By Jane E. Brody Many people aren’t overly concerned when an octogenarian occasionally forgets the best route to a favorite store, can’t remember a friend’s name or dents the car while trying to parallel park on a crowded city street. Even healthy brains work less efficiently with age, and memory, sensory perceptions and physical abilities become less reliable. But what if the person is not in their 80s but in their 30s, 40s or 50s and forgets the way home from their own street corner? That’s far more concerning. While most of the 5.3 million Americans who are living with Alzheimer’s disease or other forms of dementia are over 65, some 200,000 are younger than 65 and develop serious memory and thinking problems far earlier in life than expected. “Young-onset dementia is a particularly disheartening diagnosis because it affects individuals in the prime years,” Dr. David S. Knopman, a neurologist at the Mayo Clinic in Rochester, Minn., wrote in a July 2021 editorial in JAMA Neurology. Many of the afflicted are in their 40s and 50s, midcareer, hardly ready to retire and perhaps still raising a family. Dementia in a younger adult is especially traumatic and challenging for families to acknowledge, and many practicing physicians fail to recognize it or even suspect it may be an underlying cause of symptoms. “Complaints about brain fog in young patients are very common and are mostly benign,” Dr. Knopman told me. “It’s hard to know when they’re not attributable to stress, depression or anxiety or the result of normal aging. Even neurologists infrequently see patients with young-onset dementia.” Yet recent studies indicate that the problem is far more common than most doctors realize. Worldwide, as many as 3.9 million people younger than 65 may be affected, a Dutch analysis of 74 studies indicated. The study, published in JAMA Neurology in September, found that for every 100,000 people aged 30 to 64, 119 had early dementia. © 2022 The New York Times Company

Keyword: Alzheimers; Genes & Behavior
Link ID: 28161 - Posted: 01.19.2022

By Erin Garcia de Jesús For many people, one of the fastest tip-offs that they have COVID-19 is the loss of taste or smell. Now researchers have pinpointed some genetic variants in people that may make it more likely that the coronavirus might rob them of these senses. A study of nearly 70,000 adults with COVID-19 found that individuals with certain genetic tweaks on chromosome 4 were 11 percent more likely to lose the ability to smell or taste than people without the changes, researchers report January 17 in Nature Genetics. The data come from people who’d had their DNA analyzed by genetic testing company 23andMe and self-reported a case of COVID-19. Two genes, UGT2A1 and UGT2A2, that help people smell reside in the region of chromosome 4 linked to sensory loss during infection, epidemiologist Janie Shelton of 23andMe and colleagues found. Both genes make enzymes that metabolize substances called odorants, which produce distinctive smells. Sign up for e-mail updates on the latest coronavirus news and research Studies suggest that loss of smell, a hallmark symptom of COVID-19, stems from infections taking hold in smell-supporting cells called sustentacular cells (SN: 6/12/20). It’s possible that the genetic variants near UGT2A1 and UGT2A2 could affect how the two genes are turned on or off to somehow mess with smell during an infection, Shelton says. © Society for Science & the Public 2000–2022.

Keyword: Chemical Senses (Smell & Taste)
Link ID: 28160 - Posted: 01.19.2022

Sophie Fessl Mice raised in an enriched environment are better able to adapt and change than mice raised in standard cages, but why they show this higher brain plasticity has not been known. Now, a study published January 11 in Cell Reports finds that the environment could act indirectly: living in enriched environments changes the animals’ gut microbiota, which appears to modulate plasticity. The study “provides very interesting new insights into possible beneficial effects of environmental enrichment on the brain that might act via the gut,” writes Anthony Hannan, a neuroscientist at the Florey Institute of Neuroscience and Mental Health in Australia who was not involved in the study, in an email to The Scientist. “This new study has implications for how we might understand the beneficial effects of environmental enrichment, and its relevance to cognitive training and physical activity interventions in humans.” In previous studies, mice raised in what scientists call an enriched environment—one in which they have more opportunities to explore, interact with others, and receive sensory stimulation than they would in standard laboratory enclosures—have been better able to modify their neuronal circuits in response to external stimuli than mice raised in smaller, plainer cages. Paola Tognini, a neuroscientist at the University of Pisa and lead author of the new study, writes in an email to The Scientist that she “wondered if endogenous factors (signals coming from inside our body instead of the external world), such as the signals coming from the intestine, could also influence brain plasticity.” © 1986–2022 The Scientist.

Keyword: Learning & Memory; Obesity
Link ID: 28159 - Posted: 01.19.2022

By Amelia Nierenberg Most people think of melatonin as a natural nod-off aid, kind of like chamomile tea in pill form. Even the name of the popular dietary supplement sounds sleepy — that long “o” sound almost makes you yawn mid-word. But melatonin is also a hormone that our brains naturally produce, and hormones, even in minuscule amounts, can have potent effects throughout the body. “There are some clinical uses for it, but not the way that it’s marketed and used by the vast majority of the general public,” said Jennifer Martin, a psychologist and professor of medicine at the University of California, Los Angeles. Experts strongly urge people to consult their doctor or a sleep specialist before taking melatonin, in part because the supplement does not address many underlying health problems that may be disrupting sleep. Anxiety can cause insomnia, as can a host of other potentially serious ailments, such as sleep apnea, restless legs syndrome or mood disorders like depression, that may require medical treatment. Melatonin, however, is relatively inexpensive and readily available at local pharmacies in the United States (in other countries it typically requires a prescription), and many people will go out and buy it on their own. So what’s the best approach to taking melatonin? Here’s what experts had to say. During the day, the brain’s pea-sized pineal gland remains inactive. A few hours before our natural sleep time, as it starts to get dark outside and the light entering our retina fades, the gland switches on to flood the brain with melatonin. “Melatonin is sometimes called the ‘hormone of darkness’ or ‘vampire hormone,’” because it comes out at night, said Matthew Walker, a professor of neuroscience and psychology at the University of California, Berkeley, and the author of the book “Why We Sleep.” As levels of melatonin rise, levels of cortisol, the stress hormone, fall. Respiration slows. Soon, our eyelids begin to droop. Instead of a lights-out trigger, melatonin acts more like a dimmer switch, turning the day functions off and switching night functions on. So taking a melatonin supplement is sort of like taking a dose of sunset, tricking your body into feeling like it’s nighttime. It doesn’t put you to sleep as much as it tells the body that it’s time to sleep. © 2022 The New York Times Company

Keyword: Biological Rhythms; Sleep
Link ID: 28158 - Posted: 01.19.2022

By Linda Searing For people with early-stage Parkinson’s disease, four hours a week of moderate exercise may help slow the progression of the disease. Symptoms of Parkinson’s, which is a movement disorder, generally start gradually but worsen over time. FAQ: What to know about the omicron variant of the coronavirus But research published in the journal Neurology found that those who were regularly active for at least that amount of time — whether with traditional exercise or such physical activity as walking, gardening or dancing — had less decline in balance and walking ability, were better able to maintain daily activities and did better on cognitive tests five years later than those who exercised less. The researchers noted that the key to achieving these benefits was maintaining regular exercise over time, rather than how active people had been when their disease started. Parkinson’s, which is more common in men than women, usually begins about age 60 as nerve cells in the brain (neurons) become weak or damaged. Symptoms may include trembling or shaking (tremor), muscle stiffness (rigidity), slow movement (bradykinesia) and poor balance and coordination. As symptoms get worse, people may have trouble walking, talking or continuing to do routine daily activities. Although no cure exists for Parkinson’s, treatment — medication, surgery or electrical stimulation — can sometimes help ease some symptoms for a while. The researchers wrote, however, that “there is still no disease-modifying treatment to slow the disease’s progression.”

Keyword: Parkinsons
Link ID: 28157 - Posted: 01.19.2022

By Azeen Ghorayshi An upsurge in teenagers requesting hormones or surgeries to better align their bodies with their gender identities has ignited a debate among doctors over when to provide these treatments. An international group of experts focused on transgender health last month released a draft of new guidelines, the gold standard of the field that informs what insurers will reimburse for care. Many doctors and activists praised the 350-page document, which was updated for the first time in nearly a decade, for including transgender people in its drafting and for removing language requiring adults to have psychological assessments before getting access to hormone therapy. But the guidelines take a more cautious stance on teens. A new chapter dedicated to adolescents says that they must undergo mental health assessments and must have questioned their gender identity for “several years” before receiving drugs or surgeries. Experts in transgender health are divided on these adolescent recommendations, reflecting a fraught debate over how to weigh conflicting risks for young people, who typically can’t give full legal consent until they are 18 and who may be in emotional distress or more vulnerable to peer influence than adults are. Some of the drug regimens bring long-term risks, such as irreversible fertility loss. And in some cases, thought to be quite rare, transgender people later “detransition” to the gender they were assigned at birth. Given these risks, as well as the increasing number of adolescents seeking these treatments, some clinicians say that teens need more psychological assessment than adults do. “They absolutely have to be treated differently,” said Laura Edwards-Leeper, a child clinical psychologist in Beaverton, Ore., who works with transgender adolescents. Dr. Edwards-Leeper was one of seven authors of the new adolescent chapter, but the organization that publishes the guidelines, the World Professional Association for Transgender Health, did not authorize her to comment publicly on the draft’s proposed wording. © 2022 The New York Times Company

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 28156 - Posted: 01.15.2022

Meredith Wadman Progress in treating Parkinson’s disease—a progressive neurological illness that causes tremors, muscle rigidity, and dementia—has been painfully slow, in large part because scientists still don’t fully understand the molecular events that kill select brain cells. What they do know is Parkinson’s leaves behind a telltale mark: clumps of the misfolded alpha synuclein (αS) protein in the brains and guts of patients at autopsy. In its normal form, the protein is widely thought to help brain cells communicate, but researchers have now uncovered another role—αS plays an essential part in immune and inflammatory responses in the gut. The new work is “extremely well done and very exciting,” says physician-scientist Michael Schlossmacher, who studies Parkinson’s disease at the Ottawa Hospital Research Institute but was not involved with the study. He adds that the protein’s “pivotal role” in immunity may help explain why chronic infection or inflammation can lead to a higher risk of Parkinson’s. Others in the field, however, question the work’s relevance to the brain disorder. The dominant view among researchers is that misfolded αS aggregates and takes on new toxic properties, and some say the natural role of the protein, although interesting, may be irrelevant to pursuing needed treatments. Parkinson’s disease, the second most common neurodegenerative ailment after Alzheimer’s, affects one in 331, or about 1 million, people in the United States and at least 7 million people globally. Many patients are diagnosed in their 60s, as brain cells that make the neurotransmitter dopamine die and lead to symptoms. But the disease can also strike the young—including those who produce too much αS, or fail to break it down—because of rare genetic mutations. Other risk factors include sex—prevalence is 40% to 50% higher in men than in women—and some chronic inflammatory diseases, such as inflammatory bowel disease and chronic hepatitis C. Oral dopamine can mitigate symptoms, but the 60-year-old treatment isn’t a cure and ultimately fails to prevent worsening symptoms and death. © 2022 American Association for the Advancement of Science.

Keyword: Parkinsons
Link ID: 28155 - Posted: 01.15.2022

By Gina Kolata For decades, researchers have suspected that people infected with an exceedingly common virus, Epstein-Barr, might be more likely to develop multiple sclerosis, a neurological illness that affects a million people in the United States. Now, a team of researchers reports what some say is the most compelling evidence yet of a strong link between the two diseases. The virus infects nearly everyone in their teen or young adult years, and very few go on to develop multiple sclerosis. The researchers also note that it is not the only known risk factor for people who develop the illness. But they say their data points to it being the clearest of them all. While it remains to be seen whether the finding will result in treatments or cures for multiple sclerosis, the study may further motivate research into therapies and vaccines for the condition. In their study, published Thursday in Science, the group examined data from 10 million people on active duty in the United States Armed Forces over two decades. The strength of their study, said its principal investigator, Dr. Alberto Ascherio, an epidemiologist at the Harvard T.H. Chan School of Public Health, is that they were able to follow people for years and ask whether infections with Epstein-Barr preceded multiple sclerosis. Among the service members in the study, 801 developed multiple sclerosis, a disabling disease that occurs when the immune system attacks the fatty insulation that protects nerves in the brain and spinal cord. Most who develop the disease are diagnosed between the ages of 20 and 50. The disease is rare, though — an individual’s chance of getting multiple sclerosis is half of one percent. At the same time, the virus in question, Epstein-Barr, is common, infecting nearly everyone in the population at some point. Although few are aware that they were infected, some develop mononucleosis. The virus remains in the body for life. © 2022 The New York Times Company

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 28154 - Posted: 01.15.2022

By Winston Choi-Schagrin SOUTH ST. PAUL, Minn. — Chuck McGinley, a chemical engineer, stepped out of his car, eyed the smokestack of an animal processing plant rising above the treetops, and inhaled deeply. At first he smelled nothing except the faint, sweet fragrance of the nearby trees. Suddenly, the wind picked up. “We have an oh-my-God smell!” Mr. McGinley exclaimed. Immediately one of his colleagues pressed a Nasal Ranger to his nose. The 14-inch-long smell-measuring device, which looks like a cross between a radar gun and a bugle, is one of Mr. McGinley’s most significant inventions. Using terms from one of Mr. McGinley’s other standard tools, an odor wheel, a chart akin to an artist’s color wheel that he has been fine-tuning for decades, the team described the stink. “Sour,” one person said. “Decay, with possibly some petroleum,” said another. Then, as quickly as it had arrived, the smell disappeared. “The wind decided it was going to gift us only a short sniff,” Mr. McGinley said. “To tease us.” Intuitively, humans know to avoid bad smells. Yet for a half-century, Mr. McGinley, 76, has returned again and again to society’s stinkiest sites, places very much like this one, in order to measure, describe and demystify smell. Climate Fwd There’s an ongoing crisis — and tons of news. Our newsletter keeps you up to date. Get it sent to your inbox. From his unconventional lab in a Minnesota suburb (it actually feels more like a ski lodge) Mr. McGinley and his son Mike have established an outsize influence over the measurement and understanding of odor. They have equipped scientists around the world with tools the elder Mr. McGinley invented, advised governments on odor regulations and empowered communities near smelly places to find a vocabulary for their complaints and a way to measure what their noses are telling them. In many ways, the growing demand for Mr. McGinley’s services and instruments signals society’s heightened awareness of the power of odor and its potential to make people physically ill or diminish their quality of life. His inventions have taken on a powerful role in a movement to recognize odor as a pollutant, not merely an annoyance, worthy of closer study and perhaps tighter regulation. © 2022 The New York Times Company

Keyword: Chemical Senses (Smell & Taste)
Link ID: 28153 - Posted: 01.15.2022

Melinda Wenner Moyer Like many paediatricians, Dani Dumitriu braced herself for the impact of the SARS-CoV-2 coronavirus when it first surged in her wards. She was relieved when most newborn babies at her hospital who had been exposed to COVID-19 seemed to do just fine. Knowledge of the effects of Zika and other viruses that can cause birth defects meant that doctors were looking out for problems. But hints of a more subtle and insidious trend followed close behind. Dumitriu and her team at the NewYork–Presbyterian Morgan Stanley Children’s Hospital in New York City had more than two years of data on infant development — since late 2017, they had been analysing the communication and motor skills of babies up to six months old. Dumitriu thought it would be interesting to compare the results from babies born before and during the pandemic. She asked her colleague Morgan Firestein, a postdoctoral researcher at Columbia University in New York City, to assess whether there were neurodevelopmental differences between the two groups. A few days later, Firestein called Dumitriu in a panic. “She was like, ‘We’re in a crisis, I don’t know what to do, because we not only have an effect of a pandemic, but it’s a significant one,’” Dumitriu recalled. She was up most of that night, poring over the data. The infants born during the pandemic scored lower, on average, on tests of gross motor, fine motor and communication skills compared with those born before it (both groups were assessed by their parents using an established questionnaire)1. It didn’t matter whether their birth parent had been infected with the virus or not; there seemed to be something about the environment of the pandemic itself. Dumitriu was stunned. “We were like, oh, my God,” she recalled. “We’re talking about hundreds of millions of babies.” Although children have generally fared well when infected with SARS-CoV-2, preliminary research suggests that pandemic-related stress during pregnancy could be negatively affecting fetal brain development in some children. Moreover, frazzled parents and carers might be interacting differently or less with their young children in ways that could affect a child’s physical and mental abilities.

Keyword: Development of the Brain; Learning & Memory
Link ID: 28152 - Posted: 01.12.2022

By Judith Graham The reports from coronavirus patients are disconcerting. Only a few hours before, they were enjoying a cup of pungent coffee or the fragrance of flowers in a garden. Then, as if a switch had been flipped, those smells disappeared. F Young and old alike are affected — more than 80 to 90 percent of those diagnosed with the virus, according to some estimates. While most people recover in a few months, 16 percent take half a year or longer to do so, research has found. According to new estimates, up to 1.6 million Americans have chronic smell problems because of covid-19, the disease caused by the coronavirus. Seniors are especially vulnerable, experts say. “We know that many older adults have a compromised sense of smell to begin with. Add to that the insult of covid, and it made these problems worse,” said Jayant Pinto, a professor of surgery and a specialist in sinus and nasal diseases at the University of Chicago Medical Center. Advertisement Recent data highlights the interaction between covid-19, advanced age and loss of smell. When Italian researchers evaluated 101 patients who had been hospitalized for mild to moderate covid-19, 50 showed objective signs of smell impairment six months later. Those 65 or older were nearly twice as likely to be impaired; those 75 or older were more than 2½ times as likely. Most people aren’t aware of the extent to which smell can be diminished in later life. More than half of 65-to-80-year-olds have some degree of smell loss, or olfactory dysfunction, as it’s known in the scientific literature. That rises to as high as 80 percent for those even older. People affected often report concerns about safety, less enjoyment eating and an impaired quality of life. But because the ability to detect, identify and discriminate among odors declines gradually, most older adults — up to 75 percent of those with some degree of smell loss — don’t realize they’re affected.

Keyword: Chemical Senses (Smell & Taste)
Link ID: 28151 - Posted: 01.12.2022

By Lisa Sanders, M.D. The mother stood in the baggage-claim area of the Buffalo Niagara International Airport, waiting for her 37-year-old son, who had just flown in from North Carolina. The carousel was nearly empty by the time she caught sight of him. She was shocked by how sick he looked. His face was pale and thin, his hair and clothes rumpled as if he felt too awful to care. Most surprising of all: He was being rolled toward her in a wheelchair. “I had some trouble with the stairs,” he explained. He thanked the attendant and then struggled to get to his feet. He didn’t make it. Before he got more than a few inches off the seat, his arms and then his legs began to shake and wobble, and he fell heavily back into the chair. His mother collected his bag and pushed him out to where her husband was waiting in the car. On the drive home, the young man struggled to explain what was going on. He had always considered himself to be pretty strong and healthy, but these past few weeks had been rough. It started in his legs. He felt wobbly. When he walked, his hips, legs and especially his feet felt as if they might not be able to hold him up. He saw his physician assistant about it — he worried that it was caused by the cholesterol-lowering medication he had started taking — but the P.A. assured him it wasn’t. He was running a few times a week, but he had to stop because his legs were done well before the run was. And he didn’t feel as sharp as he used to be. His brain seemed foggy and slow. Then this morning he had trouble climbing the stairs to the plane. That was scary. The guy behind him helped by holding up his backpack, but his feet felt like dead weights. He had to use his arms to help get his body up high enough to take each step. Once on the plane, he supported himself on the headrests to get to his assigned seat. They offered the wheelchair when he arrived in Buffalo, and he gratefully accepted. His mother tentatively asked if he thought he should see a doctor. She knew he hated it when she tried to tell him what to do. He had flown up to see a football game with her ex-husband, his father, and a hockey game with his stepbrother. If he didn’t feel any better after that, he conceded, it would be time to see a doctor. © 2022 The New York Times Company

Keyword: Movement Disorders; Drug Abuse
Link ID: 28150 - Posted: 01.12.2022

Don Arnold All memory storage devices, from your brain to the RAM in your computer, store information by changing their physical qualities. Over 130 years ago, pioneering neuroscientist Santiago Ramón y Cajal first suggested that the brain stores information by rearranging the connections, or synapses, between neurons. Since then, neuroscientists have attempted to understand the physical changes associated with memory formation. But visualizing and mapping synapses is challenging to do. For one, synapses are very small and tightly packed together. They’re roughly 10 billion times smaller than the smallest object a standard clinical MRI can visualize. Furthermore, there are approximately 1 billion synapses in the mouse brains researchers often use to study brain function, and they’re all the same opaque to translucent color as the tissue surrounding them. A new imaging technique my colleagues and I developed, however, has allowed us to map synapses during memory formation. We found that the process of forming new memories changes how brain cells are connected to one another. While some areas of the brain create more connections, others lose them. Mapping new memories in fish Previously, researchers focused on recording the electrical signals produced by neurons. While these studies have confirmed that neurons change their response to particular stimuli after a memory is formed, they couldn’t pinpoint what drives those changes. © 2010–2022, The Conversation US, Inc.

Keyword: Learning & Memory
Link ID: 28149 - Posted: 01.12.2022

By Maria Temming It might seem like a fish needs a car like — well, like a fish needs a bicycle. But a new experiment suggests that fish actually make pretty good drivers. In the experiment, several goldfish learned to drive what is essentially the opposite of a submarine — a tank of water on wheels — to destinations in a room. That these fish could maneuver on land suggests that fishes’ understanding of space and navigation is not limited to their natural environment — and perhaps has something in common with landlubber animals’ internal sense of direction, researchers report in the Feb. 15 Behavioural Brain Research. Researchers at Ben-Gurion University of the Negev in Beer-Sheva, Israel taught six goldfish to steer a motorized water tank. The fishmobile was equipped with a camera that continually tracked a fish driver’s position and orientation inside the tank. Whenever the fish swam near one of the tank’s walls, facing outward, the vehicle trundled off in that direction. This goldfish knows how to use its wheels. Successfully navigating in a tank on land suggests that the animals understand space and direction in a way that lets them explore even in unfamiliar habitats. Fish were schooled on how to drive during about a dozen 30-minute sessions. The researchers trained each fish to drive from the center of a small room toward a pink board on one wall by giving the fish a treat whenever it reached the wall. During their first sessions, the fish averaged about 2.5 successful trips to the target. During their final sessions, fish averaged about 17.5 successful trips. By the end of driver’s ed, the animals also took faster, more direct routes to their goal. © Society for Science & the Public 2000–2022.

Keyword: Learning & Memory
Link ID: 28148 - Posted: 01.12.2022

By Sabrina Imbler Common bottlenose dolphins have sex frequently — very likely multiple times in a day. Copulation lasts only a few seconds, but social sex, which is used to maintain social bonds, can last much longer, happen more frequently and involve myriad heterosexual and homosexual pairings of dolphins and their body parts. Anything is possible, and, as new research suggests, probably pleasurable for swimmers of both sexes. According to a paper published on Monday in the journal Current Biology, female bottlenose dolphins most likely experience pleasure through their clitorises. The findings come as little surprise to scientists who research these dolphins. “The only thing that surprises me is how long it has taken us as scientists to look at the basic reproductive anatomy,” Sarah Mesnick, an ecologist at NOAA Fisheries who was not involved with the research, said, speaking of the clitoris. She added, “It took a team of brilliant women,” referring to two of the authors. “A lot of people assume that humans are unique in having sex for pleasure,” Justa Heinen-Kay, a researcher at the University of Minnesota who was not involved with the paper, wrote in an email. “This research challenges that notion.” And learning more about the anatomy of marine mammals’ genitalia has clear implications for their survival, Dr. Mesnick said: “The more we know about the social behavior of these animals, the better we’re able to understand their evolution and help use that to manage and conserve them.” Historically, researchers have focused on male genitalia, driven by prejudice toward male subjects, prejudice against female choice in sexual selection and the fact that it can be easier to study something that sticks out. “Female genitalia were assumed to be simple and uninteresting,” Dr. Heinen-Kay said. “But the more that researchers study female genitalia, the more we’re learning that this isn’t the case at all.” She added that this shift may be driven in part by the increasing number of women researchers. © 2022 The New York Times Company

Keyword: Sexual Behavior; Evolution
Link ID: 28147 - Posted: 01.12.2022

Stephen Wooding The sweetness of sugar is one of life’s great pleasures. People’s love for sweet is so visceral, food companies lure consumers to their products by adding sugar to almost everything they make: yogurt, ketchup, fruit snacks, breakfast cereals and even supposed health foods like granola bars. Schoolchildren learn as early as kindergarten that sweet treats belong in the smallest tip of the food pyramid, and adults learn from the media about sugar’s role in unwanted weight gain. It’s hard to imagine a greater disconnect between a powerful attraction to something and a rational disdain for it. How did people end up in this predicament? I’m an anthropologist who studies the evolution of taste perception. I believe insights into our species’ evolutionary history can provide important clues about why it’s so hard to say no to sweet. The basic activities of day-to-day life, such as raising the young, finding shelter and securing enough food, all required energy in the form of calories. Individuals more proficient at garnering calories tended to be more successful at all these tasks. They survived longer and had more surviving children – they had greater fitness, in evolutionary terms. One contributor to success was how good they were at foraging. Being able to detect sweet things – sugars – could give someone a big leg up. In nature, sweetness signals the presence of sugars, an excellent source of calories. So foragers able to perceive sweetness could detect whether sugar was present in potential foods, especially plants, and how much. © 2010–2022, The Conversation US, Inc.

Keyword: Chemical Senses (Smell & Taste); Evolution
Link ID: 28146 - Posted: 01.12.2022

Alejandra Marquez Janse & Christopher Intagliata Imagine you're moving to a new country on the other side of the world. Besides the geographical and cultural changes, you will find a key difference will be the language. But will your pets notice the difference? It was a question that nagged at Laura Cuaya, a brain researcher at the Neuroethology of Communication Lab at at Eötvös Loránd University in Budapest. "When I moved from Mexico to Hungary to start my post-doc research, all was new for me. Obviously, here, people in Budapest speak Hungarian. So you've had a different language, completely different for me," she said. The language was also new to her two dogs: Kun Kun and Odín. "People are super friendly with their dogs [in Budapest]. And my dogs, they are interested in interacting with people," Cuaya said. "But I wonder, did they also notice people here ... spoke a different language?" Cuaya set out to find the answer. She and her colleagues designed an experiment with 18 volunteer dogs — including her two border collies — to see if they could differentiate between two languages. Kun Kun and Odín were used to hearing Spanish; the other dogs Hungarian. The dogs sat still within an MRI machine, while listening to an excerpt from the story The Little Prince. They heard one version in Spanish, and another in Hungarian. Then the scientists analyzed the dogs' brain activity. © 2022 npr

Keyword: Language; Evolution
Link ID: 28145 - Posted: 01.08.2022

Jon Hamilton When baby mice cry, they do it to a beat that is synchronized to the rise and fall of their own breath. It's a pattern that researchers say could help explain why human infants can cry at birth — and how they learn to speak. Mice are born with a cluster of cells in the brainstem that appears to coordinate the rhythms of breathing and vocalizations, a team reports in the journal Neuron. If similar cells exist in human newborns, they could serve as an important building block for speech: the ability to produce one or many syllables between each breath. The cells also could explain why so many human languages are spoken at roughly the same tempo. "This suggests that there is a hardwired network of neurons that is fundamental to speech," says Dr. Kevin Yackle, the study's senior author and a researcher at the University of California, San Francisco. Scientists who study human speech have spent decades debating how much of our ability is innate and how much is learned. The research adds to the evidence that human speech relies — at least in part — on biological "building blocks" that are present from birth, says David Poeppel, a professor of psychology and neural science at New York University who was not involved in the study. But "there is just a big difference between a mouse brain and a human brain," Poeppel says. So the human version of this building block may not look the same. © 2022 npr

Keyword: Language; Evolution
Link ID: 28144 - Posted: 01.08.2022

by Peter Hess Of all the brain chemistry that autism researchers study, few molecules have garnered as much attention as the so-called ‘social hormone,’ oxytocin. Some autistic children appear to have low blood levels of oxytocin, which has led several teams to test oxytocin delivered intranasally as an autism therapy. So far, though, such clinical trials have yielded inconsistent results. Here we explain what scientists know so far about oxytocin’s connection to autism. What does oxytocin do in the brain and body? Oxytocin serves multiple purposes, such as promoting trust between people, moderating our response to threats, and supporting lactation and mother-child bonding. The hormone is produced primarily in the hypothalamus, a brain region that mediates basic bodily functions, including hunger, thirst and body temperature. Oxytocin-producing neurons in the hypothalamus project into other parts of the brain, such as the nucleus accumbens, where the hormone regulates social-reward learning. In the brain’s sensory system, including the olfactory bulb, oxytocin seems to help balance excitatory and inhibitory signals, improving social-information processing, at least in rats. In the amygdala, oxytocin appears to help dull threat responses to negative social information and foster social recognition. The pituitary gland controls the release of oxytocin into the bloodstream. Blood oxytocin is crucial to start uterine muscle contractions during childbirth. It also supports lactation by facilitating the milk letdown reflex, stimulating the flow of milk into the nipple. © 2022 Simons Foundation

Keyword: Hormones & Behavior; Autism
Link ID: 28143 - Posted: 01.08.2022

By Charles F. Zorumski One minute you’re enjoying a nice buzz, the next your brain stops recording events that are taking place. The result can mean having vague or no memory of a time period ranging anywhere from a few minutes up to several hours. Scary—isn’t it? Unfortunately, alcohol-induced blackouts aren’t a rarity, either. A 2015 survey of English teenagers who drank showed 30 percent of 15-year-olds and 75 percent of 19-year-olds suffered alcohol-induced blackouts. In medical terms this memory loss is a form of temporary anterograde amnesia, a condition where the ability to form new memories is, for a limited time, impaired. That means you can’t remember a stretch of time because your brain was unable to record and store memories in the first place. Neuroscientists do not fully understand how blackouts occur. Researchers long assumed alcohol impairs memory because it kills brain cells. Indeed, long-standing alcohol abuse can damage nerve cells and permanently impact memory and learning. It is unlikely, however, that brain damage is behind acute blackouts. It is clear that processes in the hippocampus—the area of brain involved in the formation, storage and retrieval of new memories—are disturbed. Specifically, it appears alcohol impairs the so-called long-term potentiation of synapses at the pyramidal cells in the hippocampus. Alcohol alters the activity of certain glutamate receptors, thereby boosting the production of specific steroid hormones. This in turn slows the long-term potentiation of hippocampal synapses. Normally this mechanism, responsible for strengthening the synaptic transfer of information between neurons, is the basis of memory formation. © 2022 Scientific American,

Keyword: Drug Abuse; Learning & Memory
Link ID: 28142 - Posted: 01.08.2022