average, the males’ sleep time per day was around 20% lower during the breeding season than during the non-breeding season ― and one male’s sleep time per day was more than 50% lower. At the end of breeding season, two of the males died within a few hours of one another. The other eight became sterile. To determine whether sleep loss occurs in the wild, Zaid and her colleagues trapped 38 animals from a related species called agile antechinus (A. agilis) before and during breeding season and measured the animals’ oxalic acid, a chemical in the blood whose levels drop when an animal is short on sleep. Males’ oxalic acid levels fell sharply during the breeding season. Unlike the captive females, wild females showed drops as well, suggesting that males were waking them up for shenanigans. Mysterious death © 2024 Springer Nature Limited

Keyword: Sleep; Sexual Behavior
Link ID: 29113 - Posted: 01.27.2024

By Sandra G. Boodman On the day after Christmas 2021, Abigail Aguilar, 18, and nearly three months pregnant, walked into her mother’s bedroom and in a flat, emotionless voice announced, “Mom, I’m going to slit my throat.” For weeks Quintina Sims had grappled with her daughter’s increasingly bizarre and frightening behavior. Aguilar had also been plagued by unremitting nausea, splitting headaches and weakness so severe her stepfather sometimes had to carry her to the bathroom. Doctors had largely brushed off her symptoms as the normal manifestations of early pregnancy. Aguilar’s threat triggered a cascade of events that would end in a hospital 130 miles south of her Kern County, Calif., home where doctors mobilized in an effort to discover what was making the previously healthy teenager so sick. After treatment after treatment failed, Sims, now 42, would be called upon to make what she called “the hardest decision of my life” — one that appears to have saved her daughter. Aguilar, who will turn 21 in a few weeks, is now working full time as a preschool teacher’s assistant and studying child development at a community college. She remembers very little of her harrowing six-week stay at Loma Linda University Medical Center, but says the months she spent recovering proved to be clarifying. “It made me realize that I had to value my life a lot more,” Aguilar said. “And I learned that my family was always going to be there for me.” An unexpected surprise In the fall of 2021, Aguilar, a recent high school graduate, was living with her grandparents in Los Angeles, working in a movie theater and going to college part time. In October, she discovered she was pregnant; the baby was due in July 2022. “It was a surprise,” she recalled. Aguilar, who was unmarried, struggled with what to do. She decided to have the baby, a decision her mother supported. “At first everything was fine,” Aguilar said.

Keyword: Schizophrenia; Hormones & Behavior
Link ID: 29112 - Posted: 01.23.2024

By Kenna Hughes-Castleberry Crows, ravens and other birds in the Corvidae family have a head for numbers. Not only can they make quantity estimations (as can many other animal species), but they can learn to associate number values with abstract symbols, such as “3.” The biological basis of this latter talent stems from specific number-associated neurons in a brain region called the nidopallium caudolaterale (NCL), a new study shows. The region also supports long-term memory, goal-oriented thinking and number processing. Discovery of the specialized neurons in the NCL “helps us understand the origins of our counting and math capabilities,” says study investigator Andreas Nieder, professor of animal physiology at the University of Tübingen. Until now, number-associated neurons — cells that fire especially frequently in response to an animal seeing a specific number — had been found only in the prefrontal cortex of primates, which shared a common ancestor with corvids some 300 million years ago. The new findings imply that the ability to form number-sign associations evolved independently and convergently in the two lineages. “Studying whether animals have similar concepts or represent numerosity in ways that are similar to what humans do helps us establish when in our evolutionary history these abilities may have emerged and whether these abilities emerge only in species with particular ecologies or social structures,” says Jennifer Vonk, professor of psychology at Oakland University, who was not involved in the new study. Corvids are considered especially intelligent birds, with previous studies showing that they can create and use tools, and may even experience self-recognition. Nieder has studied corvids’ and other animals’ “number sense,” or the ability to understand numerical values, for more than a decade. His previous work revealed specialized neurons in the NCL that recognize and respond to different quantities of items — including the number zero. But he tested the neurons only with simple pictures and signs that have inherent meaning for the crows, such as size. © 2023 Simons Foundation.

Keyword: Intelligence; Evolution
Link ID: 29111 - Posted: 01.23.2024

By Ewen Callaway Researchers have used the protein-structure-prediction tool AlphaFold to identify1 hundreds of thousands of potential new psychedelic molecules — which could help to develop new kinds of antidepressant. The research shows, for the first time, that AlphaFold predictions — available at the touch of a button — can be just as useful for drug discovery as experimentally derived protein structures, which can take months, or even years, to determine. The development is a boost for AlphaFold, the artificial-intelligence (AI) tool developed by DeepMind in London that has been a game changer in biology. The public AlphaFold database holds structure predictions for nearly every known protein. Protein structures of molecules implicated in disease are used in the pharmaceutical industry to identify and improve promising medicines. But some scientists had been starting to doubt whether AlphaFold’s predictions could stand in for gold standard experimental models in the hunt for new drugs. “AlphaFold is an absolute revolution. If we have a good structure, we should be able to use it for drug design,” says Jens Carlsson, a computational chemist at the University of Uppsala in Sweden. Efforts to apply AlphaFold to finding new drugs have been met with considerable scepticism, says Brian Shoichet, a pharmaceutical chemist at the University of California, San Francisco. “There is a lot of hype. Whenever anybody says ‘such and such is going to revolutionize drug discovery’, it warrants some scepticism.” Shoichet counts more than ten studies that have found AlphaFold’s predictions to be less useful than protein structures obtained with experimental methods, such as X-ray crystallography, when used to identify potential drugs in a modelling method called protein–ligand docking. © 2024 Springer Nature Limited

Keyword: Drug Abuse
Link ID: 29110 - Posted: 01.23.2024

By Evelyn Lake Functional MRI (fMRI), though expensive, has many properties of an ideal clinical tool. It’s safe and noninvasive. It is widely available in some countries, and increasingly so on a global scale. Its “blood oxygen level dependent,” or BOLD, signal is altered in people with almost any neurological condition and is rich enough to contain information specific to each person, offering the potential for a personalized approach to medical care across a wide spectrum of neurological conditions. But despite enormous interest and investment in fMRI — and its wide use in basic neuroscience research — it still lacks broad clinical utility; it is mainly employed for surgical planning. For fMRI to inform a wider range of clinical decision-making, we need better ways of deciphering what underlying changes in the brain drive changes to the BOLD signal. If someone with Alzheimer’s disease has an increase in functional connectivity (a measure of synchrony between brain regions), for example, does this indicate that synapses are being lost? Or does it suggest that the brain is forming compensatory pathways to help the person avoid further cognitive decline? Or something else entirely? Depending on the answer, one can imagine different courses of treatment. Put simply, we cannot extract sufficient information from fMRI and patient outcomes alone to determine which scenarios are playing out and therefore what we should do when we observe changes in our fMRI readouts. To better understand what fMRI actually shows, we need to use complementary methodologies, such as the emerging optical imaging tool of wide-field fluorescence calcium imaging. Combining modalities presents significant technical challenges but offers the potential for deeper insights: observing the BOLD signal alongside other signals that report more directly on what is occurring in brain tissue. Using these more direct measurements instead of fMRI in clinical practice is not an option — they are unethical to use in people or invasive, requiring physical or optical access to the brain. © 2023 Simons Foundation.

Keyword: Brain imaging
Link ID: 29109 - Posted: 01.23.2024

Karla Kaun Many people are wired to seek and respond to rewards. Your brain interprets food as rewarding when you are hungry and water as rewarding when you are thirsty. But addictive substances like alcohol and drugs of abuse can overwhelm the natural reward pathways in your brain, resulting in intolerable cravings and reduced impulse control. A popular misconception is that addiction is a result of low willpower. But an explosion of knowledge and technology in the field of molecular genetics has changed our basic understanding of addiction drastically over the past decade. The general consensus among scientists and health care professionals is that there is a strong neurobiological and genetic basis for addiction. As a behavioral neurogeneticist leading a team investigating the molecular mechanisms of addiction, I combine neuroscience with genetics to understand how alcohol and drugs influence the brain. In the past decade, I have seen changes in our understanding of the molecular mechanisms of addiction, largely due to a better understanding of how genes are dynamically regulated in the brain. New ways of thinking about how addictions form have the potential to change how we approach treatment. Each of your brain cells has your genetic code stored in long strands of DNA. For all that DNA to fit into a cell, it needs to be packed tightly. This is achieved by winding the DNA around “spools” of protein called histones. Areas where DNA is unwound contain active genes coding for proteins that serve important functions within the cell. When gene activity changes, the proteins your cells produce also change. Such changes can range from a single neuronal connection in your brain to how you behave. This genetic choreography suggests that while your genes affect how your brain develops, which genes are turned on or off when you are learning new things is dynamic and adapts to suit your daily needs. © 2010–2024, The Conversation US, Inc.

Keyword: Drug Abuse; Epigenetics
Link ID: 29108 - Posted: 01.23.2024

By Mark Johnson There had been early clues, but it was a family game of dominoes around Christmas 2021 that convinced Susan Stewart that something was wrong with her husband. Charlie Stewart, then 75 and retired, struggled to match the dots on different domino tiles. Susan assumed it was a vision problem. Charlie’s memory was fine, and he had no family history of dementia. But months later the Marin County, Calif., couple were shocked to learn that his domino confusion was a sign he had a lesser-known variant of Alzheimer’s disease. For patients with this variant, called posterior cortical atrophy, the disease begins with problems affecting vision rather than memory. The unusual early symptoms mean that thousands of people may go years before receiving the correct diagnosis, experts said. That may change with the first large-scale international study of the condition, published Monday in the journal Lancet Neurology. An international team led by researchers at the University of California at San Francisco studied records of 1,092 PCA patients from 16 countries and found that, on average, the syndrome begins affecting patients at age 59 ― about five to six years earlier than most patients with the more common form of Alzheimer’s. Although the number of patients with PCA has not been established, researchers say that the variant may account for as many as 10 percent of all Alzheimer’s cases; that would put the number of Americans with the condition close to 700,000. “We have a lot of work to do to raise awareness about the syndrome,” said Gil D. Rabinovici, one of the study’s authors and director of the UCSF Alzheimer’s Disease Research Center. “One thing that we found in our large study is that by the time people are diagnosed, they’ve had [the disease] for quite a few years.” The study authors said they hope greater awareness of the syndrome will help doctors diagnose it earlier and will encourage researchers to include patients with PCA in future Alzheimer’s clinical trials. Unusual symptoms delay diagnosis

Keyword: Alzheimers; Vision
Link ID: 29107 - Posted: 01.23.2024

By Mariana Lenharo Neuroscientist Lucia Melloni didn’t expect to be reminded of her parents’ divorce when she attended a meeting about consciousness research in 2018. But, much like her parents, the assembled academics couldn’t agree on anything. The group of neuroscientists and philosophers had convened at the Allen Institute for Brain Science in Seattle, Washington, to devise a way to empirically test competing theories of consciousness against each other: a process called adversarial collaboration. Devising a killer experiment was fraught. “Of course, each of them was proposing experiments for which they already knew the expected results,” says Melloni, who led the collaboration and is based at the Max Planck Institute for Empirical Aesthetics in Frankfurt, Germany. Melloni, falling back on her childhood role, became the go-between. The collaboration Melloni is leading is one of five launched by the Templeton World Charity Foundation, a philanthropic organization based in Nassau, the Bahamas. The charity funds research into topics such as spirituality, polarization and religion; in 2019, it committed US$20 million to the five projects. The aim of each collaboration is to move consciousness research forward by getting scientists to produce evidence that supports one theory and falsifies the predictions of another. Melloni’s group is testing two prominent ideas: integrated information theory (IIT), which claims that consciousness amounts to the degree of ‘integrated information’ generated by a system such as the human brain; and global neuronal workspace theory (GNWT), which claims that mental content, such as perceptions and thoughts, becomes conscious when the information is broadcast across the brain through a specialized network, or workspace. She and her co-leaders had to mediate between the main theorists, and seldom invited them into the same room. Their struggle to get the collaboration off the ground is mirrored in wider fractures in the field. © 2024 Springer Nature Limited

Keyword: Consciousness
Link ID: 29106 - Posted: 01.18.2024

By Holly Barker Sensory issues associated with autism may be caused by fluctuating neuronal noise — the background hum of electrical activity in the brain — according to a new mouse study. Up to 90 percent of autistic people report sensory problems, including heightened sensitivity to sounds or an aversion to certain smells. Yet others barely register sensory cues and may seek out sensations by making loud noises or rocking back and forth. But thinking in terms of hyper- or hyposensitivity may be an oversimplification, says Andreas Frick, lead investigator and research director at INSERM. “It’s becoming clear now that things are a lot more nuanced.” For instance, the brain’s response to visual patterns — measured using electroencephalography (EEG) recordings — varies more between viewings in autistic people than in those without the condition, one study found. And functional MRI has detected similar variability among autistic people, suggesting sensory problems may arise from inconsistent brain responses. In the new study, Frick and his colleagues found variability in the activity of individual neurons in a mouse model of fragile X syndrome, one of the leading causes of autism. That variability in neuronal response maps to fluctuations in the levels of noise in the brain, the study found. Noise within the brain isn’t necessarily a bad thing. In fact, an optimum amount is ideal: a little can give neurons the ‘push’ they might need to fire an action potential, while too much can make it difficult for the brain to distinguish between different stimuli. But in animals modeling fragile X syndrome, noise fluctuates such that they process sensory information less reliably, Frick says. © 2023 Simons Foundation.

Keyword: Autism
Link ID: 29105 - Posted: 01.18.2024

Nicola Davis Science correspondent Breaking up is hard to do, but it seems the brain may have a mechanism to help get over an ex. Researchers studying prairie voles say the rodents, which form monogamous relationships, experience a burst of the pleasure hormone dopamine in their brain when seeking and reuniting with their partner. However, after being separated for a lengthy period, they no longer experience such a surge. “We tend to think of it as ‘getting over a breakup’ because these voles can actually form a new bond after this change in dopamine dynamics – something they can’t do while the bond is still intact,” said Dr Zoe Donaldson, a behavioural neuroscientist at CU Boulder and senior author of the work. Writing in the journal Current Biology, the team describe how they carried out a series of experiments in which voles had to press levers to access either their mate or an unknown vole located on the other side of a see-through door. The team found the voles had a greater release of dopamine in their brain when pressing levers and opening doors to meet their mate than when meeting the novel vole. They also huddled more with their mate on meeting, and experienced a greater rise in dopamine while doing so. Donaldson said: “We think the difference is tied to knowing you are about to reunite with a partner and reflects that it is more rewarding to reunite with a partner than go hang out with a vole they don’t know.” However, these differences in dopamine levels were no longer present after they separated pairs of voles for four weeks – a considerable period in the lifetime of the rodents. Differences in huddling behaviour also decreased. The researchers say the findings suggest a devaluation of the bond between pairs of voles, rather than that they have forgotten each other. © 2024 Guardian News & Media Limited

Keyword: Sexual Behavior; Evolution
Link ID: 29104 - Posted: 01.18.2024

By Jude Coleman When it comes to tail wagging among dogs, some questions still hound researchers. We know that domesticated dogs (Canis familiaris) use their tails to communicate — with other dogs as well as humans — and even what various types of wags mean, researchers note in a new review of the scientific literature. But we don’t know why dogs seem to wag more than other canines or even how much of it is under their control, ethologist Silvia Leonetti and colleagues report January 17 in Biology Letters. “Among all possible animal behavior that humans experience in everyday life, domestic dog tail wagging is one of the most common,” says Leonetti, who is now at the University of Turin in Italy. “But a lot of dog behavior remains a scientific enigma.” So Leonetti and her colleagues pored through previous studies to figure out what elements of tail wagging are understood and which remain mysterious. They also hypothesized about the behavior’s origins: Perhaps tail wagging placates some human need for rhythm, the researchers suggest, or maybe the behavior is a genetic tagalong, a trait tied to others that humans bred into domesticated dogs. “People think wagging tail equals happy dog. But it’s actually a lot more complicated than that,” says Emily Bray, an expert in canine cognition at the University of Arizona in Tucson who was not involved with the work. Understanding why dogs wag their tails is important partly from an animal welfare perspective, she says, as it could help dog owners read their pups’ cues better. One main thing that researchers know about tail wagging is that it’s used predominantly for communication instead of locomotion, like a whale, or swatting away bugs, like a horse. Wagging also means different things depending on how the tail is wagged, such as its height or side-to-side movement. © Society for Science & the Public 2000–2024.

Keyword: Animal Communication; Emotions
Link ID: 29103 - Posted: 01.18.2024