Aaron E. Carroll Many high-school-aged children across the United States now find themselves waking up much earlier than they’d prefer as they return to school. They set their alarms, and their parents force them out of bed in the morning, convinced that this is a necessary part of youth and good preparation for the rest of their lives. It’s not. It’s arbitrary, forced on them against their nature, and a poor economic decision as well. The National Heart, Lung and Blood Institute recommends that teenagers get between nine and 10 hours of sleep. Most in the United States don’t. It’s not their fault. My oldest child, Jacob, is in 10th grade. He plays on the junior varsity tennis team, but his life isn’t consumed by too many extracurricular activities. He’s a hard worker, and he spends a fair amount of time each evening doing homework. I think most nights he’s probably asleep by 10 or 10:30. His school bus picks him up at 6:40 a.m. To catch it, he needs to wake up not long after 6. Nine hours of sleep is a pipe dream, let alone 10. There’s an argument to be made that we should cut back on his activities or make him go to bed earlier so that he gets more sleep. Teens aren’t wired for that, though. They want to go to bed later and sleep later. It’s not the activities that prevent them from getting enough sleep — it’s the school start times that require them to wake up so early. More than 90 percent of high schools and more than 80 percent of middle schools start before 8:30 a.m. Some argue that delaying school start times would just cause teenagers to stay up later. Research doesn’t support that idea. A systematic review published a year ago examined how school start delays affect students’ sleep and other outcomes. Six studies, two of which were randomized controlled trials, showed that delaying the start of school from 25 to 60 minutes corresponded with increased sleep time of 25 to 77 minutes per week night. In other words, when students were allowed to sleep later in the morning, they still went to bed at the same time, and got more sleep. © 2017 The New York Times Company

Keyword: Biological Rhythms; Development of the Brain
Link ID: 24060 - Posted: 09.13.2017

By Giorgia Guglielmi The trillions of bacteria that live in our intestines, known collectively as the gut microbiome, have been linked to maladies from eye disease to rheumatoid arthritis. Now, two new studies have added another disease: multiple sclerosis (MS), an autoimmune disorder that strips away nerve cells’ protective covers, leading to muscle weakness, blindness, and even death. What’s more, the studies suggest how our gut microbes make the immune system turn against nerve cells—a finding that could lead to treatments, like drugs based on microbial byproducts, that might improve the course of the disease. MS affects 2.5 million people worldwide, but little is known about what causes the disease, which progressively disrupts information flow from and within the brain. Most researchers think it starts when genetically predisposed people encounter an as-yet-unknown environmental trigger. Previous studies have identified particular bacteria present in increased amounts in the guts of MS patients. But the new papers “took it to the next level” in trying to understand how these bacteria affect the immune system, says Francisco Quintana, a neuroimmunologist at Brigham and Women’s Hospital in Boston not involved with the work. “These are going to be landmark studies.” In the first paper, a team of researchers led by Sergio Baranzini, a human geneticist at the University of California, San Francisco, analyzed the microbiomes of 71 people with MS and 71 healthy individuals, aged 19 to 71. They found that two bacterial groups, Acinetobacter and Akkermansia, were four times more abundant in MS patients than in individuals with no disease. Another group, Parabacteroides, was four times as abundant in healthy people. © 2017 American Association for the Advancement of Science

Keyword: Multiple Sclerosis
Link ID: 24059 - Posted: 09.13.2017

By Clare Wilson Have we had our first peek at the source of nightmares? When rats are given a fright while they are awake, the fear centre of their brains gets reactivated when they next go to sleep. This could explain why people who go through frightening experiences often have nightmares afterwards, says György Buzsáki of New York University. Rats store mental maps of the world they experience in their hippocampi – two curved structures in the brain. Different places are processed by distinct groups of neurons in the hippocampi that fire together in sequence as rats run around a maze, for example. Later, after exploring an environment like this, these firing sequences have been seen replaying as the animals sleep, as if dreaming of the routes they’d taken. This process is thought to allow memories to become consolidated for longer term storage, and has recently been detected in people for the first time. Buzsáki’s team wondered if such memory replay might include not just spatial information but also how the animal was feeling at the time. They tested this by giving a rat an unpleasant but harmless experience – a puff of air in the face from a computer keyboard cleaner – at a particular spot along a route. As expected, the rats learned to fear that particular place. “They slow down before the location of the air puff, then run superfast away from it,” says Buzsáki’s colleague, Gabrielle Girardeau. “If you do it in the face of a human, they don’t like it either.” © Copyright New Scientist Ltd.

Keyword: Sleep; Learning & Memory
Link ID: 24058 - Posted: 09.12.2017

By Michelle Roberts Health editor, BBC News online There is "surprisingly limited" evidence that light drinking during pregnancy poses any risk to the baby, say UK researchers. They reviewed all the available studies done on the topic since the 1950s and found no convincing proof that a drink or two a week is harmful. The Bristol University team stress this does not mean it is completely safe. They say women should avoid all alcohol throughout pregnancy "just in case", as per official guidelines. But women who have had small amounts to drink in pregnancy should be reassured that they are unlikely to have harmed their baby. The Chief Medical Officer for the UK, Prof Dame Sally Davies, updated her advice last year to advocate total abstinence. Before that, pregnant women had been told they could drink one or two units - equivalent to one or two small glasses of wine - a week. There is no proven safe amount that women can drink during pregnancy, although the risks of drinking heavily in pregnancy are well known. Getting drunk or binge drinking during pregnancy increases the risk of miscarriage and premature birth and can lead to mental and physical problems in the baby, called foetal alcohol syndrome. The risks associated with light drinking, however, are less clear. Dr Luisa Zuccolo and colleagues found 26 relevant studies on the topic. Their review found no overwhelming proof of harm - but, in seven of the studies, light drinking was associated, on average, with an 8% higher risk of having a small baby, compared with drinking no alcohol at all. The review, in BMJ Open, also notes it appeared to increase the risk of having a premature birth. © 2017 BBC.

Keyword: Development of the Brain; Drug Abuse
Link ID: 24057 - Posted: 09.12.2017

By Helen Thomson DON’T mind the gap. A woman has reached the age of 24 without anyone realising she was missing a large part of her brain. The case highlights just how adaptable the organ is. The discovery was made when the woman was admitted to the Chinese PLA General Hospital of Jinan Military Area Command in Shandong Province complaining of dizziness and nausea. She told doctors she’d had problems walking steadily for most of her life, and her mother reported that she hadn’t walked until she was 7 and that her speech only became intelligible at the age of 6. Doctors did a CAT scan and immediately identified the source of the problem – her entire cerebellum was missing (see scan, above). The space where it should be was empty of tissue. Instead it was filled with cerebrospinal fluid, which cushions the brain and provides defence against disease. The cerebellum – sometimes known as the “little brain” – is located underneath the two hemispheres. It looks different from the rest of the brain because it consists of much smaller and more compact folds of tissue. It represents about 10 per cent of the brain’s total volume but contains 50 per cent of its neurons. Although it is not unheard of to have part of your brain missing, either congenitally or from surgery, the woman joins an elite club of just nine people who are known to have lived without their entire cerebellum. A detailed description of how the disorder affects a living adult is almost non-existent, say doctors from the Chinese hospital, because most people with the condition die at a young age and the problem is only discovered on autopsy (Brain, doi.org/vh7). © Copyright New Scientist Ltd.

Keyword: Development of the Brain
Link ID: 24056 - Posted: 09.12.2017

Sarah Knapton, Science Editor Depression could be treated using anti-inflammatory drugs, scientists now believe, after determining that it is a physical illness caused by a faulty immune system. Around one in 13 people in Britain suffers from anxiety or depression and last year the NHS issued 64.7 million prescriptions for antidepressants, double the amount given out a decade ago. Current treatment is largely centred around restoring mood-boosting chemicals in the brain, such as serotonin, but experts now think an overactive immune system triggers inflammation throughout the entire body, sparking feelings of hopelessness, unhappiness and fatigue. It may be a symptom of the immune system failing to switch off after a trauma or illness, and is a similar to the low mood people often experience when they are fighting a virus, like flu. A raft of recent papers, and unexpected results from clinical trials, have shown that treating inflammation seems to alleviate depression. Likewise when doctors give drugs to boost the immune system to fight illness it is often accompanied by depressive mood - in the same way as how many people feel down after a vaccination. Professor Ed Bullmore, Head of the Department of Psychiatry at the University of Cambridge, believes a new field of ‘immuno-neurology’ is on the horizon. © Telegraph Media Group Limited 2017

Keyword: Depression
Link ID: 24055 - Posted: 09.11.2017

A family has settled a lawsuit against People for the Ethical Treatment of Animals (Peta) after it took a girl’s unattended dog and put it down. The legal outcome ends an attempt to in effect put Peta on trial for euthanising hundreds of animals each year. Wilber Zarate from Virginia had sued the group for taking his daughter’s chihuahua from a mobile home park on the state’s eastern shore and euthanising it before the end of a required five-day grace period. Zarate alleged Peta operated under a broad policy of euthanising animals, including healthy ones, because it “considers pet ownership to be a form of involuntary bondage”. Peta denied the allegations and maintained the incident in 2014 was a “terrible mistake”. Two women affiliated with Peta – Victoria Carey and Jennifer Wood – travelled to Accomack County, Virginia, because they said a mobile home park owner asked for help capturing wild dogs and feral cats. The women removed an unattended and unleashed chihuahua named Maya, which was a Christmas present to nine-year-old Cynthia Zarate. Maya was put down later that day, a violation of a state law that requires a five-day grace period. Peta was fined $500 for the violation. A trial had been scheduled for September, during which Zarate’s attorneys had planned to question current and former Peta employees about its euthanasia policy. © 2017 Guardian News and Media Limited

Keyword: Animal Rights
Link ID: 24054 - Posted: 09.11.2017

By JANE E. BRODY Many years ago I was plagued with debilitating headaches associated with a number of seemingly unrelated activities that included cooking for company and sewing drapes for the house. I thought I might be allergic to natural gas or certain fabrics until one day I realized that I tensed my facial muscles when I concentrated intently on a project. The cure was surprisingly simple: I became aware of how my body was reacting and changed it through self-induced behavior modification. I consciously relaxed my muscles whenever I focused on a task that could precipitate a tension-induced headache. Fast-forward about five decades: Now it was my back that ached when I hurriedly cooked even a simple meal. And once again, after months of pain, I realized that I was transferring stress to the muscles of my back and had to learn to relax them, and to allow more time to complete a project to mitigate the stress. Happy to report, I recently prepared dinner for eight with nary a pain. I don’t mean to suggest that every ache and pain can be cured by self-awareness and changing one’s behavior. But recent research has demonstrated that the mind – along with other nonpharmacological remedies — can be powerful medicine to relieve many kinds of chronic or recurrent pains, especially low back pain. As Dr. James Campbell, a neurosurgeon and pain specialist, put it, “The best treatment for pain is right under our noses.” He suggests not “catastrophizing” – not assuming that the pain represents something disastrous that keeps you from leading the life you’ve chosen. Acute pain is nature’s warning signal that something is wrong that should be attended to. Chronic pain, however, is no longer a useful warning signal, yet it can lead to perpetual suffering if people remain afraid of it, the doctor said. © 2017 The New York Times Company

Keyword: Pain & Touch
Link ID: 24053 - Posted: 09.11.2017

By David Grimm It started in May with a web post by People for the Ethical Treatment of Animals (PETA). “Tell Yale University to Stop Tormenting Birds!” the headline read, followed by text accusing postdoc Christine Lattin of wasteful experiments and animal abuse in her research on stress in wild house sparrows. Then the emails from PETA supporters began flooding Lattin’s inbox: “You should kill yourself, you sick bitch!” Then the messages on Facebook and Twitter: “What you’re doing is so sick and evil.” “I hope someone throws you into the fire …” By the end of August, PETA—based in Norfolk, Virginia—had organized three protests against Lattin, and she says she was getting 40 to 50 messages a day. “Every time I went to check my email or Twitter, my heart started racing. I worried there might be another message. I worried about the safety of my family.” In some ways, Lattin’s story is nothing new. PETA and other animal rights groups have hounded researchers for decades in hopes of shutting down animal experiments in the United States and elsewhere. But Lattin is an unusual target. She’s a self-professed animal lover with a background in bird rescue; her studies are far less invasive than the research PETA has traditionally gone after; and she’s only a postdoc, much younger and less established than any scientist the group has singled out before. That has prompted critics to accuse PETA of trying to destroy Lattin’s career. “She’s at the most vulnerable point in the academic spectrum,” says Kevin Folta, a molecular biologist at the University of Florida in Gainesville. (Folta was targeted by activists opposed to genetically engineered crops after reports that he did not disclose funding from agriculture giant Monsanto; Folta say he did nothing wrong.) PETA’s campaign, he says, “is a warning shot for anyone even thinking about doing animal research.” © 2017 American Association for the Advancement of Science.

Keyword: Animal Rights
Link ID: 24052 - Posted: 09.09.2017

Nicola Davis A pioneering approach to tackling a host of diseases using an electrical implant could eventually reduce or even end pill-taking for some patients, researchers have claimed. The technology relies on electrical stimulation of the vagus nerve – a bundle of nerve fibres that runs from the brain to the abdomen, branching off to organs including the heart, spleen, lungs and gut, and which relays signals from the body’s organs to the brain and vice versa. The pacemaker-like device is typically implanted below the left collarbone with wires running to the vagus nerve in the neck and is already used to tackle treatment-resistant epilepsy and depression. But a growing body of researchers say that such “hacking” of the body’s neural circuits could alleviate the symptoms of diseases including rheumatoid arthritis and Crohn’s disease by tapping into a recently discovered link between the brain and the immune system. That, they say, could bring hope for those with currently untreatable conditions while raising the possibility for others of dramatically reducing medication, or even cutting it out altogether. “In your lifetime and mine we are going to see millions of people with devices so they don’t have to take drugs,” said Kevin Tracey, president of the Feinstein Institute for Medical Research and co-founder of bioelectronics company, SetPoint Medical.

Keyword: Stress; Depression
Link ID: 24051 - Posted: 09.09.2017

By NICHOLAS BAKALAR High carbohydrate intake is associated with a higher risk of mortality, and high fat intake with a lower risk, researchers report. An international team of scientists studied diet and mortality in 135,335 people between 35 and 70 years old in 18 countries, following them for an average of more than seven years. Diet information depended on self-reports, and the scientists controlled for factors including age, sex, smoking, physical activity and body mass index. The study is in The Lancet. Compared with people who ate the lowest 20 percent of carbohydrates, those who ate the highest 20 percent had a 28 percent increased risk of death. But high carbohydrate intake was not associated with cardiovascular death. People with the highest 20 percent in total fat intake — an average of 35.3 percent of calories from fat — had about a 23 percent reduced risk of death compared with the lowest 20 percent (an average of 10.6 percent of calories from fat). Consuming higher saturated fat, polyunsaturated fat and monounsaturated fat were all associated with lower mortality. Higher fat diets were also associated with a lower risk of stroke. “Guidelines recommend low saturated fat, and some recommend really low amounts,” said a co-author, Andrew Mente, an epidemiologist at McMaster University in Ontario. “Our study, which captures intake at the lowest levels, shows that this may be harmful.” Current federal guidelines recommend a diet that provides no more than 35 percent of calories from fat. © 2017 The New York Times Company

Keyword: Obesity
Link ID: 24050 - Posted: 09.09.2017

Laura Sanders The brain chemical missing in Parkinson’s disease may have a hand in its own death. Dopamine, the neurotransmitter that helps keep body movements fluid, can kick off a toxic chain reaction that ultimately kills the nerve cells that make it, a new study suggests. By studying lab dishes of human nerve cells, or neurons, derived from Parkinson’s patients, researchers found that a harmful form of dopamine can inflict damage on cells in multiple ways. The result, published online September 7 in Science, “brings multiple pieces of the puzzle together,” says neuroscientist Teresa Hastings of the University of Pittsburgh School of Medicine. The finding also hints at a potential treatment for the estimated 10 million people worldwide with Parkinson’s: Less cellular damage occurred when some of the neurons were treated early on with antioxidants, molecules that can scoop up harmful chemicals inside cells. Study coauthor Dimitri Krainc, a neurologist and neuroscientist at Northwestern University Feinberg School of Medicine in Chicago, and colleagues took skin biopsies from healthy people and people with one of two types of Parkinson’s disease, inherited or spontaneously arising. The researchers then coaxed these skin cells into becoming dopamine-producing neurons. These cells were similar to those found in the substantia nigra, the movement-related region of the brain that degenerates in Parkinson’s. |© Society for Science & the Public 2000 - 2017.

Keyword: Parkinsons
Link ID: 24049 - Posted: 09.08.2017

Bruno Martin “I heard a thud behind me,” says zoologist Stefan Greif, recalling the first time he noticed a bat crash into a metal plate propped up against a wall in his lab’s flight chamber. Now, in a study published on 7 September in Science1, a team led by Greif — of the Max Planck Institute for Ornithology in Seewiesen, Germany — explains why bats often slam into vertical panes, such as glass windows.These smooth surfaces interfere with bats’ echolocation by reflecting sound away from the creatures. Bats rely on echolocation to navigate in the dark. They locate and identify objects by sending out shrill calls and listening to the echoes that bounce back. Greif and his colleagues tested the echolocation of 21 wild-caught greater mouse-eared bats (Myotis myotis) in the lab. The researchers placed a featureless metal plate on a side wall at the end of a flight tunnel. The bats interpreted the smooth surface — but not the adjacent, felt-covered walls — as a clear flight path. Over an an average of around 20 trials for each bat, 19 of them crashed into the panel at least once. The researchers also put up smooth, vertical plates near wild bat colonies, and saw similar results. The animals became confused owing to a property of smooth surfaces called ‘acoustic mirroring’. Whereas rough objects bounce some echoes back towards the bat, says Greif, a smooth surface reflects all echolocation calls away from the source. This makes a smooth wall appear as empty space to the bats, until they are directly in front of it. Only once a bat is facing the surface are their perpendicular echoes reflected back, which alerts the bat to its mistake. This explains why some bats attempted to swerve out of harm’s way at the last second — but often too late. © 2017 Macmillan Publishers Limited

Keyword: Hearing
Link ID: 24048 - Posted: 09.08.2017

Claudia Dreifus Dr. Gregory Berns, 53, a neuroscientist at Emory University in Atlanta, spends his days scanning the brains of dogs, trying to figure out what they’re thinking. The research is detailed in a new book, “What It’s Like to Be a Dog.” Among the findings: Your dog may really love you for you — not for your food. We spoke during his recent visit to New York City and later by telephone. The conversation below has been edited and condensed for space and clarity. How did your canine studies begin? It really started with the mission that killed bin Laden. There had been this dog, Cairo, who’d leapt out of the helicopter with the Navy SEALs. Watching the news coverage gave me an idea. Helicopters are incredibly noisy. Dogs have extremely sensitive hearing. I thought, “Gee, if the military can train dogs to get into noisy helicopters, it might be possible to get them into noisy M.R.I.s.” Why? To find out what dogs think and feel. A year earlier, my favorite dog, a pug named Newton, had died. I thought about him a lot. I wondered if he’d loved me, or if our relationship had been more about the food I’d provided. As a neuroscientist, I’d seen how M.R.I. studies helped us understand which parts of the human brain were involved in emotional processes. Perhaps M.R.I. testing could teach us similar things about dogs. I wondered if dogs had analogous functions in their brains to what we humans have. The big impediment doing this type of testing was to find some way to get dogs into an M.R.I. and get them to hold still for long enough to obtain useful images. © 2017 The New York Times Company

Keyword: Brain imaging; Emotions
Link ID: 24047 - Posted: 09.08.2017

Devin Coldewey We count on machine learning systems for everything from creating playlists to driving cars, but like any tool, they can be bent towards dangerous and unethical purposes as well. Today's illustration of this fact is a new paper from Stanford researchers, who have created a machine learning system that they claim can tell from a few pictures whether a person is gay or straight. The research is as surprising as it is disconcerting. In addition to exposing an already vulnerable population to a new form of systematized abuse, it strikes directly at the egalitarian notion that we can't (and shouldn't) judge a person by their appearance, nor guess at something as private as sexual orientation from something as simple as a snapshot or two. But the accuracy of the system reported in the paper seems to leave no room for mistake: this is not only possible, it has been achieved. It relies on cues apparently more subtle than most can perceive — cues many would suggest do not exist. And it demonstrates, as it is intended to, a class of threat to privacy that is entirely unique to the imminent era of ubiquitous computer vision. Before discussing the system itself, it should be made clear that this research was by all indications done with good intentions. In an extensive set of authors' notes that anyone commenting on the topic ought to read, Michal Kosinski and Yilun Wang address a variety of objections and questions. Most relevant are perhaps their remarks as to why the paper was released at all: We were really disturbed by these results and spent much time considering whether they should be made public at all. We did not want to enable the very risks that we are warning against. The ability to control when and to whom to reveal one’s sexual orientation is crucial not only for one’s well-being, but also for one’s safety.

Keyword: Sexual Behavior
Link ID: 24046 - Posted: 09.08.2017

James Gorman African wild dogs sneeze. And that’s a first. No other social animal has been reported to cast a vote, of sorts, by sneezing, although in humans sneezing may once have expressed a negative opinion, as in, “nothing to sneeze at.” Wild dog sneezing is different. For one thing it seems to indicate a positive reaction to a proposal before a group of dogs. When a pack of these dogs is getting ready to hunt, scientists reported Tuesday, the more sneezes, the more likely they are to actually get moving. Just about all social organisms make group decisions that require reaching a consensus. If monkeys or meerkats are looking for a better place to forage, they need to reach a consensus about moving on among a minimum number of animals — called a quorum, just like in Congress. Even some bacteria do this before releasing toxins or lighting up with bioluminescence. Bacteria use chemical signals but larger animals often use sounds as a way of saying, I’m in. However, among grunts, huffs, piping signals and others, the sneeze had not been reported as one of those signals until a group of American, British and Australian researchers published their observations of African dogs in the Proceedings of the Royal Society B. They were studying the dogs where they live in Botswana to see how they decide to go on a hunt. Like most carnivores, the wild dogs sleep a lot. But at some point one of the pack will start what is called a rally, getting all the other members excited and milling around as if they want to play. Sometimes the rallies are successful, and off the pack goes. Sometimes the pack members lie down and go back to sleep. Neil R. Jordan of the University of New South Wales in Sydney, the senior author of the report, noticed that the successful rallies there seemed to have more sneezing. © 2017 The New York Times Company

Keyword: Aggression
Link ID: 24045 - Posted: 09.07.2017

By Andy Coghlan A type of therapy originally designed for insomnia has been found to also help a range of mental health issues, including negative thoughts, anxiety, depression and psychosis. Daniel Freeman, at the University of Oxford, and his colleagues have been testing Sleepio, a type of cognitive behavioural therapy available online. The ten-week course is intended to restore healthy sleep patterns in people with insomnia, and Freeman wanted to see if it could also relieve other problems. Learn more about the science of sleep: In our expert talk at New Scientist Live in London His team asked nearly 1900 students who have difficulty sleeping to try using Sleepio, and nearly 1870 others to try following standard advice for insomnia. Both groups filled in questionnaires beforehand that assessed their sleep patterns, as well as tendencies to experience paranoia and hallucinations. They repeated these questionnaires at three, ten and 22 weeks into the experiment. Overall, those using Sleepio slept 50 per cent better than the control group, says Freeman. Compared to this group, the Sleepio users also had a 30 per cent reduction in hallucinations, 25 per cent reduction in paranoia, and their anxiety and depression levels were 20 per cent lower. © Copyright New Scientist Ltd.

Keyword: Sleep; Depression
Link ID: 24044 - Posted: 09.07.2017

By Bob Grant Eating a diet high in fat and low in carbohydrates keeps mice living longer, healthier lives, according to two separate studies published in Cell Metabolism today (September 5). One of the studies, conducted by researchers at the University of California, San Francisco, and the Buck Institute for Research on Aging in California, cycled mice on and off a ketogenic diet, which forces the body to produce fatty acids called ketone bodies to fuel metabolism through the severe limiting of carbohydrates. Those mice, which were given non-ketogenic diets one week and ketogenic diets the next, avoided obesity and memory decline and displayed reductions in midlife mortality, compared to mice on a control diet. The other study, performed by scientists at the Buck Institute in collaboration with researchers at the University of California, Davis, kept mice on a ketogenic diet for 14 months and showed similar results, with the addition of improvements in motor function, grip strength, and other indicators of muscle mass. “The fact that we had such an effect on memory and preservation of brain function is really exciting,” Eric Verdin, CEO of the Buck Institute and coauthor of the study that alternated ketogenic and non-ketogenic diets, says in a statement. “The older mice on the ketogenic diet had a better memory than the younger mice. That’s really remarkable.” © 1986-2017 The Scientist

Keyword: Obesity
Link ID: 24043 - Posted: 09.07.2017

A test that involves drawing a spiral on a sheet of paper could be used to diagnose early Parkinson's disease. Australian researchers have trialled software that measures writing speed and pen pressure on the page. Both are useful for detecting the disease, which causes shaking and muscle rigidity. The Melbourne team said the test could be used by GPs to screen their patients after middle age and to monitor the effect of treatments. The study, published in Frontiers of Neurology, involved 55 people - 27 had Parkinson's and 28 did not. Speed of writing and pen pressure while sketching are lower among Parkinson's patients, particularly those with a severe form of the disease. Image copyright RMIT University Image caption Treatment options are effective only when the disease is diagnosed early In the trial, a tablet computer with special software took measurements during the drawing test and was able to distinguish those with the disease, and how severe it was. Poonam Zham, study researcher from RMIT University, said: "Our aim was to develop an affordable and automated electronic system for early-stage diagnosis of Parkinson's disease, which could be easily used by a community doctor or nursing staff." The system combines pen speed and pressure into one measurement, which can be used to tell how severe the disease is. David Dexter, deputy research director at Parkinson's UK, said current tests for the disease were not able to accurately measure how advanced someone's condition was. "This can impact on the ability to select the right people for clinical research, which is essential to develop new and better treatments for Parkinson's. "This new test could provide a more accurate assessment by measuring a wider range of features that may be affected by Parkinson's, such as co-ordination, pressure, speed and cognitive function." He added that the test could be a "stepping stone" to better clinical trials for Parkinson's. © 2017 BBC.

Keyword: Parkinsons
Link ID: 24042 - Posted: 09.07.2017

Laura Sanders Peer inside the brain of someone learning. You might be lucky enough to spy a synapse pop into existence. That physical bridge between two nerve cells seals new knowledge into the brain. As new information arrives, synapses form and strengthen, while others weaken, making way for new connections. You might see more subtle changes, too, like fluctuations in the levels of signaling molecules, or even slight boosts in nerve cell activity. Over the last few decades, scientists have zoomed in on these microscopic changes that happen as the brain learns. And while that detailed scrutiny has revealed a lot about the synapses that wire our brains, it isn’t enough. Neuroscientists still lack a complete picture of how the brain learns. They may have been looking too closely. When it comes to the neuroscience of learning, zeroing in on synapse action misses the forest for the trees. A new, zoomed-out approach attempts to make sense of the large-scale changes that enable learning. By studying the shifting interactions between many different brain regions over time, scientists are beginning to grasp how the brain takes in new information and holds onto it. These kinds of studies rely on powerful math. Brain scientists are co-opting approaches developed in other network-based sciences, borrowing tools that reveal in precise, numerical terms the shape and function of the neural pathways that shift as human brains learn. © Society for Science & the Public 2000 - 2017.

Keyword: Learning & Memory
Link ID: 24041 - Posted: 09.06.2017