By Emily Cataneo It’s 1922. You’re a scientist presented with a hundred youths who, you’re told, will grow up to lead conventional adult lives — with one exception. In 40 years, one of the one hundred is going to become impulsive and criminal. You run blood tests on the subjects and discover nothing that indicates that one of them will go off the rails in four decades. And yet sure enough, 40 years later, one bad egg has started shoplifting and threatening strangers. With no physical evidence to explain his behavior, you conclude that this man has chosen to act out of his own free will. Now, imagine the same experiment starting in 2022. This time, you use the blood samples to sequence everyone’s genome. In one, you find a mutation that codes for something called tau protein in the brain and you realize that this individual will not become a criminal in 40 years out of choice, but rather due to dementia. It turns out he did not shoplift out of free will, but because of physical forces beyond his control. Now, take the experiment a step further. If a man opens fire in an elementary school and kills scores of children and teachers, should he be held responsible? Should he be reviled and punished? Or should observers, even the mourning families, accept that under the right circumstances, that shooter could have been them? Does the shooter have free will while the man with dementia does not? Can you explain why? These provocative, even disturbing questions about similar scenarios underlie two new books about whether humans have control over our personalities, opinions, actions, and fates. “Free Agents: How Evolution Gave Us Free Will,” by professor of genetics and neuroscience Kevin J. Mitchell, and “Determined: A Science of Life Without Free Will,” by biology and neurology professor Robert M. Sapolsky, both undertake the expansive task of using the tools of science to probe the question of whether we possess free will, a question with stark moral and existential implications for the way we structure human society.

Keyword: Consciousness
Link ID: 29009 - Posted: 11.18.2023

By Tina Hesman Saey WASHINGTON — Scientists have uncovered a clue about why it takes so long for Huntington’s disease to develop. And they may have a lead on how to stop the fatal brain disease. Huntington’s is caused by a mistakenly repeated bit of a gene called HTT. Until recently, researchers thought the number of repeats a person is born with doesn’t change, though repeats may expand when passed to future generations. But in some brain cells, the repeats can grow over time to hundreds of copies, geneticist Bob Handsaker reported November 2 at the annual meeting of the American Society of Human Genetics. Once the number of repeats passes a certain point, the activity of thousands of other genes in the brain cells changes drastically, leading the cells to die. These findings suggest that adding repeats to the HTT gene in vulnerable brain cells is what is driving Huntington’s disease, says Handsaker, of the Broad Institute of MIT and Harvard in Cambridge, Mass. The research also suggests that preventing the repeats from growing may stop the development of the disease. The new work gives “serious insight into the disease mechanism,” says Russell Snell, a geneticist at the University of Auckland in New Zealand who was not involved in the work. About 41,000 people in the United States have symptomatic Huntington’s disease, and another 200,000 are at risk of developing it. Inheriting just one copy of a repeat-riddled HTT gene produces symptoms. Even though individuals are born with the disease-causing gene, symptoms don’t usually appear until people are in their 30s to 50s. Those symptoms include depression, mood swings, forgetfulness, balance problems, involuntary movements and slurred speech. Eventually, a person with the disease may be paralyzed and can die from complications such as pneumonia or heart failure. © Society for Science & the Public 2000–2023.

Keyword: Huntingtons
Link ID: 29008 - Posted: 11.15.2023

Sean O'Donnell Human-driven climate change is increasingly shaping the Earth’s living environments. Rising temperatures, rapid shifts in rainfall and seasonality, and ocean acidification are presenting altered environments to many animal species. How do animals adjust to these new, often extreme, conditions? Animal nervous systems play a central role in both enabling and limiting how they respond to changing climates. Two of my main research interests as a biologist and neuroscientist involve understanding how animals accommodate temperature extremes and identifying the forces that shape the structure and function of animal nervous systems, especially brains. The intersection of these interests led me to explore the effects of climate on nervous systems and how animals will likely respond to rapidly shifting environments. All major functions of the nervous system – sense detection, mental processing and behavior direction – are critical. They allow animals to navigate their environments in ways that enable their survival and reproduction. Climate change will likely affect these functions, often for the worse. Changing temperatures shift the energy balance of ecosystems – from plants that produce energy from sunlight to the animals that consume plants and other animals – subsequently altering the sensory worlds that animals experience. It is likely that climate change will challenge all of their senses, from sight and taste to smell and touch. Animals like mammals perceive temperature in part with special receptor proteins in their nervous systems that respond to heat and cold, discriminating between moderate and extreme temperatures. These receptor proteins help animals seek appropriate habitats and may play a critical role in how animals respond to changing temperatures.

Keyword: Biological Rhythms
Link ID: 29007 - Posted: 11.15.2023

By Sean Cummings If a bite of dandelion greens or extra-dark chocolate makes you pucker, there’s good reason. Bitterness can indicate the presence of toxins in potential foods, and animals long ago honed the ability to ferret out harsh tastes. But the ability to sense bitterness may be even older than many presumed, a new study finds. It likely first evolved in vertebrates roughly 460 million years ago, when sharks and other cartilaginous fishes separated from bony vertebrates like ourselves, researchers report today in the Proceedings of the National Academy of Sciences. The bitter taste receptor identified in a pair of shark species may mirror a sort of all-purpose bitterness detector that our common ancestor possessed. “Given how quickly taste receptors change, to have this one receptor conserved over 460 million years, that’s pretty astounding,” says Craig Montell, a neurobiologist at the University of California, Santa Barbara who was not involved in the study. “The ability to react to the particular bitter chemicals that activate it must be really important.” Humans and other bony vertebrates experience bitterness thanks to taste 2 receptors, or T2Rs, which are proteins that transmit taste information to the brain. But scientists had never found T2Rs in cartilaginous vertebrates such as sharks and rays. That led many to assume these receptors had evolved after their lineage split from the bony vertebrates. Yet sharks and other cartilaginous fish do have smell receptors closely related to bitter taste receptors. That made Sigrun Korsching, a neurobiologist at the University of Cologne, wonder: Could bitter taste perception be even older than most believed? To find out, she and colleagues examined 17 genomes from various species of sharks, skates, and sawfish. Twelve of these had genes that coded for taste receptors similar to T2Rs, which they dubbed T2R1s. In the lab, the researchers implanted genes for these receptors from two of the species—bamboo sharks and catsharks—into human kidney cells, then exposed them to 94 bitter substances. These included resveratrol, found in foods such as grapes, peanuts, and cranberries, and amarogentin, a compound from the gentian plant considered one of the most astringent tastes in the world.

Keyword: Chemical Senses (Smell & Taste); Evolution
Link ID: 29006 - Posted: 11.15.2023

By Jocelyn Solis-Moreira When the alarm goes off in the early morning, it’s tempting to hit the snooze button and curl back under the warm covers for a few more minutes of slumber. This repeated postponing of the buzzer is often thought of as a bad habit—one that creates not only a lazy start to a day but also a fragmented sleep pattern that’s detrimental to health. Now, however, a growing body of recent research is contradicting this notion. A new study published in the Journal of Sleep Research found that people who regularly press the snooze button lost only about six minutes of sleep per night—and that it didn’t affect their morning sleepiness or mood. In fact, tests showed that it actually improved cognition. This adds to research in 2022 that also found chronic snoozers generally felt no sleepier than nonsnoozers. “Snoozing for a limited time in the morning is probably not bad for you,” says the new study’s lead author Tina Sundelin, a sleep researcher at Stockholm University. She says that her study is one of few that have directly tested snoozing’s effect on sleep health, and it supplies evidence that snoozing doesn’t break up sleep in a harmful way. Scientific American spoke with sleep experts on the science of snoozing and how the habit may actually be good for you—if you do it right. The Potential Benefits of Snoozing Snoozing does shorten sleep, Sundelin says, but she maintains that it’s not as bad as scientists once thought. Past research has suggested that the extra minutes snoozers get don’t really help them feel more rested—and repeatedly waking up and trying to sleep again has been thought to prevent the restorative stages of sleep, including rapid-eye movement (REM). Other research has suggested that waking someone in the middle of their sleep cycle causes them to feel sleepier throughout the day. “If you disturb someone’s sleep, it’s not good-quality sleep, and they often feel tired afterwards—but this [idea] is based on a whole night of sleep fragmentation,” explains Sundelin, who adds that most theories about snoozing are “inferred from what we know about sleep in general.” © 2023 SCIENTIFIC AMERICAN,

Keyword: Sleep
Link ID: 29005 - Posted: 11.15.2023

Max Kozlov Researchers have sifted through genomes from thousands of individuals in an effort to identify genes linked to Alzheimer’s disease. But these scientists have faced a serious obstacle: it’s hard to know for certain which of those people have Alzheimer’s. There’s no foolproof blood test for the disease, and dementia, a key symptom of Alzheimer’s, is also caused by other disorders. Early-stage Alzheimer’s might cause no symptoms at all. Now, researchers have developed artificial intelligence (AI)-based approaches that could help. One algorithm efficiently sorts through large numbers of brain images and picks out those that include characteristics of Alzheimer’s. A second machine-learning method identifies important structural features of the brain — an effort that could eventually help scientists to spot new signs of Alzheimer’s in brain scans. The goal is to use people’s brain images as visual ‘biomarkers’ of Alzheimer’s. Applying the method to large databases that also include medical information and genetic data, such as the UK Biobank, could allow scientists to pinpoint genes that contribute to the disease. In turn, this work could aid the creation of treatments and of models that predict who’s at risk of developing the disease. Combining genomics, brain imaging and AI is allowing researchers to “find brain measures that are tightly linked to a genomic driver”, says Paul Thompson, a neuroscientist at the University of Southern California in Los Angeles, who is spearheading efforts to develop these algorithms. Thompson and others described the new AI techniques on 4 November at the annual conference of the American Society of Human Genetics in Washington DC. Overwhelmed with data © 2023 Springer Nature Limited

Keyword: Alzheimers; Robotics
Link ID: 29004 - Posted: 11.13.2023

By Francesca Paris There are more Americans who say they have serious cognitive problems — with remembering, concentrating or making decisions — than at any time in the last 15 years, data from the Census Bureau shows. The increase started with the pandemic: The number of working-age adults reporting “serious difficulty” thinking has climbed by an estimated one million people. About as many adults ages 18 to 64 now report severe cognitive issues as report trouble walking or taking the stairs, for the first time since the bureau started asking the questions each month in the 2000s. The sharp increase captures the effects of long Covid for a small but significant portion of younger adults, researchers say, most likely in addition to other effects of the pandemic, including psychological distress. But they also say it’s not yet possible to fully dissect all the reasons behind the increase. Richard Deitz, an economist at the Federal Reserve Bank of New York, analyzed the data and attributed much of the increase to long Covid. “These numbers don’t do this — they don’t just start suddenly increasing sharply like this,” he said. In its monthly Current Population Survey, the census asks a sample of Americans whether they have serious problems with their memory and concentration. It defines them as disabled if they answer yes to that question or one of five others about limitations on their daily activities. The questions are unrelated to disability applications, so respondents don’t have a financial incentive to answer one way or another. At the start of 2020, the survey estimated there were fewer than 15 million Americans ages 18 to 64 with any kind of disability. That rose to about 16.5 million by September 2023. Nearly two-thirds of that increase was made up of people who had newly reported limitations on their thinking. There were also increases in census estimates of the number of adults with a vision disability or serious difficulty doing basic errands. For older working-age Americans, the pandemic ended a yearslong decline in reported rates of disability. © 2023 The New York Times Company

Keyword: Attention
Link ID: 29003 - Posted: 11.13.2023

By Frieda Klotz Tess Olmsted stopped eating sugar when she was just 12 years old. She had previously been treated for obsessive compulsive disorder, or OCD, and soon found herself following rituals around eating. “For me it was never, ‘Oh I need to get skinnier,’” she recalls. Once she started to diet, she simply couldn’t stop. Two years later, on a summer day in 2019, her father saw her on the family’s patio wearing a loose-fitting swimsuit. He soon noticed how little Tess was eating and insisted she see the pediatrician. During a subsequent appointment with a specialist, he recalls, the family learned that Tess’s blood pressure and heart rate were dangerously low. She was admitted to a hospital in life-threatening condition. Across the United States, up to 2 million adults have had anorexia, a mental health condition in which a person severely restricts their food intake, often due to an intense fear of gaining weight. Almost 1 percent of all U.S. women will experience anorexia at some point in their lives. Patients are developing the condition increasingly early in life — sometimes as young as 8 years old — and new figures suggest that symptoms in children worsened during the Covid-19 pandemic, leading to increased numbers of hospitalizations. At one treatment center in Michigan, the admission rate of young people aged 10 to 23 more than doubled during the pandemic’s first year. These sobering developments are due, in part, to the fact that there are no drugs or devices approved by the U.S. Food and Drug Administration to treat the condition. For adults, there are three first-line treatments: an adapted form of cognitive behavioral therapy, known as CBT-E; a structured psychotherapy designed with patient input; and an approach that combines psychotherapy with nutritional support. Studies have shown that these approaches can help more than 50 percent of patients. But experts acknowledge that the studies are not high quality. Patients with anorexia are hard to engage in treatment, and as a result, studies are small and drop-out rates are high.

Keyword: Anorexia & Bulimia
Link ID: 29002 - Posted: 11.13.2023

By Jan Hoffman Dr. Nic Helmstetter crab-walked down a steep, rain-slicked trail into a grove of maple and cottonwood trees to his destination: a dozen tents in a clearing by the Kalamazoo River, surrounded by the detritus of lives perpetually on the move. Discarded red plastic cups. A wet sock flung over a bush. A carpet square. And scattered across the forest floor: orange vial caps and used syringes. Kalamazoo, a small city in Western Michigan, is a way station along the drug trafficking corridor between Chicago and Detroit. In its parks, under railroad overpasses and here in the woods, people ensnared by drugs scramble to survive. Dr. Helmstetter, who makes weekly primary care rounds with a program called Street Medicine Kalamazoo, carried medications to reverse overdoses, blunt cravings and ease withdrawal-induced nausea. But increasingly, the utility of these therapies, developed to address the decades-old opioid crisis, is diminishing. They work to counteract the most devastating effects of fentanyl and heroin, but most users now routinely test positive for other substances too, predominantly stimulants such as cocaine and methamphetamine, for which there are no approved medications. Rachel, 35, her hair dyed a silvery lavender, ran to greet Dr. Helmstetter. She takes the medicine buprenorphine, which acts to dull her body’s yearning for opioids, but she was not ready to let go of meth. “I prefer both, actually,” she said. “I like to be up and down at the same time.” The United States is in a new and perilous period in its battle against illicit drugs. The scourge is not only opioids, such as fentanyl, but a rapidly growing practice that the Centers for Disease Control and Prevention labels “polysubstance use.” Over the last three years, studies of people addicted to opioids (a population estimated to be in the millions) have consistently shown that between 70 and 80 percent also take other illicit substances, a shift that is stymieing treatment efforts and confounding state, local and federal policies. “It’s no longer an opioid epidemic,” said Dr. Cara Poland, an associate professor at the Michigan State University College of Human Medicine. “This is an addiction crisis.” © 2023 The New York Times Company

Keyword: Drug Abuse
Link ID: 29001 - Posted: 11.13.2023

By Yasemin Saplakoglu More than 150 years ago, the economist and philosopher William Stanley Jevons discovered something curious about the number 4. While musing about how the mind conceives of numbers, he tossed a handful of black beans into a cardboard box. Then, after a fleeting glance, he guessed how many there were, before counting them to record the true value. After more than 1,000 trials, he saw a clear pattern. When there were four or fewer beans in the box, he always guessed the right number. But for five beans or more, his quick estimations were often incorrect. Jevons’ description of his self-experiment, published in Nature in 1871, set the “foundation of how we think about numbers,” said Steven Piantadosi, a professor of psychology and neuroscience at the University of California, Berkeley. It sparked a long-lasting and ongoing debate about why there seems to be a limit on the number of items we can accurately judge to be present in a set. Now, a new study in Nature Human Behaviour has edged closer to an answer by taking an unprecedented look at how human brain cells fire when presented with certain quantities. Its findings suggest that the brain uses a combination of two mechanisms to judge how many objects it sees. One estimates quantities. The second sharpens the accuracy of those estimates — but only for small numbers. It’s “very exciting” that the findings connect long-debated ideas to their neural underpinnings, said Piantadosi, who was not involved in the study. “There’s not many things in cognition where people have been able to pinpoint very plausible biological foundations.” Although the new study does not end the debate, the findings start to untangle the biological basis for how the brain judges quantities, which could inform bigger questions about memory, attention and even mathematics. All Rights Reserved © 2023

Keyword: Attention
Link ID: 29000 - Posted: 11.11.2023

By Veronique Greenwood When someone brushes a hand across your skin, it’s like a breeze blowing through a forest of countless small hairs. Nerves that surround your hair follicles detect that contact, and very far away in your brain, other cells fire. Some of the neurons responding to light contact might make you shiver and give you goose bumps. Some might tell you to move away. Or they might tell you to move closer. Scientists who study the sense of touch have explored which cells bear these messages, and they have made an intriguing discovery: Follicle cells triggered by hair movements release the neurotransmitters histamine and serotonin, chemical messengers linked to biological phenomena as varied as inflammation, muscle contraction and mood changes. The observation, reported in October in the journal Science Advances, lays the groundwork for tracing how gentle touch makes us feel the way it does. Studying hair follicles is challenging, because they begin to decay soon after being removed from the body, said Claire Higgins, a bioengineering professor at Imperial College London and an author of the study. So she and her colleagues went to a hair transplant clinic. There, they were able to look at freshly harvested follicles, which they gently prodded with a very small rod to simulate touch. The scientists knew from work done by other groups that the neurons in the skin surrounding hair follicles are capable of sensing movement. “When you brush your hair, you feel it because the sensory neurons are directly being stimulated,” Dr. Higgins said. But they were curious whether the cells of the follicle itself — the tube from which a hair sprouts — could be contributing to some of the feelings associated with more gentle touch. Not all of the follicle cells had movement sensors, but some did. The researchers identified these and watched them carefully as the rod touched them. “We found that when we stimulated our hair follicle cells, they actually released mood-regulating neurotransmitters serotonin and histamine,” Dr. Higgins said. © 2023 The New York Times Company

Keyword: Pain & Touch; Emotions
Link ID: 28999 - Posted: 11.11.2023

by Grace Huckins In 1961, the late psychiatrist Daniel Freedman made what would become one of the most replicated — and most mysterious — discoveries in the history of autism research. Comparing blood levels of the neurotransmitter serotonin in 4 non-autistic and 23 autistic children, he found significantly higher levels among the latter group. Since then, researchers have repeatedly identified this trait, called hyperserotonemia, in about a third of autistic people tested. It’s not difficult to theorize how hyperserotonemia might be linked to a range of autism traits. Neurons that release serotonin extend into practically every part of the brain, where they modulate signals sent among other neurons. Selective serotonin reuptake inhibitors (SSRIs), drugs that raise levels of serotonin in the brain’s synapses, treat psychiatric conditions, such as anxiety and obsessive-compulsive disorder, that can co-occur with autism. And serotonin prompts the gut to contract and facilitate digestion, which is often impaired in autistic people. So when Edwin Cook, professor of psychiatry at the University of Illinois at Chicago, began to study the biology of autism in the 1980s, hyperserotonemia seemed like an obvious place to start. “We didn’t have much [else],” he says. “There were plenty of mothers of older patients I saw who had been labeled refrigerator mothers,” a term that refers to the discredited idea that unaffectionate mothers cause autism. The serotonin finding offered a tangible, biological clue. Even today, with decades more autism research to look back on, the hyperserotonemia result stands out. “It’s one of the few robust biological clues that we’ve had in autism,” says Jeremy Veenstra-VanderWeele, professor of psychiatry at Columbia University and a former advisee of Cook’s. But so far, it has escaped explanation. Nor have researchers been able to definitively link hyperserotonemia to specific genetic, anatomical or behavioral traits in autistic people. This apparent lack of progress has led some to disregard work on the neurotransmitter, according to serotonin researcher Georgianna Gould, associate professor of physiology at the University of Texas Health Science Center at San Antonio. “I’ve actually seen reviews come back that say that serotonin has nothing to do with autism,” she says. © 2023 Simons Foundation

Keyword: Autism; Obesity
Link ID: 28998 - Posted: 11.11.2023

Liam Drew In a laboratory in San Francisco, California, a woman named Ann sits in front of a huge screen. On it is an avatar created to look like her. Thanks to a brain–computer interface (BCI), when Ann thinks of talking, the avatar speaks for her — and in her own voice, too. In 2005, a brainstem stroke left Ann almost completely paralysed and unable to speak. Last year, neurosurgeon Edward Chang, at the University of California, San Francisco, placed a grid of more than 250 electrodes on the surface of Ann’s brain, on top of the regions that once controlled her body, face and larynx. As Ann imagined speaking certain words, researchers recorded her neural activity. Then, using machine learning, they established the activity patterns corresponding to each word and to the facial movements Ann would, if she could, use to vocalize them. The system can convert speech to text at 78 words per minute: a huge improvement on previous BCI efforts and now approaching the 150 words per minute considered average for regular speech1. Compared with two years ago, Chang says, “it’s like night and day”. In an added feat, the team programmed the avatar to speak aloud in Ann’s voice, basing the output on a recording of a speech she made at her wedding. “It was extremely emotional for Ann because it was the first time that she really felt that she was speaking for almost 20 years,” says Chang. This work was one of several studies in 2023 that boosted excitement about implantable BCIs. Another study2 also translated neural activity into text at unprecedented speed. And in May, scientists reported that they had created a digital bridge between the brain and spinal cord of a man paralysed in a cycling accident3. A BCI decoded his intentions to move and directed a spinal implant to stimulate the nerves of his legs, allowing him to walk. © 2023 Springer Nature Limited

Keyword: Brain imaging; Language
Link ID: 28997 - Posted: 11.11.2023

By Azeen Ghorayshi Doctors and patients have long known that antidepressants can cause sexual problems. No libido. Pleasureless orgasms. Numb genitals. Well over half of people taking the drugs report such side effects. Now, a small but vocal group of patients is speaking out about severe sexual problems that have endured even long after they stopped taking selective serotonin reuptake inhibitors, the most popular type of antidepressants. The drugs’ effects have been devastating, they said, leaving them unable to enjoy sex or sustain romantic relationships. “My clitoris feels like a knuckle,” said Emily Grey, a 27-year-old in Vancouver, British Columbia, who took one such drug, Celexa, for depression from age 17 to 23. “It’s not a normal thing to have to come to terms with.” The safety label on Prozac, one of the most widely prescribed S.S.R.I.s, warns that sexual problems may persist after the drug is discontinued. And health authorities in Europe and Canada recently acknowledged that the medications can lead to lasting sexual issues. But researchers are only just beginning to quantify how many people have these long-term problems, known as post-S.S.R.I. sexual dysfunction. And the chronic condition remains contested among some psychiatrists, who point out that depression itself can curb sexual desire. Clinical trials have not followed people after they stop the drugs to determine whether such sexual problems stem from the medications. “I think it’s depression recurring. Until proven otherwise, that’s what it is,” said Dr. Anita Clayton, the chief of psychiatry at the University of Virginia School of Medicine and a leader of an expert group that will meet in Spain next year to formally define the condition. Dr. Clayton published some of the earliest research showing that S.S.R.I.s come with widespread sexual side effects. © 2023 The New York Times Company

Keyword: Depression; Sexual Behavior
Link ID: 28996 - Posted: 11.11.2023

Catherine Sweeney - WPLN NASHVILLE, Tenn. — High school classes start so early around this city that some kids get on buses at 5:30 in the morning. Just 10% of public schools nationwide start before 7:30 a.m., according to federal statistics. But in Nashville, classes start at 7:05 — a fact the new mayor, Freddie O'Connell, has been criticizing for years. "It's not a badge of honor," he said when he was still a city council member. Since his election in September, O'Connell has announced that pushing back school start times is a cornerstone of the education policy he is promoting. He and others around the country have been trying to stress that teenagers aren't lazy or to blame for getting too little sleep. It's science. Sponsor Message "All teenagers have this shift in their brain that causes them to not feel sleepy until about 10:45 or 11 at night," said Kyla Wahlstrom, a senior research fellow at the University of Minnesota in the College of Education and Human Development. She studies how education policy affects learning, and she used to be a teacher. "It's a shift that is biologically determined." Sleep deprivation in teenagers is linked to mental health struggles, worse grades, traffic accidents, and more. That's why states including California and Florida have mandated later start times. Individual districts across the country — including some in Tennessee — have made the same change. But resistance to later starts is less about the science than it is about logistical and financial difficulties, especially with basics like busing. Melatonin makes people feel drowsy. The brain starts producing it when it gets dark outside, and its production peaks in the middle of the night. Adolescents' brains start releasing melatonin about three hours later than adults' and younger children's brains, according to the American Chemical Society. When teens wake up early, their brains are still producing melatonin. © 2023 npr

Keyword: Biological Rhythms; Sleep
Link ID: 28995 - Posted: 11.11.2023

Emily Waltz A highly experimental implant that delivers electrical stimulation to the spinal cord has substantially improved mobility for one man with advanced Parkinson’s disease, according to a report published today in Nature Medicine1. Stimulating spinal cord helps paralysed people to walk again The technology, developed by researchers at the Swiss Federal Institute of Technology in Lausanne (EPFL), enables the man to walk fluidly and to navigate terrain without falling — something he couldn’t do before the treatment. Parkinson’s causes uncontrollable movements and difficulty with coordination that worsens over time. The effects of the treatment have lasted for two years. “There are no therapies to address the severe gait problems that occur at a later stage of Parkinson’s, so it’s impressive to see him walking,” says Jocelyne Bloch, a neurosurgeon at the EPFL and a lead author of the paper. But with only one individual tested, it remains unclear whether the approach will work for other people with the disease. The next step “would be to do a randomized, controlled trial”, says Susan Harkema, a neuroscientist at the University of Louisville in Kentucky who works on stimulation therapy in people with spinal cord injuries. Spinal cord stimulation involves surgically implanting a neuroprosthetic device that delivers pulses of electricity to specific regions of the spinal cord in an effort to activate dysfunctional neural circuits. The technique has been used experimentally to enable people paralysed by spinal cord injury to stand on their own, and even to walk short distances. © 2023 Springer Nature Limited

Keyword: Parkinsons; Robotics
Link ID: 28994 - Posted: 11.08.2023

Ross Pomeroy Numerous hypotheses attempt to explain obesity‘s meteoric rise over the past few decades. There’s the energy balance hypothesis, which states that weight gain is due to consuming more calories than the amount expended. There’s the carbohydrate-insulin hypothesis, which argues that excess consumption of carbohydrates stimulates an insulin response that drives cells to accumulate fat. Then there’s the protein-leverage hypothesis, which suggests that we don’t eat enough protein, driving incessant hunger. Now, researchers have put forth a new hypothesis that places the blame on a sugar ubiquitous in modern food: fructose. Commonly known as “fruit sugar,” fructose is a simple, monosaccharide sugar found in many plants. But the compound that sweetens your watermelon, apples, and oranges can mess with your cells’ energy metabolism, Richard Johnson, a professor of medicine at the University of Colorado, and his co-authors Laura G. Sánchez-Lozada and Miguel A. Lanaspa explain in a paper published October 17 in the journal Obesity. “We suggest that obesity is not a disease of energy excess but rather a disease of energy crisis,” they wrote. The fructose hypothesis As studies in rodents have elucidated, fructose uniquely suppresses the function of mitochondria compared to other nutrients. When these cellular powerhouses are slowed, the cells get stuck in a low-energy state, triggering hunger and thirst. Eating nutrients including fats and protein eventually restores cellular energy levels, but not before we’ve eaten more calories than we need. This excess gets stored as fat. In the long term, frequent fructose exposure can damage mitochondria and reduce the amount of mitochondria in cells, the researchers say, locking people in a low-energy state which drives chronic overeating.

Keyword: Obesity
Link ID: 28993 - Posted: 11.08.2023

Saima Sidik When the scent of morning coffee wafts past the nose, the brain encodes which nostril it enters, new research shows1. Integrating information from both nostrils might help us to identify the odour. The results were published today in Current Biology. A region of the brain called the piriform cortex, which spans the brain’s two hemispheres, is known to receive and process information about scents. However, scientists were unsure whether the two sides of the piriform cortex react to smells in unison or independently. To investigate this question, researchers recruited people with epilepsy who were undergoing brain surgery to identify the areas of their brains responsible for their seizures. Participants were awake for the surgery, during which the scientists delivered scents to one or both nostrils through tiny tubes that reached roughly one centimetre into each nostril. The authors took advantage of electrodes placed in the study participants’ brains to take readings of activity in the piriform cortex. In reality, scents rarely hit only one nostril. Instead, they’re likely to enter one nostril slightly ahead of the other. “The question to ask is, well, can the brain exploit these potential differences?” says Naz Dikecligil, a neuroscientist at the University of Pennsylvania in Philadelphia and a co-author of the study. The findings suggest that the brain does make use of the different arrival times. When an odour was delivered to a single nostril, the side of the brain closest to that nostril reacted first, and a reaction then followed in the opposite side of the brain. “There seem to be actually two odour representations, corresponding to odour information coming from each nostril,” Dikecligil says. When the researchers provided a scent to both nostrils simultaneously, they saw that both sides of the brain recognized the scent faster than either did when it was delivered through only one nostril. This suggests that the two sides do synergize to some degree, even though one lags behind the other in encoding a scent, Dikecligil says. © 2023 Springer Nature Limited

Keyword: Chemical Senses (Smell & Taste)
Link ID: 28992 - Posted: 11.08.2023

By Claudia López Lloreda Genetic tweaks in kingfishers might help cushion the blow when the diving birds plunge beak first into the water to catch fish. Analysis of the genetic instruction book of some diving kingfishers identified changes in genes related to brain function as well as retina and blood vessel development, which might protect against damage during dives, researchers report October 24 in Communications Biology. The results suggest the different species of diving kingfishers may have adapted to survive their dives unscathed in some of the same ways, but it’s still unclear how the genetic changes protect the birds. Hitting speeds of up to 40 kilometers per hour, kingfisher dives put huge amounts of potentially damaging pressure on the birds’ heads, beaks and brains. The birds dive repeatedly, smacking their heads into the water in ways that could cause concussions in humans, says Shannon Hackett, an evolutionary biologist and curator at the Field Museum in Chicago. “So there has to be something that protects them from the terrible consequences of repeatedly hitting their heads against a hard substrate.” Hackett first became interested in how the birds protect their brains while she worked with her son’s hockey team and started worrying about the effect of repeated hits on the human brain. Around the same time, evolutionary biologist Chad Eliason joined the museum to study kingfishers and their plunge diving behavior. In the new study, Hackett, Eliason and colleagues analyzed the complete genome of 30 kingfisher species, some that plunge dive and others that don’t, from specimens frozen and stored at the museum. The preserved birds came from all over the world; some of the diving species came from mainland areas and others from islands and had evolved to dive independently rather than from the same plunge-diving ancestor. The team wanted to know if the different diving species had evolved similar genetic changes to arrive at the same behaviors. Many kingfisher species have developed this behavior, but it was unclear whether this was through genetic convergence, similar to how many species of birds have lost their flight or how bats and dolphins independently developed echolocation (SN: 9/6/2013). © Society for Science & the Public 2000–2023.

Keyword: Brain Injury/Concussion; Evolution
Link ID: 28991 - Posted: 11.08.2023

By Caren Chesler In 2019, Debra Halsch was diagnosed with smoldering multiple myeloma, a rare blood and bone marrow disorder that can develop into a type of blood cancer. Her doctors recommended chemotherapy, she said, but she feared the taxing side effects the drugs might wreak on her body. Instead, the life coach from Piermont, New York tried meditation. A friend had told Halsch, now 57, about Joe Dispenza, who holds week-long meditation retreats that regularly attract thousands of people and carry a $2,299 price tag. Halsch signed up for one in Cancun, Mexico and soon became a devotee. She now meditates for at least two hours a day and says her health has improved as a result. Goop, the health and lifestyle brand launched by actor and entrepreneur Gwyneth Paltrow in 2008, will have its own series on Netflix beginning January 24. Dispenza, a chiropractor who has written various self-help books, has said he believes the mind can heal the body. After all, he says he healed himself back in 1986, when a truck hit him while he was bicycling, breaking six vertebrae. Instead of surgery, Dispenza says he spent hours each day recreating his spine in his mind, visualizing it healthy and healed. After 11 weeks, the story goes, he was back on his feet. Halsch said she believes she can do the same for her illness. “If our thoughts and emotions can make our bodies sick, they can make us well, too,” she said. In an email to Undark, Rhadell Hovda, chief operating officer for Dispenza’s parent company, Encephalon, Inc., emphasized that Dispenza does not claim meditation can treat or cure cancer. However, he does “follow the evidence when it is presented,” and has encountered people at workshops and retreats “who claimed to have healed from many conditions.” For more than two decades, various studies have suggested that meditation and mindfulness — that is, being aware of the present moment — can help reduce and improve pain management, lending some credence to the notion that the brain can affect the body. Such results have helped the field grow into a multibillion-dollar industry, populated by meditation apps, guided workshops, and upscale retreats.

Keyword: Attention; Stress
Link ID: 28990 - Posted: 11.08.2023