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By Roni Caryn Rabin A sudden shortage of one of the safest anti-anxiety drugs on the market has spread alarm among people who rely on the medication, buspirone, to get through the day without debilitating anxiety and panic attacks. Physicians are also expressing concern, because there is no information about when the supply will resume, making it difficult to manage patients. Shelby Vittek, a 27-year-old writer in New Jersey, fruitlessly called dozens of drugstores in New Jersey and Pennsylvania in an attempt to locate the medication after her pharmacist told her the drug was on back-order with no end in sight. She ended up weaning herself off the drug, spreading her last three pills over six days to avoid having to go “cold turkey” before starting a difficult transition to an antidepressant. “I pretty much lost over a month of work, and have just started to feel like myself again,” she said. A 34-year-old New York woman who couldn’t get her buspirone refilled in January said she couldn’t sleep and had such severe panic attacks that she had to use Klonopin, a drug she dislikes because it is addictive. “I’m trying to take care of my anxiety, and it’s giving me a panic attack,” said the woman, a sexual assault survivor who asked not to be identified. A Pennsylvania medical school student received her mail-order shipment of medication last week with no buspirone in it and no explanation, so she scrounged around the house and dug up old pills from missed doses. Last weekend, the student, who asked not to be identified, was so anxious she could not leave the house. “This is potentially messing with people’s clinical stability,” said Dr. Dennis Glick, a psychiatrist in Greenbelt, Md. “When you have a patient with a complicated and balanced regimen, you really don’t want to just arbitrarily have someone come off the medicine.” Dr. Glick said he has been in practice for 34 years “and I honestly don’t recall issues like this interfering with care until maybe a couple of years ago.” © 2019 The New York Times Company
Keyword: Stress; Drug Abuse
Link ID: 25921 - Posted: 02.01.2019
Laura Sanders Do you floss regularly? A study published January 23 in Science Advances — and the news stories that it inspired — might have scared you into better oral hygiene by claiming to find a link between gum bacteria and Alzheimer’s disease. Those experiments hinted that the gum disease–causing bacteria Porphyromonas gingivalis was present in the brains of a small number of people who died with the degenerative brain disease. Some headlines trumpeted that the cause of Alzheimer’s had finally been found. Enzymes made by P. gingivalis, called gingipains, interact with key Alzheimer’s proteins called amyloid-beta and tau in test tube experiments and in the brains of mice, the researchers found. Gingipains prod A-beta to accumulate and tau to behave abnormally, both signs of Alzheimer’s disease in people, the experiments suggest. And compounds that block gingipains seemed to reduce the amount of A-beta in the infected mice. The findings “offer evidence that P. gingivalis and gingipains in the brain play a central role” in the development of Alzheimer’s disease, the researchers write in their study. The research was paid for and conducted in part by employees of Cortexyme, Inc., a San Francisco–based biotech company that’s developing these compounds. The results fit with an idea that’s gaining traction among Alzheimer’s researchers — that bacteria, viruses and even fungi could spark the disease (SN: 7/21/18, p. 10). But the Science Advances study is far from conclusive, cautions Rudolph Tanzi, an Alzheimer’s researcher at Massachusetts General Hospital in Boston. Science News asked him what the study can, and can’t, answer about Alzheimer’s disease. His responses are edited for length and clarity. |© Society for Science & the Public 2000 - 2019
Keyword: Alzheimers
Link ID: 25920 - Posted: 02.01.2019
By Benedict Carey The world’s most common digital habit is not easy to break, even in a fit of moral outrage over the privacy risks and political divisions Facebook has created, or amid concerns about how the habit might affect emotional health. Although four in 10 Facebook users say they have taken long breaks from it, the digital platform keeps growing. A recent study found that the average user would have to be paid $1,000 to $2,000 to be pried away for a year. So what happens if you actually do quit? A new study, the most comprehensive to date, offers a preview. Expect the consequences to be fairly immediate: More in-person time with friends and family. Less political knowledge, but also less partisan fever. A small bump in one’s daily moods and life satisfaction. And, for the average Facebook user, an extra hour a day of downtime. The study, by researchers at Stanford University and New York University, helps clarify the ceaseless debate over Facebook’s influence on the behavior, thinking and politics of its active monthly users, who number some 2.3 billion worldwide. The study was posted recently on the Social Science Research Network, an open access site. “For me, Facebook is one of those compulsive things,” said Aaron Kelly, 23, a college student in Madison, Wis. “It’s really useful, but I always felt like I was wasting time on it, distracting myself from study, using it whenever I got bored.” Mr. Kelly, who estimated that he spent about an hour a day on the platform, took part in the study “because it was kind of nice to have an excuse to deactivate and see what happened,” he said. Well before news broke that Facebook had shared users’ data without consent, scientists and habitual users debated how the platform had changed the experience of daily life. A cadre of psychologists has argued for years that the use of Facebook and other social media is linked to mental distress, especially in adolescents. Others have likened habitual Facebook use to a mental disorder, comparing it to drug addiction and even publishing magnetic-resonance images of what Facebook addiction “looks like in the brain.” © 2019 The New York Times Company
Keyword: Attention; Depression
Link ID: 25919 - Posted: 01.31.2019
By Laurie McGinley E-cigarettes are almost twice as effective at helping smokers quit as nicotine replacement therapies such as lozenges and patches, according to a new study that immediately stoked the debate over whether e-cigarettes are an important smoking-cessation tool or a health menace. The study, published online Wednesday by the New England Journal of Medicine, is the first randomized trial to test the effectiveness of modern e-cigarettes vs. nicotine-replacement products, said Peter Hajek, a psychologist at Queen Mary University of London, who led the trial. The researchers found that 18 percent of the e-cigarette users were smoke-free after a year, compared with 9.9 percent of those in the nicotine-replacement group. The participants also received behavioral support to stop smoking. For years, physicians have been reluctant to recommend e-cigarettes for smoking cessation because of a lack of clinical trial data, Hajek said. “This is now likely to change,” he added in a statement. But two editorials in the same publication threw some cold water on the trial’s results. One editorial, by Boston University researchers, said e-cigarettes should be used only when Food and Drug Administration-approved treatments do not work. Those approved therapies, as well as drugs such as bupropion, have higher effectiveness rates than the new study suggested, and much more is known about their side effects, said Belinda Borrelli, a Boston University researcher who co-wrote the editorial. © 1996-2019 The Washington Post
Keyword: Drug Abuse
Link ID: 25918 - Posted: 01.31.2019
Jon Hamilton For comedian Lewis Black, anger is a job. Black is famous for his rants about stuff he finds annoying or unfair or just plain infuriating. Onstage, he often looks ready for a fight. He leans forward. He shouts. He stabs the air with an index finger, or a middle finger. To a scientist, Black looks a lot like a belligerent dog, or an irritated gerbil. "Practically every sexually reproducing, multicellular animal shows aggressive behavior," says David Anderson, a professor of biology at Caltech and co-author of the book The Neuroscience of Emotion. "Fruit flies show aggression." When I relay that last bit to Black, he's skeptical. "Really?" he says. "Come on." But Anderson, whose lab studies fruit flies, says the evidence is compelling. "They fight over females, they fight over food, they threaten each other, they put their wings up in the air, they charge at each other," he says. But does aggressive behavior mean a fruit fly gets angry the way Black does? Anderson says that depends on how you define the term. "We use anger subjectively to refer to our experience, our conscious experience, of rage, the feeling that you are about to explode, the feeling of irritation," he says. Black feels that way a lot. And he has spent decades thinking about how anger works in his own brain. "My anger comes from a collection of things that occur during the course of a day that build up," he says. "So by the end of a day, six or seven things have happened to me that have gone into my anger bank." © 2019 npr
Keyword: Emotions; Evolution
Link ID: 25917 - Posted: 01.31.2019
Ewen Callaway Neanderthals and Denisovans might have lived side by side for tens of thousands of years, scientists report in two papers in Nature1,2. The long-awaited studies are based on the analysis of bones, artefacts and sediments from Denisova Cave in southern Siberia, which is dotted with ancient-human remains. They provide the first detailed history of the site’s 300,000-year occupation by different groups of ancient humans. “We can now tell the whole story of the entire cave, not just bits and pieces,” says Zenobia Jacobs, a geochronologist at the University of Wollongong, Australia, who co-led one of the studies. Soviet archaeologists began unravelling the story of Denisova Cave, at the foot of the Altai Mountains, in the early 1980s. Since then, scientists have found the fragmentary remains of nearly a dozen ancient humans at the site. The cave became world famous in 2010, after an analysis of the DNA from a tiny hominin finger bone found that the creature was distinct from both modern humans and Neanderthals3. It belonged to a previously unknown hominin group, later named Denisovans. Additional sequencing of the DNA in bone remains from the cave found that Denisovans were a sister group to Neanderthals, and might once have lived across Asia — where they interbred with the ancestors of some humans now living there4. © 2019 Springer Nature Publishing AG
Keyword: Evolution
Link ID: 25916 - Posted: 01.31.2019
By Carl Zimmer In 2014 John Cryan, a professor at University College Cork in Ireland, attended a meeting in California about Alzheimer’s disease. He wasn’t an expert on dementia. Instead, he studied the microbiome, the trillions of microbes inside the healthy human body. Dr. Cryan and other scientists were beginning to find hints that these microbes could influence the brain and behavior. Perhaps, he told the scientific gathering, the microbiome has a role in the development of Alzheimer’s disease. The idea was not well received. “I’ve never given a talk to so many people who didn’t believe what I was saying,” Dr. Cryan recalled. A lot has changed since then: Research continues to turn up remarkable links between the microbiome and the brain. Scientists are finding evidence that microbiome may play a role not just in Alzheimer’s disease, but Parkinson’s disease, depression, schizophrenia, autism and other conditions. For some neuroscientists, new studies have changed the way they think about the brain. One of the skeptics at that Alzheimer’s meeting was Sangram Sisodia, a neurobiologist at the University of Chicago. He wasn’t swayed by Dr. Cryan’s talk, but later he decided to put the idea to a simple test. “It was just on a lark,” said Dr. Sisodia. “We had no idea how it would turn out.” He and his colleagues gave antibiotics to mice prone to develop a version of Alzheimer’s disease, in order to kill off much of the gut bacteria in the mice. Later, when the scientists inspected the animals’ brains, they found far fewer of the protein clumps linked to dementia. Just a little disruption of the microbiome was enough to produce this effect. Young mice given antibiotics for a week had fewer clumps in their brains when they grew old, too. © 2019 The New York Times Company
Keyword: Obesity; Depression
Link ID: 25915 - Posted: 01.29.2019
Amy Lewis Cynthia Bulik began her scientific career studying childhood depression. But while she was working as a research assistant at the University of Pittsburgh in the 1980s, psychiatrist David Kupfer asked her to help write a book chapter comparing electroencephalography studies in depression and anorexia. As preparation, she shadowed a psychiatrist at a hospital inpatient unit for people with eating disorders. Bulik was intrigued by what she witnessed there. “These people were my age, my sex, and weighed half as much as I did,” she says. “They seemed very eloquent and interactive, but at the same time, in this one area of their psychology and biology, they occupied a completely different space.” Now the founding director of the Center of Excellence for Eating Disorders at the University of North Carolina at Chapel Hill, Bulik has been unraveling the biology behind eating disorders such as anorexia nervosa (AN) ever since. Characterized by extreme caloric restriction resulting in weight loss, an intense fear of gaining weight, and a distorted body image, anorexia has the highest mortality rate of any psychiatric disorder. Death can be a result of various risks associated with the condition, from suicide to heart failure. While many AN sufferers go undiagnosed, making incidence rates hard to pin down, some researchers estimate that up to 2 percent of women and 0.3 percent of men are affected globally. © 1986 - 2019 The Scientist
Keyword: Anorexia & Bulimia; Genes & Behavior
Link ID: 25914 - Posted: 01.29.2019
By Pam Belluck In dementia research, so many paths have led nowhere that any glimmer of optimism is noteworthy. So some experts are heralding the results of a large new study, which found that people with hypertension who received intensive treatment to lower their blood pressure were less likely than those receiving standard blood pressure treatment to develop minor memory and thinking problems that often progress to dementia. The study, published Monday in JAMA, is the first large, randomized clinical trial to find something that can help many older people reduce their risk of mild cognitive impairment — an early stage of faltering function and memory that is a frequent precursor to Alzheimer’s disease and other dementias. The results apply only to those age 50 or older who have elevated blood pressure and who do not have diabetes or a history of stroke. But that’s a condition affecting a lot of people — more than 75 percent of people over 65 have hypertension, the study said. So millions might eventually benefit by reducing not only their risk of heart problems but of cognitive decline, too. “It’s kind of remarkable that they found something,” said Dr. Kristine Yaffe, a professor of psychiatry and neurology at University of California San Francisco, who was not involved in the research. “I think it actually is very exciting because it tells us that by improving vascular health in a comprehensive way, we could actually have an effect on brain health.” © 2019 The New York Times Company
Keyword: Alzheimers
Link ID: 25913 - Posted: 01.29.2019
A study has shed light on the neurocomputational contributions to the development of post-traumatic stress disorder (PTSD) in combat veterans. The findings, published in Nature Neuroscience, revealed distinct patterns for how the brain and body respond to learning danger and safety depending on the severity of PTSD symptoms. These findings could help explain why symptoms of PTSD can be severe for some people but not others. The study was funded in part by the National Institute of Mental Health, part of the National Institutes of Health. “Researchers have thought that the experience of PTSD, in many ways, is an overlearned response to survive a threatening experience,” said Susan Borja, Ph.D., chief of the NIMH Dimensional Traumatic Stress Research Program. “This study clarifies that those who have the most severe symptoms may appear behaviorally similar to those with less severe symptoms, but are responding to cues in subtly different, but profound, ways.” PTSD is a disorder that can sometimes develop after exposure to a traumatic event. People with PTSD may experience intrusive and frightening thoughts and memories of the event, experience sleep problems, feel detached or numb, or may be easily startled. While almost half of all U.S. adults will experience a traumatic event in their life, most do not develop PTSD. One theory explaining why some symptoms of PTSD develop suggests that during a traumatic event, a person may learn to view the people, locations, and objects that are present as being dangerous if they become associated with the threatening situation. While some of these things may be dangerous, some are safe. PTSD symptoms result when these safe stimuli continue to trigger fearful and defensive responses long after the trauma has occurred.
Keyword: Stress; Brain imaging
Link ID: 25912 - Posted: 01.29.2019
By Gretchen Reynolds Exercise and eating have a fraught, unsettled relationship with each other. Workouts can blunt or boost appetites. People who start an exercise program often overeat and gain weight — and yet studies and lived experience demonstrate that regular exercise is needed to avoid regaining the weight lost during a successful diet. Intrigued by these contradictory outcomes, researchers at the University of Texas Southwestern Medical Center, along with colleagues from other institutions, ran an experiment on the melanocortin circuit, a brain network in the hypothalamus known to be involved in metabolism. The resulting study, published in December in Molecular Metabolism, suggests that intense exercise might change the workings of certain neurons in ways that could have beneficial effects on appetite and metabolism. The melanocortin circuit consists mainly of two types of neurons. The neuropeptide Y (NPY) cells relay signals encouraging the body to seek food, while the pro-opiomelanocortin (POMC) neurons countermand those orders, reducing interest in food. Animals, including humans, that lack healthy POMC neurons usually become morbidly obese. The researchers focused on what exercise would do to these cells in mice, whose melanocortin circuits resemble ours. Healthy adult male mice either ran on small treadmills or, in a control group, were placed on unmoving treadmills. The exercise routine consisted of 60 minutes of fast, intense running, broken into three 20-minute blocks. Afterward, the mice were free to eat or not, as they chose. The researchers then checked neuronal activity in some of their brains by microscopically probing individual cells in living tissue to measure their electrical and biochemical signals. The tests were repeated throughout the study, which ran for as many as 10 days for some mice. © 2019 The New York Times Company
Keyword: Obesity
Link ID: 25911 - Posted: 01.29.2019
Ian Sample Science editor A group of volunteers who took a trip in the name of science have helped researchers uncover how LSD messes with activity in the brain to induce an altered state of consciousness. Brain scans of individuals high on the drug revealed that the chemical allows parts of the cortex to become flooded with signals that are normally filtered out to prevent information overload. The drug allowed more information to flow from the thalamus, a kind of neural gatekeeper, to a region called the posterior cingulate cortex, and it stemmed the flow of information to another part known as the temporal cortex. This disruption in communication may underpin some of the wacky effects reported by LSD users, from feelings of bliss and being at one with the universe to hallucinations and what scientists in the field refer to as “ego dissolution”, where one’s sense of self disintegrates. For the study, the researchers invited 25 healthy participants into the lab to be scanned under the influence of LSD and, on another occasion, after taking a placebo. They were shown around the scanner beforehand to ensure they felt comfortable going inside when the drug took hold. Had the machine suddenly taken on a threatening demeanour, the scans might not have come out so well. The scientists wanted to test a hypothesis first put forward more than a decade ago. It states LSD causes the thalamus to stop filtering information it relays to other parts of the brain. It is the breakdown of this filter that gives rise to the weird effects the drug induces, or so the thinking goes. © 2019 Guardian News and Media Limited
Keyword: Drug Abuse; Brain imaging
Link ID: 25910 - Posted: 01.29.2019
By Benedict Carey Veteran insomniacs know in their bones what science has to say about sleep deprivation and pain: that the two travel together, one fueling the other. For instance, people who develop chronic pain often lose the ability to sleep well, and quickly point to a bad back, sciatica or arthritis as the reason. The loss of sleep, in turn, can make a bad back feel worse, and the next night’s slumber even more difficult. Why sleep deprivation amplifies pain is not fully worked out, but it has to do with how the body responds to an injury such as a cut or turned ankle. First, it hurts, as nerves send a blast up the spinal cord and into the brain. There, a network of neural regions flares in reaction to the injury and works to manage, or blunt, the sensation. Think of the experience as a kind of physiological dialogue between the ground unit that took the hit and the command-control center trying to contain the damage. In a new study, a team of neuroscientists has clarified the nature of the top-down portion of that exchange, and how it is affected by sleep. In a sleep-lab experiment, the researchers found that a single night of sleep deprivation reduced a person’s pain threshold by more than 15 percent and left a clear signature in the brain’s pain-management centers. In a separate experiment, the team determined that small deviations in the average amount of sleep from one day to another predicted the level of overall pain felt the next day. “What’s exciting about these findings is that they will stimulate, and justify, doing more research to figure this system out,” said Michael J. Twery, director of the sleep disorders branch of the National Heart, Lung and Blood Institute, who was not involved in the new study. “Once we understand how sleep deprivation changes how these pathways function, we should be able to manage pain more effectively — all types of pain.” © 2019 The New York Times Company
Keyword: Sleep; Pain & Touch
Link ID: 25909 - Posted: 01.29.2019
By John Horgan I’m still brooding over the pros and cons of facing truth, or reality. My last post notes that in some situations--when we’re languishing in a nursing home, say, or agonizing over climate change--reality might be distressing, hence the temptation to avoid it. In this post, I’d like to dig deeper into the link between knowledge and mood. When we see reality, assuming that’s possible, how should we feel? And when I say reality I mean Reality, the way things really are. The Truth. Below I’ll consider three possibilities. Buddha and other sages have assured us that Reality should make us happy, no matter what the circumstances of our lives at any particular moment. And not just happy but serene, blissful, immune to the pains that afflict ordinary folk. This is the state known as enlightenment, nirvana, awakening. You plunge into the timeless cosmic consciousness underlying the flux of ordinary mortal existence, and you feel fantastic. (The catch is that, according to Buddha, when you are in this state you realize that “you” don't really exist.) Plato agreed that Truth is sublime, and perceiving it should make you feel good (and be good, but let’s leave that aside). You escape the cave of delusion, step into the incandescent realm of eternal forms and are overcome with rapture. Things might get tricky when you go back inside the cave and tell your benighted buddies what you’ve seen. They might think you're nuts and kill you, but you’ll die happy, as Plato’s mentor Socrates supposedly did. © 2019 Scientific American
Keyword: Consciousness; Emotions
Link ID: 25908 - Posted: 01.28.2019
By Jane E. Brody I had hoped to avoid ushering in the new year with yet another weight/diet column, but three circumstances prompted me to reconsider: 1) The latest data released by the Centers for Disease Control and Prevention showed that the weight of American men and women has continued its upward climb, with the average B.M.I. now almost at the cutoff for obesity; 2) The Food and Drug Administration is rolling out changes in serving sizes on packaged foods that could very well make matters worse, especially for consumers of ice cream and soda, and 3) Some good news for a change: the publication of an eminently sensible approach to weight loss, “Finally Full, Finally Slim,” written by a leading expert on portion control, Lisa R. Young, a registered dietitian and adjunct professor of nutrition at New York University. Unlike the myriad diet fads that have yet to stem the ever-increasing girth of American men and women, what Dr. Young describes is not a diet but a practical approach to food and eating that can be adapted to almost any way of life, even if most meals are eaten out or taken out. It is not prescriptive or even proscriptive. It does not cut out any category of food, like carbohydrates or fats, nor does it deprive people of their favorite foods, including sweet treats. And it works. I know, because more than half a century ago I lost 40 pounds in two years following Dr. Young’s approach, and I’ve kept the weight off ever since without dieting or deprivation. It fills me up with delicious, nutritious foods and allows me to enjoy a frequent nightcap of ice cream — half a cup (measured) at 150 calories or less. © 2019 The New York Times Company
Keyword: Obesity
Link ID: 25907 - Posted: 01.28.2019
By Scott Atran “I had seen nothing sacred, and the things that were glorious had no glory and the sacrifices were like the stockyards at Chicago if nothing was done with the meat except to bury it.”—Ernest Hemingway, A Farewell to Arms The revival of parochial nationalism in tandem with the spread of transnational terrorism has fragmented social consensus across the world. Governments and peoples are struggling to understand what to do to get along without constant conflict, or even to see if that is possible anymore. A question that drives my colleagues and me is: Can science be of any help? And here I want to focus on one particular contribution from social science: research into how sacred values can ratchet up conflict, and what might be done about it. Current forms of seemingly intractable political conflict—over the wall in America, Brexit in Britain, the Yellow Vests in France, Catalonian Independence in Spain—appear to share two critical features of more violent enduring conflicts, such as the Israel-Palestine dispute or the fight with ISIS and its ilk, which our interdisciplinary research teams of scientists, policymakers and artists at Artis International have been exploring in depth for more than a decade: entrenchment of issues, however material to begin with, in appeal to the uncompromising nature of so-called “sacred values” that people believe in, like God and country; and the belief that the one side, because of its antagonistic values, wants to exclude the other side from social or political life, or even from life itself. With support from Minerva Research Initiative of the U.S. Department of Defense and National Science Foundation, we recently published the first neuroimaging study of a radicalizing population. The research used ethnographic surveys and psychological analysis to identify 535 young Muslim men in and around Barcelona—where ISIS-supporting jihadis killed 13 people and wounded 100 more in the city center in August 2017. © 2019 Scientific American,
Keyword: Emotions; Brain imaging
Link ID: 25906 - Posted: 01.28.2019
By Smitha Mundasad Global Health Correspondent, BBC News Scientists say they have discovered the secret behind why some people are skinny while others pile on the pounds easily. Their work reveals newly discovered genetic regions linked to being very slim. The international team say this supports the idea that, for some people, being thin has more to do with inheriting a "lucky" set of genes than having a perfect diet or lifestyle. The study appears in PLOS Genetics. In the past few decades, researchers have found hundreds of genetic changes that increase the chance of a person being overweight - but there has been much less focus on the genes of people who are thin. In this investigation, scientists compared DNA samples from 1,600 healthy thin people in the UK - with a body mass index (BMI) of less than 18 - with those of 2,000 severely obese people and 10,400 people of normal weight. They also looked closely at lifestyle questionnaires - to rule out eating disorders, for example. Researchers found people who were obese were more likely to have a set of genes linked to being overweight. Meanwhile, people who were skinny not only had fewer genes linked to obesity but also had changes in gene regions newly associated with healthy thinness. Lead researcher Prof Sadaf Farooqi, from the University of Cambridge, called on people to be less judgemental about others' weight. "This research shows for the first time that healthy thin people are generally thin because they have a lower burden of genes that increase a person's chances of being overweight and not because they are morally superior, as some people like to suggest," she said. © 2019 BBC.
Keyword: Obesity; Genes & Behavior
Link ID: 25905 - Posted: 01.26.2019
Aimee Cunningham A sleep-deprived brain is awash in excess amounts of not one but two proteins whose bad behavior is implicated in Alzheimer’s disease. A new study finds excessive amounts of a protein called tau in the fluid that bathes the brain and spinal cord of extremely sleep-deprived adults. Tau, which is tied to nerve cell death, tangles and spreads throughout the brain during Alzheimer’s. An earlier report on these sleepy adults found that the protein amyloid-beta — globs of which dot the brains of Alzheimer’s patients — also increased. Samples of cerebrospinal fluid collected from eight adults, monitored during a night of normal sleep and over the course of 36 hours of sleep deprivation, revealed a 51.5 percent increase in tau in participants robbed of shut-eye. And sleep-deprived mice had twice the amount of tau as well-rested mice, researchers report online January 24 in Science. Earlier work by these researchers had suggested that the quality of sleep might affect tau levels; this time, it’s been linked to duration of sleep. With both A-beta and tau increasing with a lack of sleep, “it certainly argues that treating sleep disorders during mid-life as well as getting appropriate levels of sleep is likely to decrease risk for Alzheimer’s disease,” says coauthor David Holtzman, a neurologist and neuroscientist at Washington University School of Medicine in St. Louis. During sleep, the brain appears to flush out excess proteins and other debris (SN: 7/21/18, p. 22), so perhaps less sleep means that wash cycle is curtailed. |© Society for Science & the Public 2000 - 2019.
Keyword: Sleep; Alzheimers
Link ID: 25904 - Posted: 01.26.2019
Nicola Davis If you have trouble getting to sleep, it might be worth investing in a hammock: scientists say a gentle rocking motion not only helps people to fall asleep more rapidly but also improves the quality of sleep and the memory of the sleeper. While parents have long employed rocking as a way to calm babies and send them to sleep, some studies have suggested it helps adults too. Now researchers say they have found evidence to back this up and discovered further benefits to boot. “Rocking in people that do not have any sleep problems can still improve sleep quality, and the beneficial effects of sleep on – for instance – memory also seem to be enhanced,” said Dr Paul Franken, a co-author of the research, from the University of Lausanne in Switzerland. Writing in the journal Current Biology, he and colleagues in Lausanne and Geneva reveal that 18 young participants without sleep problems spent three nights in a laboratory: one night getting used to the environment, one night being monitored while sleeping in a stationary bed and one night being monitored with the bed gently rocking from side to side. Participants were asked to learn pairs of unrelated French words and were then tested on their ability to recall these pairs both before and after each of the test nights. Brain waves of the participants were monitored as they slept using EEG, and other metrics such as heart rate were also recorded. The brain wave data revealed that a gentle rocking did not affect the overall time participants spent asleep but did shorten their transition to “real” sleep. © 2019 Guardian News and Media Limited
Keyword: Sleep
Link ID: 25903 - Posted: 01.26.2019
By Teodora Stoica Try to explain to an alien why we sleep. Give it your best shot. “Well, we get tired. And our brain needs to rest.” “I see. So, you find another way to defend yourself during rest?” Advertisement “Well … no. Our body is paralyzed, and we lose consciousness.” There is an awkward pause. The alien tilts its head, feigning understanding. “But! We sometimes dream!” “Dream?” Blindly, unaware of how ridiculous you sound, you continue with unprecedented speed and cadence: “Yes! Dreams are fantastical stories projected from the mind into the mind, sometimes mixed with things that have already happened!” You catch your breath, and smile idiotically. “And … this helps with survival?” “Well … no. Sometimes the content confuses us in waking life,” you suddenly realize. newsletter promo Sign up for Scientific American’s free newsletters. The alien blinks silently a few times, furrowing his non-eyebrows: “Let me see if I understand. Your species spends one third of their lives paralyzed watching fantasy movies?” It is reasonable to assume the human race is doomed at this uncomfortable juncture in the conversation, and aliens will plan their stealthy attack during this incapacitated, seemingly futile stage of our existence.
Keyword: Sleep
Link ID: 25902 - Posted: 01.26.2019


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