Katharine Sanderson Liz Williams was standing pitchside at a women’s rugby match, and she did not like what she was seeing. Williams, who researches forensic biomechanics at Swansea University, UK, had equipped some of the players with a mouthguard that contained a sensor to measure the speed of head movement. She wanted to understand more about head injuries in the brutal sport. “There were a few instances when my blood went cold,” Williams said. When the women fell in a tackle, their heads would often whiplash into the ground. The sensors showed that the skull was accelerating — indicating an increased risk of brain injury. But medical staff at the match, not trained to look out for this type of head movement as a cause of injury, deemed the women fine to play on. Such whiplash injuries are much rarer when males play. Williams’ observations highlight an increasingly apparent problem. A growing body of data suggests that female athletes are at significantly greater risk of a traumatic brain injury event than male athletes. They also fare worse after a concussion and take longer to recover. As researchers gather more data, the picture becomes steadily more alarming. Female athletes are speaking out about their own experiences, including Sue Lopez, the United Kingdom’s first semi-professional female football player in the 1970s, who now has dementia — a diagnosis she has linked to concussions from heading the ball. Researchers have offered some explanations for the greater risk to women, although the science is at an early stage. Their ideas range from differences in the microstructure of the brain to the influence of hormones, coaching regimes, players’ level of experience and the management of injuries. © 2021 Springer Nature Limited

Keyword: Brain Injury/Concussion; Sexual Behavior
Link ID: 27932 - Posted: 08.04.2021

By Alistair Magowan BBC Sport Defenders are more likely to have dementia in later life compared with other playing positions in football, says new research. In 2019, a study by Professor Willie Stewart found that former footballers were about three and a half times more likely to die of neurodegenerative brain disease than the general population. But his new research says the risk is highest among defenders, who are five times more likely to have dementia than non-footballers. That compared with three times the risk for forwards, and almost no extra risk for goalkeepers compared with the population. Outfield players were four times more likely to have brain disease such as dementia. The research by the University of Glasgow, which was funded by the Football Association and players' union the Professional Footballers' Association, also found that risk increased the longer a player's football career was. And despite changes in football technology and head-injury management in recent years, there was no evidence that neurodegenerative disease risk changed for footballers in this study, whose careers spanned from about 1930 to the late 1990s. 'Footballs should be sold with a health warning about heading' Study author and consultant neuropathologist Dr Stewart said that it was time for football to eliminate the risk of heading, which he said could also cause short-term impairment of brain function. "I think footballs should be sold with a health warning saying repeated heading in football may lead to increased risks of dementia," he said. "Unlike other dementias and degenerative diseases, where we have no idea what causes them, we know the risk factor [with football] and it's entirely preventable. © 2021 BBC.

Keyword: Brain Injury/Concussion
Link ID: 27931 - Posted: 08.04.2021

By Jennifer Couzin-Frankel They rose to fame as the world’s fattest mice. At about 130 grams, the rodents were “the equivalent of 600 pounds in humans,” says diabetes researcher Philipp Scherer. They were born to genetically engineered mouse parents in his lab at the University of Texas Southwestern Medical Center. One set of parents lacked the hormone leptin, an appetite suppressant that signals when it’s time to stop eating. The other parents overproduced the hormone adiponectin, churned out by fat cells, which is thought to support metabolic health, protecting against obesity-linked diseases such as type 2 diabetes. Scherer’s mouse pups melded their parents’ traits. They ate constantly and became obese. But unlike other leptin-deficient mice (and people), the animals had healthy cholesterol and blood glucose levels and didn’t develop metabolic illnesses such as type 2 diabetes. “ They were exceptionally quote-unquote healthy,” Scherer says, though he wonders whether it’s possible to be truly well while carrying such a considerable fat burden. Despite their metabolic health, the mice didn’t live a normal life span: Their weight left them so off balance that they often flipped over and got stuck, causing dehydration and death. Still, to Scherer, who described the animals in 2007 and continues to study them, the rodents sharpened an emerging message for people as well as mice: Weight and health can be uncoupled. Many researchers and doctors—and broader societies—take it as a given that obesity means ill health. In fact, says Ruth Loos, who studies the genetics of obesity at the University of Copenhagen, “We can be obese but remain healthy.” Scherer, Loos, and other researchers worldwide are examining genes, animal models, and humans to understand how factors such as the distribution of fat in the body and the nature of fat itself can blunt or compound any health impacts of extra weight. The researchers are also working to define metabolically healthy obesity (MHO) and examine how common it is and how long it persists. © 2021 American Association for the Advancement of Science

Keyword: Obesity
Link ID: 27930 - Posted: 08.04.2021

By Katharine Q. Seelye Dr. J. Allan Hobson, a psychiatrist and pioneering sleep researcher who disputed Freud’s view that dreams held hidden psychological meaning, died on July 7 at his home in East Burke, Vt. He was 88. The cause was kidney failure resulting from diabetes, said his daughter, Julia Hobson Haggerty. For some time, sleep was not taken seriously as an academic pursuit. Even Dr. Hobson, who was a professor of psychiatry at Harvard Medical School and director of the Laboratory of Neurophysiology at the Massachusetts Mental Health Center, joked that the only known function of sleep was to cure sleepiness. But over a career that spanned more than four decades, his own research and that of others showed that sleep is crucial to normal cognitive and emotional function, including learning and memory. In more than 20 books — among them “The Dreaming Brain” (1988); “Dreaming as Delirium: How the Brain Goes Out of its Mind” (1999), and “Dream Self” (2021), a memoir — he popularized his research and that of others, including the findings that sleep begins in utero and is essential for tissue growth and repair throughout life. “He showed that sleep isn’t a nothing state,” Ralph Lydic, who conducted research with Dr. Hobson in the 1980s and is a professor of neuroscience at the University of Tennessee, said in a phone interview. “He demonstrated that the brain is as active during R.E.M. sleep as it is during wakefulness,” he added, referring to sleep characterized by rapid eye movement. “We know as much about sleep as we do in part because of him.” One of his most influential contributions to dream research came in 1977, when Dr. Hobson and a colleague, Robert McCarley, produced a cellular and mathematical model that they believed showed how dreams occur. Dreams, they said, are not mysterious codes sent by the subconscious but rather the brain’s attempt to attribute meaning to random firings of neurons in the brain. © 2021 The New York Times Company

Keyword: Sleep
Link ID: 27929 - Posted: 08.04.2021

By James Gorman You’ve heard of trash pandas: Raccoons raiding the garbage. How about trash parrots? Sulfur-crested cockatoos, which may sound exotic to Americans and Europeans, are everywhere in suburban areas of Sydney. They have adapted to the human environment, and since they are known to be clever at manipulating objects it’s not entirely surprising that they went after a rich food source. But you might say that the spread of their latest trick, to open trash cans, blows the lid off social learning and cultural evolution in animals. Not only do the birds acquire the skill by imitating others, which is social learning. But the details of technique evolve to differ in different groups as the innovation spreads, a mark of animal culture. Barbara C. Klump, a behavioral ecologist at the Max Planck Institute of Animal Behavior in Germany, and the first author of a report on the cockatoo research in the journal Science, said, “It’s actually quite a complex behavior because it has multiple steps.” Dr. Klump and her colleagues broke the behavior down into five moves. First a bird uses its bill to pry the lid from the container. Then, she said, “they open it and then they hold it and then they walk along one side and then they flip it over. And at each of these stages, there is variation.” Some birds walk left, some right, they step differently or hold their heads differently. The process is similar to the spread and evolution of human cultural innovations like language, or a classic example of animal culture, bird song, which can vary from region to region in the same species. Dr. Klump and her colleagues in Germany and Australia plotted the spread of the behavior in greater Sydney over the course of two years. The behavior became more common, but it didn’t pop up in random locations as it might if different birds were figuring out the trash bin technique on their own. It spread outward from its origin, indicating that the cockatoos were learning how to do it from each other. © 2021 The New York Times Company

Keyword: Learning & Memory; Evolution
Link ID: 27928 - Posted: 07.28.2021

Jason Ulrich and David M. Holtzman In 1907 German psychiatrist Alois Alzheimer published a case report of an unusual illness affecting the cerebral cortex. A 51-year-old woman living in an asylum in Frankfurt am Main exhibited symptoms that are all too familiar to the millions of families affected by what is now known as Alzheimer’s disease. There was memory loss, confusion and disorientation. After the patient died, Alzheimer examined her brain and made a few key observations. First, it was smaller than average, or atrophic, with a corresponding loss of neurons. Next, there were tangles of protein fibers within neurons and deposits of a different protein outside brain cells. For the next 100 years, these two pathological proteins—known as tau and amyloid—were the focus of research into the causes of the disease. But there was an additional, often forgotten clue that Alzheimer noted in the autopsy. Under the microscope lens, he saw clear changes in the structural makeup of certain nonneuronal cells. Called glia, they constitute roughly half of the brain’s cells. After being studied by only a small number of scientists since Alzheimer’s discovery, glia have now entered the spotlight. One type, called microglia, is the main kind of immune cell in the brain and may influence the progression of the disease in different ways during both early and later stages. Microglia might also explain the complex relation between amyloid and tau, the aberrant proteins that lead to neuron degeneration and memory loss. © 2021 Scientific American

Keyword: Alzheimers; Neuroimmunology
Link ID: 27927 - Posted: 07.28.2021

By Sabrina Imbler In a way, nausea is our trusty personal bodyguard. Feeling nauseated is widely accepted to be an evolutionary defense measure that protects people from pathogens and parasites. The urge to gag or vomit is “well-suited” to defend ourselves against things we swallow that might contain pathogens, according to Tom Kupfer, a psychological scientist at Nottingham Trent University in England. But vomiting is somewhat futile against a tick, an ectoparasite that latches on to skin, not stomachs. In an experiment that produced both stomach churning and skin crawling sensations — I can confirm these and some other physiological responses firsthand — Dr. Kupfer and Daniel Fessler, an evolutionary anthropologist from the University of California, Los Angeles, argue in a paper published on Wednesday in the journal Proceedings of the Royal Society B that humans have evolved to defend themselves against ectoparasites through a skin response that elicits scratching. Although some outside experts say more research is needed, the findings align with some understandings of the evolution of disgust. “It makes sense to have developed adaptive defensive strategies against the ‘nasty’ ones,” Cécile Sarabian, a cognitive ecologist studying animal disgust at the Kyoto University Primate Research Institute in Japan, wrote in an email. The disgusting investigation began in 2017 on the grounds of Chicheley Hall in Buckinghamshire, England. Here, Dr. Kupfer was presenting findings to colleagues on trypophobia, the aversion to clustered holes experienced by some people. His data showed that participants with trypophobia often reacted to holey images with the urge to itch or scratch, sometimes to the point of bleeding. Dr. Kupfer suggested that trypophobia might not represent fear, but rather a disgust reaction to signs of parasites or infectious diseases, which can both result in clusters of lesions or pustules.

Keyword: Pain & Touch
Link ID: 27926 - Posted: 07.28.2021

By Barbara Casassus PARIS—Five public research institutions in France have imposed a 3-month moratorium on the study of prions—a class of misfolding, infectious proteins that cause fatal brain diseases—after a retired lab worker who handled prions in the past was diagnosed with Creutzfeldt-Jakob disease (CJD), the most common prion disease in humans. An investigation is underway to find out whether the patient, who worked at a lab run by the National Research Institute for Agriculture, Food and Environment (INRAE), contracted the disease on the job. If so, it would be the second such case in France in the past few years. In June 2019, an INRAE lab worker named Émilie Jaumain died at age 33, 10 years after pricking her thumb during an experiment with prion-infected mice. Her family is now suing INRAE for manslaughter and endangering life; her illness had already led to tightened safety measures at French prion labs. The aim of the moratorium, which affects nine labs, is to “study the possibility of a link with the [new patient’s] former professional activity and if necessary to adapt the preventative measures in force in research laboratories,” according to a joint press release issued by the five institutions yesterday. “This is the right way to go in the circumstances,” says Ronald Melki, a structural biologist at a prion lab jointly operated by the French national research agency CNRS and the French Alternative Energies and Atomic Energy Commission (CEA). “It is always wise to ask questions about the whole working process when something goes wrong.” "The occurrence of these harsh diseases in two of our scientific colleagues clearly affects the whole prion community, which is a small 'familial' community of less than 1000 people worldwide," Emmanuel Comoy, deputy director of CEA's Unit of Prion Disorders and Related Infectious Agents, writes in an email to Science. Although prion research already has strict safety protocols, "it necessarily reinforces the awareness of the risk linked to these infectious agents," he says. © 2021 American Association for the Advancement of Science.

Keyword: Prions
Link ID: 27925 - Posted: 07.28.2021

By Tom Zeller Jr. I have headaches. Not the low-grade, annoying, “I’ve got a headache” sort of headaches. I get those, too. Most everyone does, and they are a drag. No, when I say that I get headaches, I mean that at intervals that are largely unpredictable, a knot of pain rises deep inside my head, invariably sensed behind my right eyeball. It then swiftly clicks up through the intensity scale, racing past that dull ache you might get from staring at the screen too long, leapfrogging over that doozy you had the morning after your brother’s wedding, skipping past the agonizing-but-fleeting stab of an ice-cream headache, and arriving, within a matter of minutes, at a pain so piercing and sustained that I can only grip something sturdy, rock back and forth, and grunt until it subsides. Mine are what doctors call one of the “primary headaches” — recurring and often excruciating disorders that are not byproducts of another condition (or self-inflicted by last night’s cocktails), but relentless, and in many ways still poorly understood disorders unto themselves. We know them by common names like migraine, which affects tens of millions of Americans, disproportionately women. I suffer from another flavor known as cluster headaches (technically “trigeminal autonomic cephalalgias”). And there are others, with myriad and imperfectly drawn lines distinguishing them. If you experience migraines or cluster headaches — and research suggests that more than a billion people worldwide do — you probably know something about shuttling from doctor to doctor looking for someone who “gets it.” You know what it’s like to gladly gobble up pills that don’t really work and that leave you miserable in other ways. And you might even know the same sort of incredulous exasperation that has driven me to wonder, from my fetal position on the bathroom floor: “How is it possible that science can’t fix a damn headache?” © 2021 The New York Times Company

Keyword: Pain & Touch
Link ID: 27924 - Posted: 07.24.2021

Christie Wilcox One of the most well-studied synapses in the brain continues to surprise neuroscientists. According to a May 18 study in Nature Communications, mossy fiber synapses, so named because their terminals look a bit like moss growing on the axons, have an unexpected way of regulating the flow of information in the hippocampus: the postsynaptic cells that receive neurotransmitter signals can release their own glutamate to tamp down the transmission from the cell on the presynaptic side. This so-called retrograde signaling was totally unexpected and depends on calcium influx to the postsynaptic cell, meaning researchers might have to rethink the results of past experiments that used in vitro conditions with different calcium availability. The findings are “a big deal” for neuroscientists, says Chris McBain, a synaptic physiologist at the National Institutes of Health who was not involved in the study. “Retrograde glutamatergic signaling is a really rare occurrence in the central nervous system,” he notes, and to find it in mossy fibers “adds another layer of complexity onto one of the most complex synapses.” The researchers behind the new paper, led by neurophysiologist Peter Jonas of the Institute of Science and Technology Austria, were investigating the plasticity of hippocampal neurons, the dynamic changes in connections between cells that contribute to the functioning of neural circuits and that ultimately underlie learning, memory, and other cognitive abilities. János Szabadics, a neurophysiologist at the Institute of Experimental Medicine, Budapest, puts it quite simply: “Without synaptic plasticity, the brain would be just a bag of wires,” he says. © 1986–2021 The Scientist.

Keyword: Learning & Memory
Link ID: 27923 - Posted: 07.24.2021

Nidhi Subbaraman Maeve Wallace has studied maternal health in the United States for more than a decade, and a grim statistic haunts her. Five years ago, she published a study showing that being pregnant or recently having had a baby nearly doubles a woman’s risk of being killed1. More than half of the homicides she tracked, using data from 37 states, were perpetrated with a gun. In March 2020, she saw something she hadn’t seen before: a funding opportunity from the US National Institutes of Health (NIH) to study deaths and injuries from gun violence. She had mentioned firearms in her studies before. But knowing that the topic is politically fraught, she often tucked related terms and findings deep within her papers and proposals. This time, she says, she felt emboldened to focus on guns specifically, and to ask whether policies that restrict firearms for people convicted of domestic violence would reduce the death rate for new and expecting mothers. Male partners are the killers in nearly half of homicides involving women in the United States. “This call for proposals really motivated me to ask the research questions that I may not have otherwise asked,” says Wallace, an epidemiologist at Tulane University in New Orleans, Louisiana. Wallace’s group is one of several dozen funded by a new pool of federal money for gun-violence research in the United States, which has more firearm-related deaths than any other wealthy nation. Although other countries fund research on guns, it is often in the context of trafficking and armed conflict. US federal funding of gun-violence research has not reflected the death toll, researchers say. © 2021 Springer Nature Limited

Keyword: Aggression
Link ID: 27922 - Posted: 07.24.2021

Amanda Heidt Scientists have discovered two types of glial cells in the brains of adult mice—an astrocyte and an oligodendrocyte progenitor cell—after nudging neural stem cells to rise from dormancy, according to a study published June 10 in Science. The results suggest new roles for glial cells, best known for providing support to neurons, and could prompt a better understanding of how brains remain plastic into adulthood, when the vast majority of neurons no longer undergo cell division. This study is “a very important addition to the whole story about these fascinating [stem] cells that exist in the adult brain of rodents that have the capacity to generate new cells,” says Arturo Alvarez-Buylla, a developmental neuroscientist at the University of California, San Francisco, who was not involved in the work. “Understanding adult stem cells is fundamental to really know the kinds of plasticity that exist after the developmental period is over.” Most mammalian brain cells, be they neurons or glia, are generated during embryonic development, and reservoirs of stem cells become largely, if not entirely, dormant in adulthood. The small trickle of activity that is left can help the brain respond to change, sometimes by generating new neurons to help with learning or by producing cells in response to injury or disease. One pool exists in the brains of adult humans and mice, in an area called the ventricular-subventricular zone (V-SVZ). The walls of the two lateral ventricles, cavities filled with cerebrospinal fluid, are lined with stem cells, and along these walls, the cells have a regional identity—where a stem cell lies on the wall dictates what it differentiates into. This feature has been well-characterized for neuronal subtypes, which are synthesized within discrete domains on the lateral wall. Glial cells are known to be generated at low levels along the septal wall, but the specific subtypes remain unknown because the cells along this wall generally remain inactive. © 1986–2021 The Scientist.

Keyword: Development of the Brain; Neurogenesis
Link ID: 27921 - Posted: 07.24.2021

Amanda Heidt Takotsubo syndrome, also known as broken heart syndrome, is a rare, reversible condition with symptoms mimicking a mild heart attack. A disease that disproportionately affects women, TTS is triggered by stressful events such as bankruptcy, the death of a loved one, or divorce, and results in a weakening of the heart’s left ventricle such that it becomes temporarily misshapen. Previous work has shown that TTS patients have elevated activity in their amygdala, a brain region involved in stress response. What has never been clear, however, is whether “this activity in the brain happens as a result of the syndrome or whether it began many years before,” says Shady Abohashem, a nuclear cardiologist at Harvard Medical School. Abohashem and his colleagues retrospectively analyzed full-body PET/CT scans from 104 patients, most of whom had cancer and 41 of whom had developed TTS since first being scanned, and 63 individually matched controls. The team calculated ratios of the activity in each person’s amygdala to that of two brain regions that attenuate the stress response, the temporal lobe and the prefrontal cortex. Higher amygdala activity was associated with an increased risk for TTS, and among those with the condition, patients with higher ratios had developed TTS roughly two years earlier following the imaging than those with lower ratios. “We can now show that this syndrome happens as a result of chronic stress over years that makes you vulnerable to developing the syndrome more easily and sooner than [less stressed] people,” Abohashem says. © 1986–2021 The Scientist.

Keyword: Stress
Link ID: 27920 - Posted: 07.24.2021

By Pam Belluck, Sheila Kaplan and Rebecca Robbins Two months before the Food and Drug Administration’s deadline to decide whether to approve Biogen’s controversial Alzheimer’s drug, aducanumab, a council of senior agency officials resoundingly agreed that there wasn’t enough evidence it worked. The council, a group of 15 officials who review complex issues, concluded that another clinical trial was necessary before approving the drug. Otherwise, one council member noted, approval could “result in millions of patients taking aducanumab without any indication of actually receiving any benefit, or worse, cause harm,” according to minutes of the meeting, obtained by The New York Times. “It is critical that the decision be made from a place of certainty,” the minutes said. The session, whose details have not been reported before, represented at least the third time that proponents of approving aducanumab in the F.D.A. had received a clear message that the evidence did not convincingly show the drug could slow cognitive decline. On June 7, the F.D.A. greenlighted the drug anyway — a decision that has been met with scathing rebuke from many Alzheimer’s experts and other scientists and calls for investigations into how the agency approved a treatment that has little evidence it helps patients. How and why the F.D.A. went ahead and approved the drug — an intravenous infusion, marketed as Aduhelm, that the company has since priced at $56,000 a year — has become the subject of intense scrutiny. Two congressional committees are investigating the approval and the price. Much is still unknown, but an examination by The Times has found that the process leading to approval took several unusual turns, including a decision for the F.D.A. to work far more closely with Biogen than is typical in a regulatory review. Allegations about the collaboration prompted the F.D.A. to conduct an internal inquiry after a consumer advocacy group called for an inspector general’s investigation, according to documents reviewed by The Times. The agency has not disclosed the inquiry. © 2021 The New York Times Company

Keyword: Alzheimers
Link ID: 27919 - Posted: 07.21.2021

by Peter Hess Neurons in mice with an autism-linked mutation sprout extraneous protrusions, an overgrowth that tracks with above-average motor learning. The animals lose both attributes when treated with an experimental drug that suppresses the activity of the Ras-ERK/MAPK cell signaling pathway, according to a new study. This pathway helps reshape neurons to change the strength of their connections in response to learning or other influences, part of a process known as neuroplasticity. “There is a balance between learning and forgetting in the brain,” says lead researcher Stelios Smirnakis, associate professor of neurology at Harvard University. “Understanding these pathways and how to balance them is of critical importance to a number of neurological disorders.” Hyperactivation of the Ras-ERK/MAPK pathway, which is also involved in cell growth, has been linked to cancer as well as multiple autism-related conditions. “A lot of genes in that pathway have been shown to underlie several forms of autism,” says Maria Chahrour, assistant professor of neuroscience at the University of Texas Southwestern Medical Center in Dallas, who was not involved in the study. “The pathway itself is also dysregulated in several forms of autism, so there’s a potential convergence.” The mice in the new work had an extra copy of the gene MECP2. As in previous studies and some other autism mouse models, the MECP2-duplication mice showed enhanced motor learning, mastering how to balance on a rotating rod more quickly than their wildtype counterparts. The animals’ motor learning prowess offers a model for studying how the repetitive behaviors seen in people with autism develop, the researchers say. © 2021 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 27918 - Posted: 07.21.2021

By Kim Tingley During menopause, which marks the end of a woman’s menstrual cycles, her ovaries stop producing the hormones estrogen and progesterone, bringing an end to her natural childbearing years. But those hormones also regulate how the brain functions, and the brain governs their release — meaning that menopause is a neurological process as well. “Many of the symptoms of menopause cannot possibly be directly produced by the ovaries, if you think about the hot flashes, the night sweats, the anxiety, the depression, the insomnia, the brain fog,” says Lisa Mosconi, an associate professor of neurology at Weill Cornell Medicine and director of its Women’s Brain Initiative. “Those are brain symptoms, and we should look at the brain as something that is impacted by menopause at least as much as your ovaries are.” In June, Mosconi and her colleagues published in the journal Scientific Reports one of the few studies to observe in detail what happens to the brain throughout the menopause transition, not just before and after. Using various neuroimaging techniques, they scanned the brains of more than 160 women between the ages of 40 and 65 who were in different stages of the transition to examine the organ’s structure, blood flow, metabolism and function; they did many of the same scans two years later. They also imaged the brains of men in the same age range. “What we found in women and not in men is that the brain changes quite a lot,” Mosconi says. “The transition of menopause really leads to a whole remodeling.” On average, women in the United States enter the menopause transition — defined as the first 12 consecutive months without a period — at around 50; once diagnosed, they are in postmenopause. But they may begin to have hormonal fluctuations in their 40s. (For some women, this happens in their 30s, and surgical removal of the ovaries causes immediate menopause, as do some cancer treatments.) Those fluctuations cause irregular periods and potentially a wide variety of symptoms, including hot flashes, insomnia, mood swings, trouble concentrating and changes in sexual arousal. During this phase, known as perimenopause, which averages four years in length (but can last from several months to a decade), Mosconi and colleagues observed that their female subjects experienced a loss of both gray matter (the brain cells that process information) and white matter (the fibers that connect those cells). Postmenopause, however, that loss stopped, and in some cases brain volume increased, though not to its premenopausal size. © 2021 The New York Times Company

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 27917 - Posted: 07.21.2021

By Jonathan Lambert Winter on the Qinghai-Tibetan Plateau is unfriendly to pikas. Temperatures across the barren, windy highlands routinely dip below –30° Celsius, and the grass that typically sustains the rabbitlike mammals becomes dry and brittle. It would seem the perfect time for these critters to hibernate, or subsist on stores of grass in burrows to stay warm, like the North American pika. Instead, plateau pika (Ochotona curzoniae) continue foraging in winter, but reduce their metabolism by about 30 percent to conserve energy, researchers report July 19 in the Proceedings of the National Academy of Sciences. Some pikas also resort to unusual rations: yak poop. Camera data from four sites confirmed that pikas regularly brave the cold to forage. “Clearly they’re doing something fancy with their metabolism that’s not hibernation,” says John Speakman, an ecophysiologist at the University of Aberdeen in Scotland. Speakman and colleagues measured daily energy expenditure of 156 plateau pikas in summer and winter, and implanted 27 animals with temperature sensors. While many nonhibernating animals keep warm in winter by using more energy, these pikas did the opposite (SN: 1/22/14). On average, pikas reduced their metabolism by 29.7 percent, in part by cooling their bodies a couple degrees overnight. The animals were also less active, relative to summertime levels. © Society for Science & the Public 2000–2021.

Keyword: Obesity
Link ID: 27916 - Posted: 07.21.2021

By Gretchen Reynolds We all know that lifting weights can build up our muscles. But by changing the inner workings of cells, weight training may also shrink fat, according to an enlightening new study of the molecular underpinnings of resistance exercise. The study, which involved mice and people, found that after weight training, muscles create and release little bubbles of genetic material that can flow to fat cells, jump-starting processes there related to fat burning. The results add to mounting scientific evidence that resistance exercise has unique benefits for fat loss. They also underscore how extensive and interconnected the internal effects of exercise can be. Many of us pigeonhole resistance training as muscle building, and with good reason. Lifting weights — or working against our body weight as we bob through push-ups, squats or chair dips — will noticeably boost our muscles’ size and strength. But a growing number of studies suggest weight training also reshapes our metabolisms and waistlines. In recent experiments, weight workouts goosed energy expenditure and fat burning for at least 24 hours afterward in young women, overweight men and athletes. Likewise, in a study I covered earlier this month, people who occasionally lifted weights were far less likely to become obese than those who never lifted. But how weight training revamps body fat remains murky. Part of the effect occurs because muscle is metabolically active and burns calories, so adding muscle mass by lifting should increase energy expenditure and resting metabolic rates. After six months of heavy lifting, for example, muscles will burn more calories just because they are larger. But that doesn’t fully explain the effect, because adding muscle mass requires time and repetition, while some of the metabolic effects of weight training on fat stores seem to occur immediately after exercise. © 2021 The New York Times Company

Keyword: Obesity
Link ID: 27915 - Posted: 07.21.2021

By Linda Searing Keeping your brain active later in life may delay by as much as five years the onset of Alzheimer’s disease, the most common type of dementia. Research published in the journal Neurology found that cognitively stimulating activities that involve seeking or processing information — such as reading books, magazines or newspapers, writing letters, playing card games, board games or checkers, and doing puzzles — seemed to add dementia-free time to older people’s lives. The research involved 1,903 people (average age was 80), none of whom had dementia at the start of the study and who were tracked and tested for up to 22 years. In that time, 457 participants developed Alzheimer’s. That occurred on average at age 94 for people who did the most brain-stimulating activities later in life, compared with developing Alzheimer’s at age 89 for those with the least amount of cognitive activity. Alzheimer’s, considered a degenerative brain disease, affects memory, thinking and behavior, with symptoms eventually becoming severe enough to interfere with once-routine daily tasks. Today, about 6.2 million Americans 65 and older have the disease, two-thirds of them women, according to the Alzheimer’s Association. That number is expected to reach nearly 13 million by 2050, unless ways are discovered to prevent, cure or slow the disease. The researchers found that neither education nor cognitive activity early in life were associated with the age at which a person developed Alzheimer’s. Rather, it’s what you do later in life that seems to make a difference. And, as the lead author of the story said, “It’s never too late to start doing the kinds of inexpensive, accessible activities” tracked in the study, “even in your 80s.”

Keyword: Alzheimers; Learning & Memory
Link ID: 27914 - Posted: 07.21.2021

By Pam Belluck He has not been able to speak since 2003, when he was paralyzed at age 20 by a severe stroke after a terrible car crash. Now, in a scientific milestone, researchers have tapped into the speech areas of his brain — allowing him to produce comprehensible words and sentences simply by trying to say them. When the man, known by his nickname, Pancho, tries to speak, electrodes implanted in his brain transmit signals to a computer that displays his intended words on the screen. His first recognizable sentence, researchers said, was, “My family is outside.” The achievement, published on Wednesday in the New England Journal of Medicine, could eventually help many patients with conditions that steal their ability to talk. “This is farther than we’ve ever imagined we could go,” said Melanie Fried-Oken, a professor of neurology and pediatrics at Oregon Health & Science University, who was not involved in the project. Three years ago, when Pancho, now 38, agreed to work with neuroscience researchers, they were unsure if his brain had even retained the mechanisms for speech. “That part of his brain might have been dormant, and we just didn’t know if it would ever really wake up in order for him to speak again,” said Dr. Edward Chang, chairman of neurological surgery at University of California, San Francisco, who led the research. The team implanted a rectangular sheet of 128 electrodes, designed to detect signals from speech-related sensory and motor processes linked to the mouth, lips, jaw, tongue and larynx. In 50 sessions over 81 weeks, they connected the implant to a computer by a cable attached to a port in Pancho’s head, and asked him to try to say words from a list of 50 common ones he helped suggest, including “hungry,” “music” and “computer.” As he did, electrodes transmitted signals through a form of artificial intelligence that tried to recognize the intended words. © 2021 The New York Times Company

Keyword: Brain imaging; Language
Link ID: 27913 - Posted: 07.17.2021