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By Knvul Sheikh There is some truth to the longstanding anecdote that your locks can lose color when you’re stressed. A team of researchers has found that in mice, stressful events trigger damage the stem cells that are responsible for producing pigment in hair. These stem cells, found near the base of each hair follicle, differentiate to form more specialized cells called melanocytes, which generate the brown, black, red and yellow hues in hair and skin. Stress makes the stem cells differentiate faster, exhausting their number and resulting in strands that are more likely to be transparent — gray. The study, published Wednesday in Nature, also found that the sympathetic nervous system, which prepares the body to respond to threats, plays an important role in the graying process. “Normally, the sympathetic nervous system is an emergency system for fight or flight, and it is supposed to be very beneficial or, at the very least, its effects are supposed to be transient and reversible,” said Ya-Chieh Hsu, a stem cell biologist at Harvard University who led the study. The sympathetic nervous system helps mobilize many biological responses, including increasing the flow of blood to muscles and sharpening mental focus. But the researchers found that in some cases the same system of nerves permanently depleted the stem cell population in hair follicles. The findings provide the first scientific link between stress and hair graying, Dr. Hsu said. Stress affects the whole body, so the researchers had to do some sleuthing to figure out which physiological system was conveying its effects to hair follicles. At first, the team hypothesized that stress might cause an immune attack on melanocyte stem cells. They exposed mice to acute stress by injecting the animals with an analogue of capsaicin, the chemical in chili peppers that causes irritation. But even mice that lacked immune cells ended up with gray hair. Next, the scientists looked at the effects of the stress hormone cortisol. Mice that had their adrenal glands removed so they couldn’t produce cortisol still had hair that turned gray under stress. © 2020 The New York Times Company

Keyword: Stress
Link ID: 26987 - Posted: 01.23.2020

By Will Hobson In 2017, Bennet Omalu traveled the globe to accept a series of honors and promote his autobiography, “Truth Doesn’t Have A Side.” In a visit to an Irish medical school, he told students he was a “nobody” who “discovered a disease in America’s most popular sport.” In an appearance on a religious cable TV show, he said he named the disease chronic traumatic encephalopathy, or CTE, because “it sounded intellectually sophisticated, with a very good acronym.” And since his discovery, Omalu told Sports Illustrated, researchers have uncovered evidence that shows adolescents who participate in football, hockey, wrestling and mixed martial arts are more likely to drop out of school, become addicted to drugs, struggle with mental illness, commit violent crimes and kill themselves. A Ni­ger­ian American pathologist portrayed by Will Smith in the 2015 film, “Concussion,” Omalu is partly responsible for the most important sports story of the 21st century. Since 2005, when Omalu first reported finding widespread brain damage in a former NFL player, concerns about CTE have inspired a global revolution in concussion safety and fueled an ongoing existential crisis for America’s most popular sport. Omalu’s discovery — initially ignored and then attacked by NFL-allied doctors — inspired an avalanche of scientific research that forced the league to acknowledge a link between football and brain disease. Nearly 15 years later, Omalu has withdrawn from the CTE research community and remade himself as an evangelist, traveling the world selling his frightening version of what scientists know about CTE and contact sports. In paid speaking engagements, expert witness testimony and in several books he has authored, Omalu portrays CTE as an epidemic and himself as a crusader, fighting against not just the NFL but also the medical science community, which he claims is too corrupted to acknowledge clear-cut evidence that contact sports destroy lives.

Keyword: Brain Injury/Concussion
Link ID: 26986 - Posted: 01.23.2020

By Karen Weintraub A small injury to a nerve outside the brain and spinal cord is relatively easy to repair just by stretching it, but a major gap in such a peripheral nerve poses problems. Usually, another nerve is taken from elsewhere in the body, and it causes an extra injury and returns only limited movement. Now researchers at the University of Pittsburgh have found an effective way to bridge such a gap—at least in mice and monkeys—by inserting a biodegradable tube that releases a protein called a growth factor for several months. In a study published Wednesday in Science Translational Medicine, the team showed that the tube works as a guide for the nerve to grow along the proper path, and the naturally occurring protein induces the nerve to grow faster. Kacey Marra, a professor at the university’s departments of plastic surgery and bioengineering, says she’s been working for a dozen years on the device, which she particularly hopes will help soldiers injured in combat. More than half of injured soldiers suffer nerve injuries, she says. And as the daughter and granddaughter of military men, she considers it her mission to help their successors. Combat gear does a good job of protecting a soldier’s chest and head, but arms and legs are often exposed, which is why peripheral nerve injuries are so common, Marra says. Car crashes and accidents involving machinery such as snowblowers can also damage nerves involved in hand, arm, leg and foot control. In the U.S., there are about 600,000 nerve injuries every year, she says, though she is unsure how many are severe enough to require the relocation of a second nerve because that information is not tracked yet. When the injuries are severe, the only current treatment is to take a nerve from somewhere else on the body, Marra says. But patients recover just about 50 to 60 percent of function in the damaged nerve. © 2020 Scientific American,

Keyword: Regeneration
Link ID: 26985 - Posted: 01.23.2020

Janelia and Google scientists have constructed the most complete map of the fly brain ever created, pinpointing millions of connections between 25,000 neurons. Now, a wiring diagram of the entire brain is within reach. In a darkened room in Ashburn, Virginia, rows of scientists sit at computer screens displaying vivid 3-D shapes. With a click of a mouse, they spin each shape to examine it from all sides. The scientists are working inside a concrete building at the Howard Hughes Medical Institute’s Janelia Research Campus, just off a street called Helix Drive. But their minds are somewhere else entirely – inside the brain of a fly. Each shape on the scientists’ screens represents part of a fruit fly neuron. These researchers and others at Janelia are tackling a goal that once seemed out of reach: outlining each of the fly brain’s roughly 100,000 neurons and pinpointing the millions of places they connect. Such a wiring diagram, or connectome, reveals the complete circuitry of different brain areas and how they're linked. The work could help unlock networks involved in memory formation, for example, or neural pathways that underlie movements. Gerry Rubin, vice president of HHMI and executive director of Janelia, has championed this project for more than a decade. It’s a necessary step in understanding how the brain works, he says. When the project began, Rubin estimated that with available methods, tracing the connections between every fly neuron by hand would take 250 people working for two decades – what he refers to as “a 5,000 person-year problem.”

Keyword: Brain imaging
Link ID: 26984 - Posted: 01.23.2020

Kayt Sukel Since its inception, the field of neuroscience has relied on animal models, from fruit flies to macaque monkeys, to better understand the behavior and inner workings of neurons. But while these models have led to remarkable insights about the brain in both health and in disease, they do have limitations. The very genetic differences that place us in different species also make the translation of neurobiological findings in animals to humans challenging—if not outright impossible. “We’ve now cured Alzheimer’s disease a dozen times over in mice, but we haven’t cured it in human patients,” said Matthew Blurton-James, Ph.D., a neurobiologist at the University of California, Irvine. “There’s clearly a big species difference in how this disease develops, which means our current animal models can’t get us the answers we’re searching for.” In the past few years, however, advances in technology have led to the development of innovative models to study the activity of human neurons—and how they communicate with one another. Such models, which include ex vivo tissue harvested from living human donors, organoids, and chimeric models (animal tissue modified with human genes or cells), are enabling scientists to investigate processes in ways that were previously unthinkable. “These new technologies, including those that use induced pluripotent stem cells (iPSCs), are really quite striking,” said Walter Koroshetz, M.D., director of the National Institute of Neurological Disorders and Stroke. “And the real advantage of these is that they offer us a new way to study human brain cells, particularly when it comes to developmental processes, that is incredibly valuable.” © 2020 The Dana Foundation

Keyword: Development of the Brain
Link ID: 26983 - Posted: 01.23.2020

Nicola Davis When Mount Vesuvius erupted in AD79, the damage wreaked in nearby towns was catastrophic. Now it appears the heat was so immense it turned one victim’s brain to glass – thought to be the first time this has been seen. Experts say they have discovered that splatters of a shiny, solid black material found inside the skull of a victim at Herculaneum appear to be the remains of human brain tissue transformed by heat. They say the find is remarkable since brain tissue is rarely preserved at all due to decomposition, and where it is found it has typically turned to soap. “To date, vitrified remains of the brain have never been found,” said Dr Pier Paolo Petrone, a forensic anthropologist at the University of Naples Federico II and a co-author of the study. Writing in the New England Journal of Medicine, Petrone and colleagues reveal that the glassy brains belonged to a man of about 25 who was found in the 1960s lying face-down on a wooden bed under a pile of volcanic ash – a pose that suggests he was asleep when disaster struck the town. The bed was in a small room that was part of the Collegium Augustalium, a building relating to an imperial cult that worshipped the former emperor Augustus. The victim, according to Petrone, is believed to have been the caretaker. Petrone said it was when he recently focused his research on human remains found at the college that he noticed the black fragments in the caretaker’s skull. “I noticed something shining inside the head ,” he told the Guardian. “This material was preserved exclusively in the victim’s skull, thus it had to be the vitrified remains of the brain. But it had to be proved beyond any reasonable doubt.” © 2020 Guardian News & Media Limited

Keyword: Brain imaging
Link ID: 26982 - Posted: 01.23.2020

Liz Fuller-Wright, Office of Communications Barry L. Jacobs, an emeritus professor of psychology and neuroscience who became internationally known for his research on serotonin, sleep and depression, died Friday, Jan. 10, in Princeton. He was 77 years old. Jacobs joined the Princeton faculty in 1972 and transferred to emeritus status in 2017. Among his roles at the University, he served as director of the neuroscience graduate program from 1988 to 2000. “Barry Jacobs was a truly wonderful colleague — brilliant, knowledgeable, interesting, generous, and always upbeat and friendly,” said Ronald Comer, an emeritus member of Princeton’s psychology faculty. “Deeply committed to his work and to all of neuroscience, he was just as interested in and curious about the work of his other psychology colleagues, including those of us in social and clinical psychology. As a result of his special accomplishments in neuroscience, multiple interests, extraordinary skills as a teacher and communicator, and contagious passion for science, Barry was able to develop and teach, for decades, one of the University’s most successful and popular courses, ‘The Brain: A User’s Guide’ — a course that brought the wonders of neuroscience to life for University students of all concentrations and interests.” Jacobs was born Feb. 26, 1942, in Chicago. He received his B.S. in economics from the University of Illinois-Chicago, in 1966, and his doctorate in psychology from the University of California-Los Angeles in 1971. He was a postdoctoral fellow in the psychiatry department at Stanford University Medical School before coming to Princeton. © 2020 The Trustees of Princeton University

Keyword: Drug Abuse
Link ID: 26981 - Posted: 01.23.2020

Sydney Lupkin Sometimes, the approval of a new generic drug offers more hype than hope for patients' wallets, as people with multiple sclerosis know all too well. New research shows just how little the introduction of a generic version of Copaxone — one of the most popular MS drugs — did to lower their medicine costs. MS is an autoimmune disease that gradually damages the central nervous system, disrupting communication between the brain and the rest of the body. Its symptoms are different from patient to patient across a lifetime but can include weakness, numbness, vision problems, tremors and even paralysis. There's no cure for MS, though some patients experience long remissions of symptoms. Several prescription drugs can stave off multiple sclerosis attacks and slow down the disease, says Deborah Ewing-Wilson, a neurologist with University Hospitals Cleveland Medical Center. But the cost of some of the most effective medicines — which have undergone frequent price hikes over the years — can put added stress on her patients. "They are extremely expensive," says Ewing-Wilson. On average, the medicines cost $70,000 per year, according to a 2017 study. Some prices have increased fivefold from when the drugs were first approved by the Food and Drug Administration. Even with insurance, says Ewing-Wilson, patients can be left on the hook for anywhere from $3,000 to more than $50,000 a year. Some patients tell her they need to skip their medications altogether because they're unaffordable. So when a generic version of the injectable MS drug Copaxone — also known as glatiramer acetate — was launched in 2015, Dan Hartung, a drug policy researcher at Oregon Health & Science University, and his colleagues thought that might spur some price relief. After all, if a cheap multiple sclerosis drug were available, wouldn't patients flock to it, forcing other manufacturers to lower their prices to compete? © 2020 npr

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 26980 - Posted: 01.22.2020

Roger E. Beaty, Ph.D. When we think about creativity, the arts often come to mind. Most people would agree that writers, painters, and actors are all creative. This is what psychologists who study the subject refer to as Big-C creativity: publicly-recognizable, professional-level performance. But what about creativity on a smaller scale? This is what researchers refer to as little-c creativity, and it is something that we all possess and express in our daily lives, from inventing new recipes to performing a do-it-yourself project to thinking of clever jokes to entertain the kids. One way psychologists measure creative thinking is by asking people to think of uncommon uses for common objects, such as a cup or a cardboard box. Their responses can be analyzed on different dimensions, such as fluency (the total number of ideas) and originality. Surprisingly, many people struggle with this seemingly simple task, only suggesting uses that closely resemble the typical uses for the object. The same happens in other tests that demand ideas that go beyond what we already know (i.e., “thinking outside the box”). Such innovation tasks assess just one aspect of creativity. Many new tests are being developed that tap into other creative skills, from visuospatial abilities essential for design (like drawing) to scientific abilities important for innovation and discovery. But where do creative ideas come from, and what makes some people more creative than others? Contrary to romantic notions of a purely spontaneous process, increasing evidence from psychology and neuroscience experiments indicates that creativity requires cognitive effort—in part, to overcome the distraction and “stickiness” of prior knowledge (remember how people think of common uses when asked to devise creative ones). In light of these findings, we can consider general creative thinking as a dynamic interplay between the brain’s memory and control systems. Without memory, our minds would be a blank slate—not conducive to creativity, which requires knowledge and expertise. But without mental control, we wouldn’t be able to push thinking in new directions and avoid getting stuck on what we already know. © 2020 The Dana Foundation

Keyword: Attention
Link ID: 26979 - Posted: 01.22.2020

By Gretchen Reynolds In a world that encourages inactivity, even our babies may be moving too little, according to an innovative new study of physical activity patterns during a child’s first year of life. The study, which used tiny activity trackers to monitor babies’ movements, found associations between infants’ squirming, kicking, crawling or stillness and the levels of fat around their middles, raising provocative questions about just how early any links between inactivity and obesity might begin. We already have considerable evidence, of course, that children in the Western world tend to be sedentary. According to recent estimates, most school-age children in the United States sit for more than eight hours a day, while children as young as 2 or 3 years of age can be sedentary for 90 percent or more of their waking hours. These statistics are concerning, because other studies suggest that inactive children face much higher risks of becoming overweight or obese than children who move more often. But little has been known about how much — or little — tiny babies move and if there might be correlations between their activities and their rotundity, and if such correlations matter. So, for the new study, which was published this month in Obesity, a group of researchers from Johns Hopkins University and other institutions decided to fit baby-size trackers to infants’ ankles and watch how they wiggled. They began by turning to new mothers already participating in a large, ongoing study of the health of mothers and newborns and asking if they could now track their babies’ activities. The researchers wound up recruiting 506 young boys and girls from various socioeconomic levels, more than half of them African-American. The researchers visited these infants in their homes when the babies were 3, 6, 9 and 12 months old, weighing and measuring the children, gently checking their body fat with calipers and fitting them with tiny accelerometers. © 2020 The New York Times Company

Keyword: Obesity; Development of the Brain
Link ID: 26978 - Posted: 01.22.2020

By Jade Wu Savvy Psychologist This week, let’s ask the million-dollar question: How much sleep do you really need? We all know sleep is important. Shakespeare called it the “sore labor’s bath, balm of hurt minds, great nature’s second course, chief nourisher in life’s feast.” Less poetically, headlines these days seem to be shouting: “Sleep deprivation will make you slower and dumber!” “It will give you Alzheimer's disease and heart attacks!” One mattress advertisement I saw simply said, “You can only live seven days without sleep.” Yikes. Talk about pressure to perform! Fear-mongering aside, there is good evidence that sleep is important for health, well-being, and performance. A recent meta-analysis including over 1600 participants confirmed that sleep restriction is associated with poorer attention and thinking. We’ve known for decades that sleep deprivation disrupts mood. For example, it can trigger manic episodes in those with bipolar disorder. And we’re learning now, from researchers in Sweden and Germany, that insufficient sleep can even affect the microbiota in your gut. But how much sleep is enough? Is there such a thing as too much sleep? If you ask Dr. Google, you’ll get over a billion answers. (That’s right; “billion” with a “b.”) The most common answer seems to be “eight hours.” That seems pretty straightforward. But where does this number come from? And if you’re thinking, “Dr. Google hasn’t examined me; how would she know how much sleep I need,” then you’re asking exactly the right question. © 2020 Scientific American

Keyword: Sleep
Link ID: 26977 - Posted: 01.22.2020

By Bradley Berman The day is approaching when commuters stuck in soul-crushing traffic will be freed from the drudgery of driving. Companies are investing billions to devise sensors and algorithms so motorists can turn our attention to where we like it these days: our phones. But before the great promise of multitasking on the road can be realized, we need to overcome an age-old problem: motion sickness. “The autonomous-vehicle community understands this is a real problem it has to deal with,” said Monica Jones, a transportation researcher at the University of Michigan. “That motivates me to be very systematic.” So starting in 2017, Ms. Jones led a series of studies in which more than 150 people were strapped into the front seat of a 2007 Honda Accord. They were wired with sensors and set on a ride that included roughly 50 left-hand turns and other maneuvers. Each subject was tossed along the same twisty route for a second time but also asked to complete a set of 13 simple cognitive and visual tasks on an iPad Mini. About 11 percent of the riders got nauseated or, for other reasons, asked that the car be stopped. Four percent vomited. Ms. Jones takes no joy in documenting her subjects’ getting dizzy, hyperventilating or losing their lunch. She feels their pain. Ms. Jones, a chronic sufferer of motion sickness, has experienced those discomforts in car back seats all her life. “I don’t remember not experiencing it,” she said. “As I’m getting older, it’s getting worse.” It’s also getting worse for the legions of commuters hailing Ubers or taxis and hopping in, barely lifting their gaze from a screen in the process. © 2020 The New York Times Company

Keyword: Miscellaneous
Link ID: 26976 - Posted: 01.21.2020

Edward Bullmore Unlikely as it may seem, #inflammation has become a hashtag. It seems to be everywhere suddenly, up to all sorts of tricks. Rather than simply being on our side, fighting infections and healing wounds, it turns out to have a dark side as well: the role it plays in causing us harm. It’s now clear that inflammation is part of the problem in many, if not all, diseases of the body. And targeting immune or inflammatory causes of disease has led to a series of breakthroughs, from new treatments for rheumatoid arthritis and other auto-immune diseases in the 1990s, through to the advent of immunotherapy for some cancers in the 2010s. Even more pervasively, low-grade inflammation, detectable only by blood tests, is increasingly considered to be part of the reason why common life experiences such as poverty, stress, obesity or ageing are bad for public health. Advertisement The brain is rapidly emerging as one of the new frontiers for inflammation. Doctors like myself, who went to medical school in the 20th century, were taught to think that there was an impermeable barrier between the brain and the immune system. In the 21st century, however, it has become clear that they are deeply interconnected and talk to each other all the time. Medical minds are now opening up to the idea that inflammation could be as widely and deeply implicated in brain and mind disorders as it is in bodily disorders. Advances in treatment of multiple sclerosis have shown the way. Many of the new medicines for MS were designed and proven to protect patients from brain damage caused by their own immune systems. The reasonably well-informed hope – and I emphasise those words at this stage – is that targeting brain inflammation could lead to breakthroughs in prevention and treatment of depression, dementia and psychosis on a par with the proven impact of immunological medicines for arthritis, cancer and MS. Indeed, a drug originally licensed for multiple sclerosis is already being tried as a possible immune treatment for schizophrenia. © 2020 Guardian News & Media Limited

Keyword: Alzheimers; Neuroimmunology
Link ID: 26975 - Posted: 01.21.2020

By Tina Hesman Saey Some hairy cells in the nose may trigger sneezing and allergies to dust mites, mold and other substances, new work with mice suggests. When exposed to allergens, these “brush cells” make chemicals that lead to inflammation, researchers report January 17 in Science Immunology. Only immune cells previously were thought to make such inflammatory chemicals — fatty compounds known as lipids. The findings may provide new clues about how people develop allergies. Brush cells are shaped like teardrops topped by tufts of hairlike projections. In people, mice and other animals, these cells are also found in the linings of the trachea and the intestines, where they are known as tuft cells (SN: 4/13/18). However, brush cells are far more common in the nose than in other tissues, and may help the body identify when pathogens or noxious chemicals have been inhaled, says Lora Bankova, an allergist and immunologist at Brigham and Women’s Hospital in Boston. Bankova and her colleagues discovered that, when exposed to certain molds or dust mite proteins, brush cells in mice’s noses churn out inflammation-producing lipids, called cysteinyl leukotrienes. The cells also made the lipids when encountering ATP, a chemical used by cells for energy that also signals when nearby cells are damaged, as in an infection. Mice exposed to allergens or ATP developed swelling of their nasal tissues. But mice that lacked brush cells suffered much less inflammation. Such inflammation may lead to allergies in some cases. The researchers haven’t yet confirmed that brush cells in human noses respond to allergens in the same way as these cells do in mice. © Society for Science & the Public 2000–2020

Keyword: Chemical Senses (Smell & Taste); Neuroimmunology
Link ID: 26974 - Posted: 01.21.2020

By Harry Guinness The world isn’t made for night owls. You struggle into work in the dark hours before 10 a.m. — or your morning coffee — and you’re greeted by some chipper person who has already been to the gym and is six items into his to-do list. I used to fantasize about fitting punishments for such morning people, but in the last two years I’ve seen the (morning) light, and I’ve become one of them. If you love staying up late but hate crawling through your mornings in a haze, here’s how you can do it too. After a long, draining day you finally get home, settle down in front of the TV and throw on whatever season you’re currently bingeing. Heaven. But then, when a reasonable bedtime rolls around, you don’t want to stop. It has been a hard day, aren’t you entitled to just one more episode? So you push play, trade a bit of sleep for more Netflix time and continue the cycle that keeps you tired all the time. Dr. Alex Dimitriu, founder of the Menlo Park Psychiatry and Sleep Medicine clinic, explained it like this: “Long days leave us tired and exhausted, but the reality is, our days would be less hard, and less exhausting, if we weren’t so tired through them. The trouble with being a night owl is that your sleep gets clipped in the morning hours, where most of the precious REM or dream sleep occurs. Instead of sleeping seven or eight hours per night, most night owls get forced to sleep five or six — with a hard start time in the morning.” Dr. Dimitriu can’t stress enough just how important REM sleep is. It’s “the key to our emotional and creative energy” and comparable to “self-therapy,” he said, adding that it “balances us out in more ways than I can describe” and that without enough of it, our memory and moods take a hit. If you have the freedom to wake up when you like, then things are different, but if that extra Netflix episode is forcing you to cut your sleep short, then you should try to do something about it. © 2020 The New York Times Company

Keyword: Biological Rhythms; Sleep
Link ID: 26973 - Posted: 01.21.2020

By Aaron E. Carroll Childhood obesity is a major public health problem, and has been for some time. Almost 20 percent of American children are affected by obesity, as well as about 40 percent of adults. Over all, this costs the United States around $150 billion in health care spending each year. Pediatricians like me, and many other health professionals, know it’s a problem, and yet we’ve been relatively unsuccessful in tackling it. About six years ago, some reports seemed to show that rates had stabilized in children and even decreased in those ages 2 to 5. Later studies showed this trend to be an illusion. If anything, things have gotten worse. Efforts to help can backfire. People on diets often gain weight. Although individual studies have pointed to potential interventions and solutions, these have not yet translated into actual improvements. Part of the problem may be flawed research. A recent paper in Pediatric Obesity provided a guide on how to do better. Its suggestions fall into five general themes. 1) When things look better, it’s critical to ask “compared to what?” In short, you need a control group. Over time, changes in behaviors or measurements often follow a pattern known as regression toward the mean. Outliers (in this case those who are more overweight) tend to move toward the average. Thus, interventions might look as if they’re working when they’re not. Control groups — participants who don’t receive the intervention — can help ensure that we’re seeing real effectiveness. Even then, things can get tricky. In a randomized controlled trial, it’s important to keep the comparisons directly between the intervention and control groups. A common mistake is comparing each group after the intervention with the same group before the intervention. In other words, people could compare a dieting group to itself, before and after, and compare the control group to itself, before and after, to see if the © 2020 The New York Times Company

Keyword: Obesity
Link ID: 26972 - Posted: 01.20.2020

By Donna Jackson Nakazawa More than a decade ago, I was diagnosed with a string of autoimmune diseases, one after another, including a bone marrow disorder, thyroiditis, and then Guillain-Barré syndrome, which left me paralyzed while raising two young children. I recovered from Guillain-Barré only to relapse, becoming paralyzed again. My immune system was repeatedly and mistakenly attacking my body, causing the nerves in my arms, legs, and those I needed to swallow to stop communicating with my brain, leaving me confined to — and raising my children from — bed. As I slowly began to recover and learn to walk again, I noticed that along with residual physical losses I had experienced shifts in my mood and clarity of mind. Although I’d always been an optimistic person, I felt a bleak unshakable dread, which didn’t feel like the “old me.” I also noticed cognitive glitches. Names, words, and facts were hard to bring to mind. I can still recall cutting up slices of watermelon, putting them in a bowl, and staring down at them thinking, “What is this again?” I knew the word but couldn’t remember it. I covered my lapse by bringing the bowl to the table and waiting for my children to call out, “Yay! Watermelon!” And I thought, “Yes. Of course. Watermelon.” As a science journalist whose niche spans neuroscience, immunology, and human emotion, I knew at the time that it didn’t make scientific sense that inflammation in the body could be connected to — much less cause — illness in the brain. At that time, scientific dogma held that the brain was the only organ in the body not ruled by the immune system. The brain was considered to be “immune privileged.” © 2020 STAT

Keyword: Glia; Alzheimers
Link ID: 26971 - Posted: 01.20.2020

Jennifer Rankin in Brussels A pioneering Belgian neurologist has been awarded €1m to fund further work in helping diagnose the most severe brain injuries, as he seeks to battle “the silent epidemic” and help people written off as “vegetative” who, it is believed, will never recover. Steven Laureys, head of the coma science group at Liège University hospital, plans to use the £850,000 award – larger than the Nobel prize – to improve the diagnosis of coma survivors labelled as being in a “persistent vegetative state”. That is “a horrible term” he says, although still one widely used by the general public and many clinicians. Laureys, who has spent more than two decades exploring the boundaries of human consciousness, prefers the term “unresponsive wakefulness” to describe people who are unconscious but show signs of being awake, such as opening their eyes or moving. These patients are often wrongly described as being in a coma, a condition that only lasts a few weeks, in which people are completely unresponsive. “The old view was to consider consciousness, which was one of the biggest mysteries for science to solve, as all or nothing,” he told the Guardian, shortly after he was awarded the Generet prize by Belgium’s King Baudouin Foundation this week. He said that a third of patients he treats at the Liège coma centre had been wrongly diagnosed as being in a vegetative state, despite signs of consciousness. As a young doctor in the 1990s he was frustrated by the questions that torture the families of coma survivors: can their loved ones see or hear them? Can they feel anything, including pain? Laureys and his 30-strong team of engineers and clinicians have shown that some of those with a “vegetative state” diagnosis are minimally conscious, showing signs of awareness such as responding to commands with their eyes. © 2020 Guardian News & Media Limited

Keyword: Consciousness
Link ID: 26970 - Posted: 01.20.2020

Hannah Devlin Science correspondent The death in 2002 of the former England and West Bromwich Albion striker Jeff Astle from degenerative brain disease placed the spotlight firmly on the possibility of a link between heading footballs and the risk of dementia. The coroner at the inquest ruled that Astle, 59, died from an “industrial disease” brought on by the repeated trauma of headers, and a later examination of Astle’s brain appeared to bear out this conclusion. At that time there was sparse scientific data on the issue, but since then the balance of evidence has steadily tipped further in favour of a link. It has been shown that even single episodes of concussion can have lifelong consequences. Children in Scotland could be banned from heading footballs over dementia link Read more A 2016 study based on health records of more than 100,000 people in Sweden found that after a single diagnosed concussion people were more likely to have mental health problems and less likely to graduate from high school and college. Other research has shown that people in prison or homeless are more likely to have had a past experience of concussion. In 2017, researchers from University College London examined postmortem the brains of six former footballers who had developed dementia. They found signs of brain injury called chronic traumatic encephalopathy (CTE) in four cases. Last year a study by a team at Glasgow University found that former professional footballers were three and a half times more likely to die from dementia and other serious neurological diseases. The study was the largest ever, based on the health records of 7,676 ex-players and 23,000 members of the public, and was possibly the trigger for the Scottish FA’s plan to follow US soccer in banning heading the ball for young players. © 2020 Guardian News & Media Limited

Keyword: Brain Injury/Concussion
Link ID: 26969 - Posted: 01.17.2020

By Betsy Mason Despite weighing less than half an ounce, mountain chickadees are able to survive harsh winters complete with subzero temperatures, howling winds and heavy snowfall. How do they do it? By spending the fall hiding as many as 80,000 individual seeds, which they then retrieve — by memory — during the winter. Their astounding ability to keep track of that many locations puts their memory among the most impressive in the animal kingdom. It also makes chickadees an intriguing subject for animal behavior researchers. Cognitive ecologist Vladimir Pravosudov of the University of Nevada, Reno, has dedicated his career to studying this tough little bird’s amazing memory. Writing in 2013 on the cognitive ecology of food caching in the Annual Review of Ecology, Evolution, and Systematics, he and coauthor Timothy Roth argued that answers to big questions about the evolution of cognition may lie in the brains of these little birds. In July, at a meeting of the Animal Behavior Society in Chicago, Pravosudov presented his group’s latest research on the wild chickadees that live in the Sierra Nevada mountains. He and his graduate students were able to show for the first time that an individual bird’s spatial memory has a direct impact on its survival. The team did this by building an experimental contraption that uses radio-frequency identification (RFID) technology and electronic leg bands to test individual birds’ memory in the wild and then track their longevity. The researchers found that the birds with the best memory were most likely to survive the winter. What are some of the big ideas driving your work on chickadees? If some species are smart, or not smart, the question is: Why? Cognitive ecologists like me are specifically trying to figure out which ecological factors may have shaped the evolution of these differences in cognition. In other words, the idea is to understand the ecological and evolutionary reasons for variation in cognition. © 2020 Annual Reviews, Inc

Keyword: Learning & Memory
Link ID: 26968 - Posted: 01.17.2020