Pien Huang Alexandra Chen was a trauma specialist working in Lebanon and Jordan when she noticed that a specific group of kids were struggling in schools. Chen kept getting referrals for refugee students who had fled the war in Syria. They were having trouble focusing and finishing schoolwork. Some had even dropped out of school. She wondered to what extent the different stressors they faced — exposure to violence in Syria, lack of resources or concerns for the future — affected how they navigate their daily lives. Specifically, she wondered, which had a bigger impact: past trauma or the poverty they now lived in? Experts she wrote to said they didn't know and advised her to investigate the question herself. Chen, who's now getting her Ph.D. at Harvard, worked with a team to devise a study that aimed to untangle the threads of poverty, trauma and other adversities. They studied 240 teen Syrian refugees, comparing them with a group of 210 Jordanian youth who were also considered at-risk but didn't have a background of war. The researchers gave the teenagers surveys to gauge trauma and insecurity. To determine poverty, they asked the teens whether their families had items such as bedframes, cars, TVs, smartphones, refrigerators and water heaters. © 2019 npr

Keyword: Learning & Memory; Stress
Link ID: 26762 - Posted: 10.29.2019

By Maya Vijayaraghavan On Jan. 1, my husband asked me whether he would die that year. I said no. It happened to be my birthday, and I wanted to feel jubilant despite the tragic turn of events in our life. I thought Rahul might have another year, that he might beat the odds of dying this year. In other words, his hazard ratio was favorable compared with someone else in his situation. He liked talking about something related, hazard scores — a composite score of one’s genetic risk for a particular outcome such as diagnosis of a disease. It was his thing as a neuroscientist-physician. He developed one for Alzheimer’s disease, and was on his way to developing one for amyotrophic lateral sclerosis (ALS), the disease he had been studying even before he got sick with it. In reality, he had declined significantly since his diagnosis of ALS two years prior. First, he lost his speech, then his mobility, and very quickly breathing became a struggle. But any talk of decline came with an acceptance that his life was imminently finite, and neither of us were willing to accept that outcome. But Rahul did die, six months after that conversation. I remember some of our last conversations, when things were very difficult. His forewarning that this existence with him teetering at the brink of life and death was much easier than the life I would lead as a widow, raising two young children. I think neither of us really understood that the emptiness I’d feel would be soul-crushing. That I would cry all the time. That I would miss him so much. That I would become a ghost of my former self. That this thing they call complicated grief, in which healing doesn’t occur as it’s supposed to, and which supposedly happens only after a year, is something that I feel now. That I would think constantly about the time when my husband was first diagnosed and he got into a fight with our then-3-year-old (now 5) about how he could not carry him because he did not have the strength to and not because he did not want to.

Keyword: ALS-Lou Gehrig's Disease
Link ID: 26761 - Posted: 10.28.2019

By Stephen L. Macknik Most of us look at a bird and see its avian shape in perfect alignment with the colors of its beautiful plumage. How could it be any other way? The shape and color are derived from the same object and so the brain must process shape and color together as a unified percept. Right? Wrong. The brain processes forms and color in separate neural circuits, but because these brain regions communicate with each other, our perception appears unified. To understand how this all works, let’s do an experiment on ourselves to separate (and then recombine in our brains) the colors and shapes from an image. We will use an illusion called the Color Assimilation Grid, developed by Øyvind Kolås, a digital media artist and software developer. First, let’s apply a screen to the birds (above) so that we can sample their colors but get rid of most of their shape information. We simply take the original image and blur it (to break down the shape information, not shown) and then multiply the resultant pixels in a step-by-step, pixel-by-pixel fashion with a grid screen of the same size as the original image. In the screen, white pixels equal 1 and the gray regions equal zero, so the result is a blurry colored plaid sample of the birds’ colors. Now that we have diminished the shape information and sampled the colors, we need to do the opposite: sample the shapes after diminishing the color information, so that we can later mix the two to see how shape and color assimilate in the brain. To create the shape-only image we first turn the original image to grayscale (above) and then we apply the inverse of the screen we used in the color sampling. The result is a grayscale image of the birds with the shape information preserved, superimposed with a tiny grid of empty spaces where we can later add color information without altering the rest of the image. © 2019 Scientific American

Keyword: Vision
Link ID: 26760 - Posted: 10.28.2019

By Owain Clarke BBC Wales health correspondent World-leading research is helping scientists find new ways of trying to help younger people who have had a stroke get back to work. The study led by Manchester Metropolitan University found the speed a patient can walk is a major factor in determining how likely they are able to return to the workplace. Researchers have been working with physiotherapists and patients in Wales. It includes moving rehabilitation outdoors, including the Brecon Beacons. It is hoped it could lead to new rehabilitation methods being developed to target younger stroke patients. The average age to have a stroke in the UK is 72 for men and 78 for women. But there has been a 40% worldwide rise in people under 65 who have strokes in the last decade, according to the researchers. Image copyright Manchester Metropolitan University Image caption Researchers are studying the skeletons of stroke patients to see how joints perform when they walk What does the science say? It looked at 46 patients across Wales who had a stroke when younger than 65 years old and only 23% were able to return to work It found walking speed was a key predictor of whether a younger adult who has had a stroke could return to work They calculated a walking speed threshold of 0.93m/s (3ft a second) was a good benchmark for the likelihood of returning to work - and as a result this could be a goal set during rehabilitation As well as looking at the best environment for younger patients to recover in, it is now looking at using CGI technology to study joints to find out how stroke patients walk Nikki Tomkinson had a stroke at 53. "The world started shifting" while she was out driving in Cardiff. © 2019 BBC

Keyword: Stroke
Link ID: 26759 - Posted: 10.28.2019

By Tanya Lewis The lenses in human eyes lose some ability to focus as they age. Monovision—a popular fix for this issue—involves prescription contacts (or glasses) that focus one eye for near-vision tasks such as reading and the other for far-vision tasks such as driving. About 10 million people in the U.S. currently use this form of correction, but a new study finds it may cause a potentially dangerous optical illusion. Nearly a century ago German physicist Carl Pulfrich described a visual phenomenon now known as the Pulfrich effect: When one eye sees either a darker or a lower-contrast image than the other, an object moving side to side (such as a pendulum) appears to travel in a three-dimensional arc. This is because the brain processes the darker or lower-contrast image more slowly than the lighter or higher-contrast one, creating a lag the brain perceives as 3-D motion. Johannes Burge, a psychologist at the University of Pennsylvania, and his colleagues recently found that monovision can cause a reverse Pulfrich effect. They had participants look through a device showing a different image to each eye—one blurry and one in focus—of an object moving side to side. The researchers found that viewers processed the blurrier image a couple of milliseconds faster than the sharper one, making the object seem to arc in front of the display screen. It appeared closer to the viewer as it moved to the right (if the left eye saw the blurry image) or to the left (if the right eye did). “That does not sound like a very big deal,” Burge says, but it is enough for a driver at an intersection to misjudge the location of a moving cyclist by about the width of a narrow street lane (graphic). © 2019 Scientific American

Keyword: Vision
Link ID: 26758 - Posted: 10.28.2019

Marisa Iati Police and doctors didn’t believe the 46-year-old man when he swore that he hadn’t had alcohol before he was arrested on suspicion of drunken driving. His blood alcohol level was 0.2, more than twice the legal limit for operating a car. He refused a breathalyzer test, was hospitalized and later released. But the facts remained in contention. Then researchers discovered the unusual truth: Fungi in the man’s digestive system were turning carbohydrates into alcohol — a rarely diagnosed condition known as “auto-brewery syndrome.” In people with the syndrome, fermenting fungi or bacteria in the gut produce ethanol and can cause the patients to show signs of drunkenness. The condition, also known as gut fermentation syndrome, can occur in otherwise healthy people but is more common in patients with diabetes, obesity or Crohn’s disease. “A person is intoxicated from this fermenting yeast, and it’s a horrible illness,” said Barbara Cordell, a researcher of auto-brewery syndrome and the author of “My Gut Makes Alcohol.” The condition has rarely been studied and is diagnosed infrequently. Researchers at Richmond University Medical Center in New York, however, wrote in the journal BMJ Open Gastroenterology that they believe the syndrome is underdiagnosed. The condition made news in 2014, when the driver of a truck that spilled 11,000 salmon onto a highway claimed to have auto-brewery syndrome. The next year, a New York woman was charged with driving under the influence after she registered a blood alcohol level that was more than four times the legal limit, CNN reported. A judge dismissed the charges after being shown evidence that she had auto-brewery syndrome.

Keyword: Drug Abuse
Link ID: 26757 - Posted: 10.26.2019

By Jocelyn Kaiser HOUSTON, TEXAS—Schizophrenia tends to run in families, which suggests it’s largely inherited. But a long-running search for genes underlying this severe psychiatric condition has yielded only indirect clues. Now, by scouring the DNA of tens of thousands of people, gene hunters have for the first time nabbed a handful of rare genes that, when mutated, appear to be direct contributors to the disease—and may shed light on what goes awry in a schizophrenia patient’s brain. “These are concrete genes with mutations with a clear molecular mechanism,” says Mark Daly of the Broad Institute in Cambridge, Massachusetts, and the University of Helsinki, who is principal investigator for a consortium that presented the work last week at the annual meeting of the American Society of Human Genetics (ASHG) here. “It was a fabulous talk,” says Jennifer Mulle of Emory University in Atlanta, who studies the genetics of psychiatric disorders. “We don’t understand anything about the biological pathways [in schizophrenia]. Now, these genes give us an avenue.” People with schizophrenia, which afflicts about 0.7% of the U.S. population, have a distorted sense of reality and confused thinking; they may have hallucinations and delusions. Some patients share similar genetic abnormalities, such as missing specific chunks of DNA, but how those gaps may contribute to disease isn’t known. © 2019 American Association for the Advancement of Science

Keyword: Schizophrenia; Genes & Behavior
Link ID: 26756 - Posted: 10.26.2019

Lena H. Sun Most people who died from vaping-related injuries used products containing THC, the psychoactive ingredient in marijuana, federal health officials said Friday, offering another data point tying the outbreak of lung illnesses to products made with that compound. Based on data available from 860 of the 1,604 patients who have fallen ill with the disease, about 85 percent reported using THC-containing products, compared to about 10 percent who reported exclusively vaping nicotine-containing products, officials said. Many sick patients said they bought THC vape products on the black market, and those have come under increased scrutiny. “The data do continue to point towards THC-containing products as the source of individuals’ injury,” said Anne Schuchat, principal deputy director at the Centers for Disease Control and Prevention, which is leading the investigation. Officials don’t know what about the products are harmful, “but we’re seeing THC as a marker for products that are risky,” she said. It is also becoming clearer that the surge in cases in recent months is not the result of better recognition of an existing disease, but “something riskier that is in much more frequent use,” she said. Schuchat cited the use of cutting agents that are added to THC-containing products to increase profit, and the increased availability of online videos that may have “skyrocketed” do-it-yourself instructions. One substance that has turned up in many product samples is vitamin E oil, known as vitamin E acetate. Experts in the legal marijuana industry have said it has been added to THC oil used to fill vape cartridges.

Keyword: Drug Abuse
Link ID: 26755 - Posted: 10.26.2019

By Carl Zimmer Evolutionary biologists retrace the history of life in all its wondrous forms. Some search for the origin of our species. Others hunt for the origin of birds. On Thursday, a team of researchers reported an important new insight into the origin of zombies — in this case, ants zombified by a fungus. Here’s how it works: Sometimes an ant, marching about its business outdoors, will step on a fungal spore. It sticks to the ant’s body and slips a fungal cell inside. The fungus, called Ophiocordyceps, feeds on the ant from within and multiplies into new cells. But you wouldn’t know it, because the ant goes on with its life, foraging for food to bring back to the nest. All the while, the fungus keeps growing until it makes up nearly half of the ant’s body mass. When Ophiocordyceps is finished feeding on its host, the fungal cells gather inside the ant’s body. They form a mat and push needlelike projections into the ant’s muscle cells. The fungal cells also send chemical signals to the ant’s brain, causing the host to do something strange. The ant departs its nest and climbs a nearby plant. In the tropics, where many species of Ophiocordyceps live, the fungus drives ants upward, to a leaf above the ground. The ant bites down, its jaws locking as it dies. The fungus sends out sticky threads that glue the corpse to the leaf. And now it is ready to take the next step in its life cycle: Out of the ant’s head bursts a giant stalk, which showers spores onto the ant trails below. “The ants are walking over a minefield,” said David Hughes, an expert on Ophiocordyceps at Pennsylvania State University. © 2019 The New York Times Company

Keyword: Evolution
Link ID: 26754 - Posted: 10.25.2019

By Jocelyn Kaiser HOUSTON, TEXAS—Two years ago, news headlines began to appear about a development that made many human geneticists uneasy. A U.S. company planned to offer a test for embryos created through in vitro fertilization (IVF) that screened the entire genome for DNA variants linked to cognitive ability, in order to help couples avoid having children with intellectual impairment. Many ethicists fear such multigene analyses could one day be used to screen embryos for desirable traits as well, such as tall stature or high IQ. For those disturbed by the prospect, a study reported here last week at the annual meeting of the American Society of Human Genetics (ASHG) may come as a relief: For now, the strategy would not work very well. Researchers, led by statistical geneticist Shai Carmi of the Hebrew University of Jerusalem, calculated exactly how much of a boost in IQ or height could be expected by scanning for relevant DNA markers in a batch of embryos and choosing those with the highest scores. The result: The gains would be slight, and prospective parents might even end up discarding their tallest or smartest potential offspring. The work "is the first to empirically test the viability of screening embryos" for traits that are influenced by many genes, says sociologist and demographer Melinda Mills of the University of Oxford in the United Kingdom. Such embryo screening goes beyond today's testing for single-gene disorders and currently "isn't plausible," she concludes. © 2019 American Association for the Advancement of Science.

Keyword: Intelligence; Genes & Behavior
Link ID: 26753 - Posted: 10.25.2019

By Laura Sanders CHICAGO — Brain cells grown into clumps in flasks are totally stressed-out and confused. Cells in these clumps have ambiguous identities and make more stress molecules than cells taken directly from human brains, researchers reported October 22 at the annual meeting of the Society for Neuroscience. These cellular clumps are grown using stem cells made from skin or blood, which under the right conditions can be coaxed into forming three-dimensional clusters of brain cells. These clusters, a type of organoid, are thought to re-create some aspects of early human brain development, a period that is otherwise difficult to study (SN: 2/20/18). The new results highlight underappreciated differences between these organoids and the human brains they are designed to mimic. “Most of the papers out there are extolling the virtues of these things,” says study coauthor Arnold Kriegstein, a developmental neurobiologist at the University of California, San Francisco. But the new study reveals “significant issues that nobody has addressed yet.” Kriegstein and colleagues compared genetic activity in human cells from brain tissue in early development with human cells grown in an organoid. Cells in the organoids had more active genes involved in stress responses. What’s more, these organoid cells didn’t fit into the neat categories of cells in actual brain tissue. Instead, some of the organoid cells showed features of two distinct categories simultaneously. “They are not normal,” Kriegstein says. © Society for Science & the Public 2000–2019.

Keyword: Development of the Brain
Link ID: 26752 - Posted: 10.25.2019

By Veronique Greenwood To the rippling sound of an aquarium pump, a small crab comes around the corner. It moves sideways, sticking close to the walls. But when it catches sight of a mussel — laid as a reward at the end of the maze it has just walked — the crab breaks into a skipping run, throwing itself on the treat with abandon. This crustacean, one of many shore crabs scooped by researchers from under a pier in Swansea, Wales, had just completed an intriguing feat: Without any guidance from researchers, it found its way to the end of a small maze. According to a paper in Biology Letters on Wednesday, shore crabs can learn to navigate a lab-rat-style maze and remember it weeks later. While crabs that have never seen the maze before bump around aimlessly, experienced crabs race to the finish line with no wrong turns. The study, one of the few to look at whether crustaceans can perform such feats, suggests that crabs are quite capable of remembering routes. Maze running could also be a way to measure the effects of changes in the sea, like ocean acidification and warming, on crabs’ cognitive abilities. Crabs often clamber through complex landscapes in their daily lives, says Edward Pope, a marine biologist at Swansea University who is an author of the new study. So, it is not particularly surprising that crabs would be able to find their way through a maze and even be able to remember it later. What was surprising, however, was just how clear the results of the study were. During the first week of the experiment, no crabs got to the end of the maze without taking wrong turns, some of them detouring six or seven times. By week four, some could race to the end flawlessly. Even the worst-performing crab took no more than three wrong turns. To see how the crabs would perform when there was no food in the maze, and thus no trace in the water of a snack to guide them, the researchers waited a couple of weeks and put the crabs back in the maze. They also tested crabs that had never seen the maze. “The conditioned animals all ran to the end of the maze expecting there to be food,” Dr. Pope said. © 2019 The New York Times Company

Keyword: Learning & Memory; Evolution
Link ID: 26751 - Posted: 10.25.2019

Researchers have discovered in mice how one of the few genes definitively linked to schizophrenia, called SETD1A, likely confers risk for the illness. Mice genetically engineered to lack a functioning version of the enzyme-coding gene showed abnormalities in working memory, mimicking those commonly seen in schizophrenia patients. Restoring the gene’s function corrected the working memory deficit. Counteracting the gene’s deficiencies also repaired neuronal circuit deficits in adult mice – suggesting clues for potential treatment strategies. A team of scientists led by Joseph Gogos, M.D., Ph.D., of Columbia University, New York City, reported on their research – supported by the National Institutes of Health – in Neuron. “You could call SETD1A a master regulator,” explained David Panchision Ph.D., of the NIH’s National Institute of Mental Health (NIMH), which co-funded the study. “This schizophrenia risk gene codes for an enzyme that influences the expression of many other genes. In mice, a hobbled version of SETD1A disrupted gene expression in a network harboring other genomic suspects in schizophrenia. Remarkably, the resulting abnormalities were reversible.” Researchers have identified both common and rare genetic variations that contribute to risk for schizophrenia. Mutant SETD1A is one of just a few rare genes known to unequivocally confer risk for schizophrenia. While common genetic variations linked to schizophrenia individually exert only tiny effects on risk, having just one mutant copy of SETD1A is sufficient to confer a large increase in disease risk. SETD1A plays a key role in epigenomic regulation – the switching on-and-off of genes in response to experience – a molecular process widespread in the brain. Mutations in SETD1A have primarily been found in people with schizophrenia, suggesting that this rare gene variation might hold important clues to the underlying disease process.

Keyword: Schizophrenia; Genes & Behavior
Link ID: 26750 - Posted: 10.25.2019

By Kim Tingley In the United States and other Western countries, diet and nutrition researchers face an urgent imperative: Figure out how to solve the crisis of obesity. About 40 percent of the adults and 19 percent of the children and adolescents in the United States have obesity, according to the Centers for Disease Control and Prevention. More and more of them face the increased risks of suffering from diabetes, cardiovascular disease and countless other negative health effects. This situation looks like a single problem from a population standpoint — one that simple guidelines for balancing calorie consumption and expenditure should be able to solve. Instead, a seeming infinitude of variables influence what each of us eats and how the body responds. That is: Obesity, like cancer, “is not one disease,” says Elizabeth Mayer-Davis, a professor of nutrition and medicine at the University of North Carolina at Chapel Hill. In order to treat it, “you really have to be thinking about biology and behavior and society and culture and policy all at the same time. Because if you miss any one of those pieces, your intervention or your diet — it’s less likely to actually work.” The same diet can affect even identical twins differently. “It’s also why there have been so many conflicting studies in nutrition,” Mayer-Davis says. “The public is very frustrated.” Indeed, just last month a paper in Annals of Internal Medicine created controversy when it argued that there’s not enough evidence to say whether red and processed meats are bad for us, despite years of guidance claiming just that. It also reignited a growing debate: How valuable can universal diet guidelines be for individuals? In recent decades, popular weight-loss plans have largely seesawed between low-fat strategies, which U.S. health agencies have also promoted, and low-carbohydrate ones. Many of them appear to work especially well for some people and not well for others; on average, however, in studies comparing the two kinds of regimens, participants lose the same moderate amount of weight. In those cases when opposing diets produce equivalent results, Kevin Hall, a researcher at the National Institutes of Health, wondered if there was, in fact, an explanation other than the nutrients. He noticed that many of those diets tended to have at least one rule in common: Avoid ultraprocessed food, the sort of packaged fare containing artificial flavorings and ingredients you wouldn’t find in your kitchen that make processed food cheap, convenient, tasty and shelf-stable — and popular. It currently accounts for 57 percent of the American diet (a proportion that is rising). Previous studies have found correlations between ultraprocessed-food consumption and obesity but no proof that it’s a cause. © 2019 The New York Times Company

Keyword: Obesity
Link ID: 26749 - Posted: 10.25.2019

By Gina Kolata Thousands of people have received brain scans, as well as cognitive and genetic tests, while participating in research studies. Though the data may be widely distributed among scientists, most participants assume their privacy is protected because researchers remove their names and other identifying information from their records. But could a curious family member identify one of them just from a brain scan? Could a company mining medical records to sell targeted ads do so, or someone who wants to embarrass a study participant? The answer is yes, investigators at the Mayo Clinic reported on Wednesday. A magnetic resonance imaging scan includes the entire head, including the subject’s face. And while the countenance is blurry, imaging technology has advanced to the point that the face can be reconstructed from the scan. Under some circumstances, that face can be matched to an individual with facial recognition software. In a letter published in the New England Journal of Medicine, researchers at the Mayo Clinic showed that the required steps are not complex. But privacy experts questioned whether the process could be replicated on a much larger scale with today’s technology. The subjects were 84 healthy participants in a long-term study of about 2,000 residents of Olmsted County, Minn. Participants get brain scans to look for signs of Alzheimer’s disease, as well as cognitive, blood and genetic tests. © 2019 The New York Times Company

Keyword: Brain imaging
Link ID: 26748 - Posted: 10.24.2019

By Elizabeth Pennisi The more researchers look, the more connections they find between the microbes in our intestines and those in our brain. Gut bacteria appear to influence everything from depression to autism. Now, a study on how mice overcome fear is starting to reveal more about the mysterious link between gut and mind. “This work is amazing,” says Peng Zheng, a neuroscientist at Chongqing Medical University in China who was not involved with the research. The study, he says, could provide new insight into several mental disorders. The research used a classic Pavlovian test: Shock a mouse on the foot while playing a tone and the rodent will quickly learn to associate the noise with pain, flinching whenever it hears the sound. But the association doesn’t last forever. After several sessions of hearing the tone but not getting the shock, the mouse will forget the association, and the sound will have no effect. This “forgetting” is important for people as well; it’s impaired, for example, in those with chronic anxiety and post-traumatic stress disorder. David Artis, an immunologist and microbiologist at Weill Cornell Medicine in New York City, wondered whether gut bacteria played any role in the learning and forgetting responses. He and colleagues treated mice with antibiotics to totally rid them of the bacteria in their gut, collectively known as the microbiome. They then played a tone and right after gave the mouse a mild shock, doing this multiple times. © 2019 American Association for the Advancement of Science.

Keyword: Obesity
Link ID: 26747 - Posted: 10.24.2019

People with long-term health problems such as arthritis are more likely to feel pain on humid days, a study has suggested. Folklore suggests the cold makes pain worse - but there is actually little research into the weather's effects. And this University of Manchester study of 2,500 people, which collected data via smartphones, found symptoms were actually worse on warmer, damper days. Researchers hope the findings will steer future research into why that is. Hearing someone say their knee is playing up because of the weather is pretty common - usually because of the cold, Some say they can even predict the weather based on how their joints feel. But carrying out scientific research into how different types of weather affect pain has been difficult. Previous studies have been small, or short-term. In this research, called Cloudy with a Chance of Pain, scientists recruited 2,500 people with arthritis, fibromyalgia, migraine and neuropathic pain from across the UK. They recorded pain symptoms each day, for between one and 15 months, while their phones recorded the weather where they were. Damp and windy days with low pressure increased the chances of experiencing more pain than normal by about 20%. So if someone's chances of a painful day with average weather were five in 100, they would increase to six in 100 on a damp and windy day. Cold, damp days also made pain worse. But there was no association with temperature alone, or rainfall. 'Pain forecast' Prof Will Dixon, of the Centre for Epidemiology Versus Arthritis, at the University of Manchester, who led the study said: "Weather has been thought to affect symptoms in patients with arthritis since [ancient Greek physician] Hippocrates. © 2019 BBC

Keyword: Pain & Touch
Link ID: 26746 - Posted: 10.24.2019

By Kelly Servick CHICAGO, ILLINOIS—By harnessing the power of imagination, researchers have nearly doubled the speed at which completely paralyzed patients may be able to communicate with the outside world. People who are “locked in”—fully paralyzed by stroke or neurological disease—have trouble trying to communicate even a single sentence. Electrodes implanted in a part of the brain involved in motion have allowed some paralyzed patients to move a cursor and select onscreen letters with their thoughts. Users have typed up to 39 characters per minute, but that’s still about three times slower than natural handwriting. In the new experiments, a volunteer paralyzed from the neck down instead imagined moving his arm to write each letter of the alphabet. That brain activity helped train a computer model known as a neural network to interpret the commands, tracing the intended trajectory of his imagined pen tip to create letters (above). Eventually, the computer could read out the volunteer’s imagined sentences with roughly 95% accuracy at a speed of about 66 characters per minute, the team reported here this week at the annual meeting of the Society for Neuroscience. The researchers expect the speed to increase with more practice. As they refine the technology, they will also use their neural recordings to better understand how the brain plans and orchestrates fine motor movements. © 2019 American Association for the Advancement of Science.

Keyword: Robotics; Brain imaging
Link ID: 26745 - Posted: 10.24.2019

By Nicholas Bakalar Trans fatty acids, known to increase the risk for heart disease, stroke and diabetes, have now been linked to an increased risk for dementia. Researchers measured blood levels of elaidic acid, the most common trans fats, in 1,628 men and women 60 and older and free of dementia. Over the following 10 years, 377 developed some type of dementia. Trans fats, which are added to processed food in the form of partially hydrogenated vegetable oils, increase levels of LDL, or “bad” cholesterol. Meat and dairy products naturally contain small amounts of trans fats, but whether these fats raise bad cholesterol is unknown. After controlling for other factors, the scientists found that compared with those in the lowest one-quarter in blood levels of elaidic acid, those in the highest were 50 percent more likely to develop any form of dementia and 39 percent more likely to develop Alzheimer’s disease in particular. Elaidic acid levels were not associated with vascular dementia considered alone. The study is in Neurology. The senior author, Dr. Toshiharu Ninomiya, a professor of public health at Kyushu University in Japan, said the study is observational so cannot prove cause and effect. “It is difficult to avoid trans fats completely, and the risk of a small amount of trans fats is unclear,” he said. “But it would be better to try to avoid them as much as possible.” © 2019 The New York Times Company

Keyword: Obesity
Link ID: 26744 - Posted: 10.24.2019

By Meredith Wadman, Kelly Servick Biogen stunned investors and scientists alike today, announcing it will resurrect an Alzheimer’s drug it had declared a failure in March; the company plans in early 2020 to ask the U.S. Food and Drug Administration for marketing approval of aducanumab, an antibody designed to bind and eliminate the protein beta-amyloid in the brain. As STAT reports, Biogen says the about-face came after it assessed clinical trial data from a larger number of patients than it first analyzed. Whereas an initial “futility” analysis of data from two late-stage clinical trials found that the drug failed to meaningfully slow progression of early Alzheimer’s disease, the company now concludes that, due primarily to the responses of people on the higher of two doses of the antibody, the drug did significantly slow people’s cognitive decline and their functional decline, meaning their ability to cope with activities of daily living. Biogen’s first analysis used data from 1748 patients who had completed 18 months on a low dose or a high dose of the drug; the new analysis, whose underlying data are not yet publicly available nor described in a journal article, included 2066 such patients. Bart De Strooper, who directs the UK Dementia Research Institute at University College London, called the news “fantastic. … We currently have no effective treatments to slow or halt the progression of Alzheimer’s disease and I hope this signifies a turning point.” He also suggested the result could revive the once-dominant theory that the neurodegenerative condition is largely due to the brain’s accumulation of toxic amyloid. “We should now redouble our efforts to tackle this central problem in Alzheimer’s disease.” © 2019 American Association for the Advancement of Science

Keyword: Alzheimers
Link ID: 26743 - Posted: 10.23.2019