Jon Hamilton Scientists are working to develop new treatments for Alzheimer's disease by looking beyond amyloid plaques, which have been the focus of most Alzheimer's drug development in the past 20 years. Science Photo Library — ZEPHYR./Getty Images Immune cells, toxic protein tangles and brain waves are among the targets of future Alzheimer's treatments, scientists say. These approaches are noteworthy because they do not directly attack the sticky amyloid plaques in the brain that are a hallmark of Alzheimer's. The plaques have been the focus of most Alzheimer's drug development in the past 20 years. And the drug Aduhelm was given conditional approval by the Food and Drug Administration in June based primarily on the medication's ability to remove amyloid from the brain. But many researchers believe amyloid drugs alone can't stop Alzheimer's. "The field has been moving beyond amyloid for many years now," says Malú Gámez Tansey, co-director of the Center for Translational Research in Neurodegenerative Disease at the University of Florida. Tansey and a number of other researchers offered a wide range of alternative strategies at the Alzheimer's Association International Conference in Denver last month. Here are three of the most promising: © 2021 npr

Keyword: Alzheimers; Development of the Brain
Link ID: 27940 - Posted: 08.11.2021

By Rachel Fritts As you age, your brain slows down. You may forget where you left your glasses or have trouble picking up a new skill. Now there’s hope from rodent experiments that some of these declines could be reversed—but it takes guts. New research shows a transplant of gut microbes, in the form of feces, from young mice to old ones can turn back the clock on the aging brain. The study is “a tour de force” for the scope of data it collected, says Sean Gibbons, a gut microbe researcher at the Institute for Systems Biology. Still, he says, more work must be done before anyone considers doing anything similar with humans. The bacteria in our intestines influence everything from our daily moods to our overall health. This “gut microbiome” also changes over the course of our lives. But whereas some studies have shown young blood can have rejuvenating effects on old mice, the microbiome’s impact on age-related declines hasn’t been clear. To test whether a young microbiome could reverse signs of aging, researchers took fecal samples from 3- to 4-month-old mice, the equivalent of young adults, and transplanted them into 20-month-old animals—ancient by mouse standards. The scientists fed a slurry of feces to the old mice using a feeding tube twice a week for 8 weeks. As controls, old mice received transplants from fellow old mice, and young from young. The first thing the team noticed was that the gut microbiomes of the old mice given young mouse microbes began to resemble those of the younger ones. The common gut microbe Enterococcus became much more abundant in old mice, just as it is in young mice, for example. © 2021 American Association for the Advancement of Science

Keyword: Obesity; Development of the Brain
Link ID: 27939 - Posted: 08.11.2021

By Lisa Sanders, M.D. The burning started as soon as the 59-year-old woman put the drops into her eye. She blinked to try to rinse away the medication with her tears. She leaned forward to the mirror. Her left eye was red and angry-looking. She’d been using these eye drops for nearly a year to treat her newly diagnosed glaucoma, adding artificial tears for the dry eyes that appeared a few months later. And while she’d had plenty of problems with her eyes since all this started, this fiery pain was new. The vision in her left eye had been bad for a few years by then, but with an operation nearly two years earlier to remove an abnormal membrane on her retina and more recent cataract surgery, she had hoped she would have her old vision back by now. She was a physician-researcher and spent much of her time reading and writing, so her vision was very important to her livelihood. But despite the efforts of her eye doctors — and at this point she had many — she still couldn’t see well. It was when she was getting ready for the cataract surgery that the patient learned she had glaucoma. After her initial exam, her new eye surgeon told her that the pressure inside her left eye was abnormally high, and she was already showing signs of damage from it. He wanted her to see one of his colleagues, Dr. Amanda Bicket, a glaucoma specialist who was then at the Wilmer Eye Institute at Johns Hopkins. A quick phone call later, she had an appointment to see the doctor that day. It was urgent that this be evaluated and treated before her upcoming surgery. © 2021 The New York Times Company

Keyword: Vision
Link ID: 27938 - Posted: 08.11.2021

By Annie Roth As anyone who has ever tried to eat french fries on a beach will attest, stealing is not an uncommon behavior among birds. In fact, many birds are quite skilled at bold and brazen theft. Scientists have documented several species of birds, including magpies, bowerbirds, and black kites, looting everything from discarded plastic to expensive jewelry to decorate their nests. And then there are birds who want hair, and will go to great lengths to get their beaks on it. Hair from dogs, raccoons and even humans has been found in the nests of birds, which scientists believe makes the nests better insulated. For a long time, scientists assumed that birds had to collect hair that had been shed or scavenge it from mammal carcasses. However, a new study, published last week in the journal Ecology, shows that several species of bird, including chickadees and titmice, don’t just scavenge hair, they steal it. The study, based largely on analysis of YouTube videos, shows numerous examples of birds pulling tufts of hair from living mammals, including humans. This phenomenon, which the study’s authors have dubbed “kleptotrichy,” has been well-documented by birders on the web, but this is the first time scientists have formally recognized it. “This is just another example of something that was overlooked in the scientific literature but was common knowledge in the bird watching and bird feeding community,” said Henry Pollock, a postdoctoral researcher in ornithology at the University of Illinois and co-author of the new study. Last spring, Dr. Pollock was participating in his university’s annual spring bird count when a tufted titmouse caught his eye. It was flitting near a raccoon sleeping soundly on a tree branch, inching closer and closer to it. Then, to Dr. Pollock’s amusement, the tiny bird began plucking tufts of the raccoon’s fur. The titmouse managed to steal over 20 beak-fulls of the raccoon’s fur without waking it. © 2021 The New York Times Company

Keyword: Learning & Memory; Evolution
Link ID: 27937 - Posted: 08.07.2021

By Pamela Feliciano As social beings, when thinking about autism we tend to focus on its social challenges, such as difficulty communicating, making friends and showing empathy. I am a geneticist and the mother of a teenage boy with autism. I too worry most about whether he’ll have the conversational skills to do basic things like grocery shopping or whether he will ever have a real friend. But I assure you that the nonsocial features of autism are also front and center in our lives: intense insistence on sameness, atypical responses to sensory stimuli and a remarkable ability to detect small details. Many attempts have been made to explain all the symptoms of autism holistically, but no one theory has yet explained all the condition’s puzzling and diverse features. Now, a growing number of neurocognitive scientists think that many traits found in people with autism spectrum disorder (ASD) may be explained centrally by impairments in predictive skills—and have begun testing this hypothesis. Generally, the human brain determines what’s coming next based on the status quo, plus what we recall from previous experiences. Scientists theorize that people with ASD have differences that disturb their ability to predict. It’s not that people with autism can’t make predictions; it’s that their predictions are flawed because they perceive the world “too accurately.” Their predictions are less influenced by prior experiences and more influenced by what they are experiencing in the moment. They overemphasize the “now.” © 2021 Scientific American

Keyword: Autism
Link ID: 27936 - Posted: 08.07.2021

By Jane E. Brody No one with debilitating symptoms likes to be told “it’s all in your head.” Yet, this is often what distressed patients with irritable bowel syndrome hear, implicitly or explicitly, when a medical work-up reveals no apparent explanation for their repeated bouts of abdominal pain, bloating, diarrhea or constipation. In fact, irritable bowel syndrome, or I.B.S., is a real problem causing real symptoms, no matter how hard its sufferers may wish it gone. But unlike an infection or tumor, I.B.S. is what medicine calls a functional disorder: a condition with no identifiable cause. Patients have no visible signs of damage or disease in their digestive tracts. Rather, the prevailing theory holds that overly sensitive nerves in the patient’s gastrointestinal tract send distress signals to the brain that result in pain and malfunction. However, as medical science progresses, experts are beginning to find physical explanations for disorders that previously had no known biological cause. For example, conditions like epilepsy, Alzheimer’s disease and migraine were once considered functional disorders, but are now known to have measurable physical or biochemical underpinnings. And recent research has revealed at least one likely explanation for the symptoms of I.B.S.: an infection in the digestive tract that triggers a localized allergic reaction in the gut. As Dr. Marc E. Rothenberg wrote in The New England Journal of Medicine in June, “Patients with I.B.S. often report that their symptoms started at the time of a gastrointestinal infection.” Dr. Rothenberg, who is the director of the division of allergy and immunology at Cincinnati Children’s Hospital Medical Center, explained in an interview that the infection can temporarily disrupt the layer of cells that normally lines the bowel. These cells form a barrier that prevents allergy-inducing proteins in foods from being absorbed. When that barrier is penetrated, people can become intolerant to foods that previously caused them no issue. Sign up for the Well Newsletter Get the best of Well, with the latest on health, fitness and nutrition. Get it sent to your inbox. © 2021 The New York Times Company

Keyword: Stress
Link ID: 27935 - Posted: 08.07.2021

Jake Buehler As the midday sun hangs over the Scandinavian spruce forest, a swarm of hopeful suitors takes to the air. They are dance flies, and it is time to attract a mate. Zigzagging and twirling, the flies show off their wide, darkened wings and feathery leg scales. They inflate their abdomens like balloons, making themselves look bigger and more appealing to a potential partner. Suddenly, the swarm electrifies with excitement at the arrival of a new fly, the one they have all been waiting for: a male. It’s time for the preening flock of females to shine. The flies are flipping the classic drama reenacted across the animal kingdom, in which eager males with dazzling plumage, snarls of antlers or other extraordinary traits compete for a chance to woo a reluctant female. Such competitions between males for the favor of choosy females are enshrined in evolutionary theory as “sexual selection,” with the females’ choices molding the evolution of the males’ instruments of seduction over generations. Yet it’s becoming clear that this traditional picture of sexual selection is woefully incomplete. Dramatic and obvious reversals of the selection scenario, like that of the dance flies, aren’t often observed in nature, but recent research suggests that throughout the tree of animal life, females jockey for the attention of males far more than was believed. A new study hosted on the preprint server biorxiv.org has found that in animals as diverse as sea urchins and salamanders, females are subject to sexual selection — not as harshly as males are, but enough to make biologists rethink the balance of evolutionary forces shaping species in their accounts of the history of life. All Rights Reserved © 2021

Keyword: Sexual Behavior; Evolution
Link ID: 27934 - Posted: 08.07.2021

By Christina Caron Q: How common is adult A.D.H.D.? What are the symptoms and is it possible for someone who was not diagnosed with it as a child to be diagnosed as an adult? A: Attention deficit hyperactivity disorder, or A.D.H.D., is a neurodevelopmental disorder often characterized by inattention, disorganization, hyperactivity and impulsivity. It is one of the most common mental health disorders. According to the World Federation of A.D.H.D., it is thought to occur in nearly 6 percent of children and 2.5 percent of adults. In the United States, 5.4 million children, or about 8 percent of all U.S. children ages 3 to 17, were estimated to have A.D.H.D. in 2016, the Centers for Disease Control and Prevention reported. For decades, experts believed that A.D.H.D. occurred only among children and ended after adolescence. But a number of studies in the ’90s showed that A.D.H.D. can continue into adulthood. Experts now say that at least 60 percent of children with A.D.H.D. will also have symptoms as adults. It’s not surprising that so many people are now wondering whether they might have the disorder, especially if their symptoms were exacerbated by the pandemic. The Attention Deficit Disorder Association, an organization founded in 1990 for adults with A.D.H.D, saw its membership nearly double between 2019 and 2021. In addition, Children and Adults With Attention-Deficit/Hyperactivity Disorder, or CHADD, reported that the highest proportion of people who call their A.D.H.D. help line are adults seeking guidance and resources for themselves. © 2021 The New York Times Company

Keyword: ADHD
Link ID: 27933 - Posted: 08.07.2021

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