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By David Shultz We still may not know what causes consciousness in humans, but scientists are at least learning how to detect its presence. A new application of a common clinical test, the positron emission tomography (PET) scan, seems to be able to differentiate between minimally conscious brains and those in a vegetative state. The work could help doctors figure out which brain trauma patients are the most likely to recover—and even shed light on the nature of consciousness. “This is really cool what these guys did here,” says neuroscientist Nicholas Schiff at Cornell University, who was not involved in the study. “We’re going to make great use of it.” PET scans work by introducing a small amount of radionuclides into the body. These radioactive compounds act as a tracer and naturally emit subatomic particles called positrons over time, and the gamma rays indirectly produced by this process can be detected by imaging equipment. The most common PET scan uses fluorodeoxyglucose (FDG) as the tracer in order to show how glucose concentrations change in tissue over time—a proxy for metabolic activity. Compared with other imaging techniques, PET scans are relatively cheap and easy to perform, and are routinely used to survey for cancer, heart problems, and other diseases. In the new study, researchers used FDG-PET scans to analyze the resting cerebral metabolic rate—the amount of energy being used by the tissue—of 131 patients with a so-called disorder of consciousness and 28 healthy controls. Disorders of consciousness can refer to a wide range of problems, ranging from a full-blown coma to a minimally conscious state in which patients may experience brief periods where they can communicate and follow instructions. Between these two extremes, patients may be said to be in a vegetative state or exhibit unresponsive wakefulness, characterized by open eyes and basic reflexes, but no signs of awareness. Most disorders of consciousness result from head trauma, and where someone falls on the consciousness continuum is typically determined by the severity of the injury. © 2016 American Association for the Advancement of Science
By Roland Pease BBC Radio Science Unit Researchers have invented a DNA "tape recorder" that can trace the family history of every cell in an organism. The technique is being hailed as a breakthrough in understanding how the trillions of complex cells in a body are descended from a single egg. "It has the potential to provide profound insights into how normal, diseased or damaged tissues are constructed and maintained," one UK biologist told the BBC. The work appears in Science journal. The human body has around 40 trillion cells, each with a highly specialised function. Yet each can trace its history back to the same starting point - a fertilised egg. Developmental biology is the business of unravelling how the genetic code unfolds at each cycle of cell division, how the body plan develops, and how tissues become specialised. But much of what it has revealed has depended on inference rather than a complete cell-by-cell history. "I actually started working on this problem as a graduate student in 2000," confessed Jay Shendure, lead researcher on the new scientific paper. "Could we find a way to record these relationships between cells in some compact form we could later read out in adult organisms?" The project failed then because there was no mechanism to record events in a cell's history. That changed with recent developments in so called CRISPR gene editing, a technique that allows researchers to make much more precise alterations to the DNA in living organisms. The molecular tape recorder developed by Prof Shendure's team at the University of Washington in Seattle, US, is a length of DNA inserted into the genome that contains a series of edit points which can be changed throughout an organism's life. © 2016 BBC.
By BENEDICT CAREY Suzanne Corkin, whose painstaking work with a famous amnesiac known as H.M. helped clarify the biology of memory and its disorders, died on Tuesday in Danvers, Mass. She was 79. Her daughter, Jocelyn Corkin, said the cause was liver cancer. Dr. Corkin met the man who would become a lifelong subject and collaborator in 1964, when she was a graduate student in Montreal at the McGill University laboratory of the neuroscientist Brenda Milner. Henry Molaison — known in published reports as H.M., to protect his privacy — was a modest, middle-aged former motor repairman who had lost the ability to form new memories after having two slivers of his brain removed to treat severe seizures when he was 27. In a series of experiments, Dr. Milner had shown that a part of the brain called the hippocampus was critical to the consolidation of long-term memories. Most scientists had previously thought that memory was not dependent on any one cortical area. Mr. Molaison lived in Hartford, and Dr. Milner had to take the train down to Boston and drive from there to Connecticut to see him. It was a long trip, and transporting him to Montreal proved to be so complicated, largely because of his condition, that Dr. Milner did it just once. Yet rigorous study of H.M., she knew, would require proximity and a devoted facility — with hospital beds — to accommodate extended experiments. The psychology department at the Massachusetts Institute of Technology offered both, and with her mentor’s help, Dr. Corkin landed a position there. Thus began a decades-long collaboration between Dr. Corkin and Mr. Molaison that would extend the work of Dr. Milner, focus intense interest on the hippocampus, and make H.M. the most famous patient in the history of modern brain science. © 2016 The New York Times Company
Keyword: Learning & Memory
Link ID: 22258 - Posted: 05.28.2016
By Jordana Cepelewicz General consensus among Alzheimer’s researchers has it that the disease’s main culprit, a protein called amyloid beta, is an unfortunate waste product that is not known to play any useful role in the body—and one that can have devastating consequences. When not properly cleared from the brain it builds up into plaques that destroy synapses, the junctions between nerve cells, resulting in cognitive decline and memory loss. The protein has thus become a major drug target in the search for a cure to Alzheimer’s. Now a team of researchers at Harvard Medical School and Massachusetts General Hospital are proposing a very different story. In a study published this week in Science Translational Medicine, neurologists Rudolph Tanzi and Robert Moir report evidence that amyloid beta serves a crucial purpose: protecting the brain from invading microbes. “The original idea goes back to 2010 or so when Rob had a few too many Coronas,” Tanzi jokes. Moir had come across surprising similarities between amyloid beta and LL37, a protein that acts as a foot soldier in the brain’s innate immune system, killing potentially harmful bugs and alerting other cells to their presence. “These types of proteins, although small, are very sophisticated in what they do,” Moir says. “And they’re very ancient, going back to the dawn of multicellular life.” © 2016 Scientific American,
Martha Bebinger Labels for the first long-acting opioid addiction treatment device are rolling off printing machines Friday. Trainings begin Saturday for doctors who want to learn to insert four matchstick-size rods under the skin. They contain the drug buprenorphine, which staves off opioid cravings. The implant, called Probuphine, was approved by the Food and Drug Administration on Thursday, and is expected to be available to patients by the end of June. "This is just the starting point for us to continue to fight for the cause of patients with opioid addiction," said Behshad Sheldon, CEO of Braeburn Pharmaceuticals, which manufactures Probuphine. But debate continues about how effective the implant will be and whether insurers will cover it. Nora Volkow, head of the National Institute on Drug Abuse, calls Probuphine a game changer, saying it will help addiction patients stay on their meds while their brain circuits recover from the ravages of drug use. And addiction experts say it will be much harder for patients prescribed the implant to sell their medication on the street, which can be a problem with addiction patients prescribed pills. "I think it's fantastic news," said Dr. Sarah Wakeman, medical director of the Substance Use Disorder Initiative at Massachusetts General Hospital. "We need as many tools in the toolbox as possible to deal with the opioid epidemic." © 2016 npr
Keyword: Drug Abuse
Link ID: 22256 - Posted: 05.28.2016
By GINA KOLATA Could it be that Alzheimer’s disease stems from the toxic remnants of the brain’s attempt to fight off infection? Provocative new research by a team of investigators at Harvard leads to this startling hypothesis, which could explain the origins of plaque, the mysterious hard little balls that pockmark the brains of people with Alzheimer’s. It is still early days, but Alzheimer’s experts not associated with the work are captivated by the idea that infections, including ones that are too mild to elicit symptoms, may produce a fierce reaction that leaves debris in the brain, causing Alzheimer’s. The idea is surprising, but it makes sense, and the Harvard group’s data, published Wednesday in the journal Science Translational Medicine, supports it. If it holds up, the hypothesis has major implications for preventing and treating this degenerative brain disease. The Harvard researchers report a scenario seemingly out of science fiction. A virus, fungus or bacterium gets into the brain, passing through a membrane — the blood-brain barrier — that becomes leaky as people age. The brain’s defense system rushes in to stop the invader by making a sticky cage out of proteins, called beta amyloid. The microbe, like a fly in a spider web, becomes trapped in the cage and dies. What is left behind is the cage — a plaque that is the hallmark of Alzheimer’s. So far, the group has confirmed this hypothesis in neurons growing in petri dishes as well as in yeast, roundworms, fruit flies and mice. There is much more work to be done to determine if a similar sequence happens in humans, but plans — and funding — are in place to start those studies, involving a multicenter project that will examine human brains. “It’s interesting and provocative,” said Dr. Michael W. Weiner, a radiology professor at the University of California, San Francisco, and a principal investigator of the Alzheimer’s Disease Neuroimaging Initiative, a large national effort to track the progression of the disease and look for biomarkers like blood proteins and brain imaging to signal the disease’s presence. © 2016 The New York Times Company
Ronald Crystal The goal of antiaddiction vaccines is to prevent addictive molecules from reaching the brain, where they produce their effects and can create chemical dependencies. Vaccines can accomplish this task, in theory, by generating antibodies—proteins produced by the immune system—that bind to addictive particles and essentially stop them in their tracks. But challenges remain. Among them, addictive molecules are often too small to be spotted by the human immune system. Thus, they can circulate in the body undetected. Researchers have developed two basic strategies for overcoming this problem. One invokes so-called active immunity by tethering an addictive molecule to a larger molecule, such as the proteins that encase a common cold virus. This viral shell does not make people sick but does prompt the immune system to produce high levels of antibodies against it and whatever is attached to it. In our laboratory, we have tested this method in animal models and successfully blocked chemical forms of cocaine or nicotine from reaching the brain. Another approach researchers are testing generates what is known as passive immunity against addictive molecules in the body. They have cultured monoclonal antibodies that can bind selectively to addictive molecules. The hurdle with this particular method is that monoclonal antibodies are expensive to produce and need to be administrated frequently to be effective. © 2016 Scientific American
By RUSSELL GOLDMAN There’s an elephant at a zoo outside Seoul that speaks Korean. — You mean, it understands some Korean commands, the way a dog can be trained to understand “sit” or “stay”? No, I mean it can actually say Korean words out loud. — Pics or it didn’t happen. Here, watch the video. To be fair, the elephant, a 26-year-old Asian male named Koshik, doesn’t really speak Korean, any more than a parrot can speak Korean (or English or Klingon). But parrots are supposed to, well, parrot — and elephants are not. And Koshik knows how to say at least five Korean words, which are about five more than I do. The really amazing part is how he does it. Koshik places his trunk inside his mouth and uses it to modulate the tone and pitch of the sounds his voice makes, a bit like a person putting his fingers in his mouth to whistle. In this way, Koshik is able to emulate human speech “in such detail that Korean native speakers can readily understand and transcribe the imitations,” according to the journal Current Biology. What’s in his vocabulary? Things he hears all the time from his keepers: the Korean words for hello, sit down, lie down, good and no. Elephant Speaks Korean | Video Video by LiveScienceVideos Lest you think this is just another circus trick that any Jumbo, Dumbo or Babar could pull off, the team of international scientists who wrote the journal article say Koshik’s skills represent “a wholly novel method of vocal production and formant control in this or any other species.” Like many innovations, Koshik’s may have been born of sad necessity. Researchers say he started to imitate his keepers’s sounds only after he was separated from other elephants at the age of 5 — and that his desire to speak like a human arose from sheer loneliness. © 2016 The New York Times Company
By Teal Burrell In neuroscience, neurons get all the glory. Or rather, they used to. Researchers are beginning to discover the importance of something outside the neurons—a structure called the perineuronal net. This net might reveal how memories are stored and how various diseases ravage the brain. The realization of important roles for structures outside neurons serves as a reminder that the brain is a lot more complicated than we thought. Or, it’s exactly as complicated as neuroscientists thought it was 130 years ago. In 1882, Italian physician and scientist Camillo Golgi described a structure that enveloped cells in the brain in a thin layer. He later named it the pericellular net. His word choice was deliberate; he carefully avoided the word “neuron” since he was engaged in a battle with another neuroscience luminary, Santiago Ramón y Cajal, over whether the nervous system was a continuous meshwork of cells that were fused together—Golgi’s take—or a collection of discrete cells, called neurons—Ramón y Cajal’s view. Ramón y Cajal wasn’t having it. He argued Golgi was wrong about the existence of such a net, blaming the findings on Golgi’s eponymous staining technique, which, incidentally, is still used today. Ramón y Cajal’s influence was enough to shut down the debate. While some Golgi supporters labored in vain to prove the nets existed, their findings never took hold. Instead, over the next century, neuroscientists focused exclusively on neurons, the discrete cells of the nervous system that relay information between one another, giving rise to movements, perceptions, and emotions. (The two adversaries would begrudgingly share a Nobel Prize in 1906 for their work describing the nervous system.) © 1996-2016 WGBH Educational Foundation
Link ID: 22252 - Posted: 05.26.2016
By Amina Zafar, Tragically Hip frontman Gord Downie's resilience and openness about his terminal glioblastoma and his plans to tour could help to reduce stigma and improve awareness, some cancer experts say. Tuesday's news revealed that the singer has an aggressive form of cancer that originated in his brain. An MRI scan last week showed the tumour has responded well to surgery, radiation and chemotherapy, doctors said. "I was quickly impressed by Gord's resilience and courage," Downie's neuro-oncologist, Dr. James Perry of Sunnybrook Health Sciences Centre, told a news conference. Perry said it's daunting for many of his patients to reveal the diagnosis to their family, children and co-workers. "The news today, while sad, also creates for us in brain tumour research an unprecedented opportunity to create awareness and to create an opportunity for fundraising for research that's desperately needed to improve the odds for all people with this disease," Perry said. Dr. James Perry, head of neurology at Toronto's Sunnybrook Health Sciences Centre, calls Gord Downie's sad news an unprecedented opportunity to fundraise for brain tumour research. (Aaron Vincent Elkaim/Canadian Press) "Gord's courage in coming forward with his diagnosis will be a beacon for all patients with glioblastoma in Canada. They will see a survivor continuing with his craft despite its many challenges." ©2016 CBC/Radio-Canada.
Link ID: 22251 - Posted: 05.26.2016
Bradley George All sorts of health information is now a few taps away on your smartphone, from how many steps you take — to how well you sleep at night. But what if you could use your phone and a computer to test your vision? A company is doing just that — and eye care professionals are upset. Some states have even banned it. A Chicago-based company called Opternative offers the test. The site asks some questions about your eyes and overall health; it also wants to know your shoe size to make sure you're the right distance from your computer monitor. You keep your smartphone in your hand and use the Web browser to answer questions about what you see on the computer screen. Like a traditional eye test, there are shapes, lines and letters. It takes about 30 minutes. "We're trying to identify how bad your vision is, so we're kind of testing your vision to failure, is the way I would describe it," says Aaron Dallek, CEO of Opternative. Dallek co-founded the company with an optometrist, who was searching for ways to offer eye exams online. "Me being a lifetime glasses and contact wearer, I was like 'Where do we start?' So, that was about 3 1/2 years ago, and we've been working on it ever since," Dallek says. © 2016 npr
Link ID: 22250 - Posted: 05.26.2016
Susan Milius Forget it, peacocks. Nice try, elk. Sure, sexy feathers and antlers are showy, but the sperm of a fruit fly could be the most over-the-top, exaggerated male ornamentation of all. In certain fruit fly species, such as Drosophila bifurca, males measuring just a few millimeters produce sperm with a tail as long as 5.8-centimeters, researchers report May 25 in Nature. Adjusted for body size, the disproportionately supersized sperm outdoes such exuberant body parts as pheasant display feathers, deer antlers, scarab beetle horns and the forward-grasping forceps of earwigs. Fruit flies’ giant sperm have been challenging to explain, says study coauthor Scott Pitnick of Syracuse University in New York. Now he and his colleagues propose that a complex interplay of male and female benefits has accelerated sperm length in a runaway-train scenario. Males with longer sperm deliver fewer sperm, bucking a more-is-better trend. Yet, they still manage to transfer a few dozen to a few hundred per mating. And as newly arrived sperm compete to displace those already waiting in a female’s storage organ, longer is better. Fewer sperm per mating means females tend to mate more often, intensifying the sperm-vs.-sperm competition. Females that have the longest storage organs, which favor the longest sperm, benefit too: Males producing megasperm, the researchers found, tend to be the ones with good genes likely to produce robust offspring. “Sex,” says Pitnick, “is a powerful force.” © Society for Science & the Public 2000 - 2016
Sara Reardon Children from impoverished families are more prone to mental illness, and alterations in DNA structure could be to blame, according to a study published on 24 May in Molecular Psychiatry1. Poverty brings with it a number of different stressors, such as poor nutrition, increased prevalence of smoking and the general struggle of trying to get by. All of these can affect a child’s development, particularly in the brain, where the structure of areas involved in response to stress and decision-making have been linked to low socioeconomic status. Poor children are more prone to mental illnesses such as depression than their peers from wealthier families, but they are also more likely to have cognitive problems. Some of these differences are clearly visible in the brain structure and seem to appear at birth, which suggests that prenatal exposure to these stressors can be involved2. But neurodevelopment does not stop at birth. Neuroscientist Ahmad Hariri of Duke University in Durham, North Carolina, suspected that continual exposure to stressors might affect older children as well. He decided to test this idea by studying chemical tags known as methyl groups, which alter DNA structure to regulate how genes are expressed. There is some evidence that methylation patterns can be passed down through generations, but they are also altered by environmental factors, such as smoking. © 2016 Nature Publishing Group,
Dean Burnett A recent report by the National Obesity Forum stated that official advice about low-fat diets is wrong. As ever, there’s now heated debate over how valid/accurate this claim is. But let’s step back a moment and ask a revealing question: why do official government dietary guidelines even exist? Why are they necessary? From an entirely logical position, eating food fulfils several requirements. It provides the energy to do things, helps us build up stores of energy for when needed, and provides the materials required to build and maintain our bodies. Therefore, the human body requires a regular intake of nutrients, vitamins and calories to maintain day-to-day functioning. As a result, the human body has developed an intricate digestive system to monitor and regulate our food intake. The digestive system is quite cool. It has a sophisticated nervous system that can operate pretty much independently, so is often regarded as separate from the main one, leading some to describe it as a “second brain”, there to encourage, monitor and process the consumption and digestion of food. It also utilises hormones, namely leptin and ghrelin, which decrease and increase appetite respectively depending on how much food the body has/needs. It’s a painstakingly complex and precise system that’s evolved over aeons to make sure we eat what and when we need to, and get the most out of our food. However, at some point the human brain got involved, then everything went to hell. This is why we can now be presented with foodstuffs we’re repeatedly told are unhealthy, even dangerous, and say “Thanks. Extra chilli sauce on mine, please”.
by Bruce Bower For a landmark 1977 paper, psychologist Andrew Meltzoff stuck his tongue out at 2- to 3-week-old babies. Someone had to do it. After watching Meltzoff razz them for 15 seconds, babies often stuck out their own tongues within the next 2½ minutes. Newborns also tended to respond in kind when the young researcher opened his mouth wide, pushed out his lips like a duck and opened and closed the fingers of one hand. Meltzoff, now at the University of Washington in Seattle, and a colleague were the first to report that babies copy adults’ simple physical deeds within weeks of birth. Until then, most scientists assumed that imitation began at around 9 months of age. Newborns don’t care that imitation is the sincerest form of flattery. For them, it may be a key to interacting with (and figuring out) those large, smiley people who come to be known as mommy and daddy. And that’s job number one for tykes hoping to learn how to talk and hang out with a circle of friends. Meltzoff suspected that babies enter the world able to compare their own movements — even those they can feel but not see, such as a projecting tongue — to corresponding adult actions. Meltzoff’s report has inspired dozens of papers on infant imitation. Some have supported his results, some haven’t. A new report, published May 5 in Current Biology, falls in the latter group. The study of 106 Australian babies tracked from 1 to 9 weeks of age concludes that infants don’t imitate anyone. © Society for Science & the Public 2000 - 201
Keyword: Development of the Brain
Link ID: 22246 - Posted: 05.25.2016
By Lisa Rapaport (Reuters Health) - Attention deficit hyperactivity disorder (ADHD), usually diagnosed in children, may show up for the first time in adulthood, two recent studies suggest. And not only can ADHD appear for the first time after childhood, but the symptoms for adult-onset ADHD may be different from symptoms experienced by kids, the researchers found. “Although the nature of symptoms differs somewhat between children and adults, all age groups show impairments in multiple domains – school, family and friendships for kids and school, occupation, marriage and driving for adults,” said Stephen Faraone, a psychiatry researcher at SUNY Upstate Medical University in Syracuse, New York and author of an editorial accompanying the two studies in JAMA Psychiatry. Faraone cautions, however, that some newly diagnosed adults might have had undetected ADHD as children. Support from parents and teachers or high intelligence, for example, might prevent ADHD symptoms from emerging earlier in life. It’s not clear whether study participants “were completely free of psychopathology prior to adulthood,” Faraone said in an email. One of the studies, from Brazil, tracked more than 5,200 people born in 1993 until they were 18 or 19 years old. © 2016 Scientific American
by Helen Thompson In hunting down delicious fish, Flipper may have a secret weapon: snot. Dolphins emit a series of quick, high-frequency sounds — probably by forcing air over tissues in the nasal passage — to find and track potential prey. “It’s kind of like making a raspberry,” says Aaron Thode of the Scripps Institution of Oceanography in San Diego. Thode and colleagues tweaked a human speech modeling technique to reproduce dolphin sounds and discern the intricacies of their unique style of sound production. He presented the results on May 24 in Salt Lake City at the annual meeting of the Acoustical Society of America. Dolphin chirps have two parts: a thump and a ring. Their model worked on the assumption that lumps of tissue bumping together produce the thump, and those tissues pulling apart produce the ring. But to match the high frequencies of live bottlenose dolphins, the researchers had to make the surfaces of those tissues sticky. That suggests that mucus lining the nasal passage tissue is crucial to dolphin sonar. The vocal model also successfully mimicked whistling noises used to communicate with other dolphins and faulty clicks that probably result from inadequate snot. Such techniques could be adapted to study sound production or echolocation in sperm whales and other dolphin relatives. © Society for Science & the Public 2000 - 2016.
Link ID: 22244 - Posted: 05.25.2016
By Ian Randall As if you needed another reason to hate the gym, it now turns out that exercise can exhaust not only your muscles, but also your eyes. Fear not, however, for coffee can perk them right up again. During strenuous exercise, our muscles tire as they run out of fuel and build up waste products. Muscle performance can also be affected by a phenomenon called “central fatigue,” in which an imbalance in the body’s chemical messengers prevents the central nervous system from directing muscle movements effectively. It was not known, however, whether central fatigue might also affect motor systems not directly involved in the exercise itself—such as those that move the eyes. To find out, researchers gave 11 volunteers a carbohydrate solution either with a moderate dose of caffeine—which is known to stimulate the central nervous system—or as a placebo without, during 3 hours of vigorous cycling. After exercising, the scientists tested the cyclists with eye-tracking cameras to see how well their brains could still control their visual system. The team found that exercise reduced the speed of rapid eye movements by about 8%, impeding their ability to capture new visual information. The caffeine—the equivalent of two strong cups of coffee—was sufficient to counteract this effect, with some cyclists even displaying increased eye movement speeds, the team reports today in Scientific Reports. So it might be a good idea to get someone else to drive you home after that marathon. © 2016 American Association for the Advancement of Science.
Link ID: 22243 - Posted: 05.25.2016
By Diana Kwon More than one in 10 Americans older than 12 takes antidepressants, according to a 2011 report by the National Center for Health Statistics. A significant but unknown number of children younger than 12 take them, too. Although most such drugs are not approved for young children, doctors have prescribed them off-label for years because they have been thought to have relatively mild side effects. Yet recent reports have revealed that important data about the safety of these drugs—especially their risks for children and adolescents—have been withheld from the medical community and the public. In the latest and most comprehensive analysis, published in January in the BMJ, researchers at the Nordic Cochrane Center in Copenhagen showed that pharmaceutical companies have not been revealing the full extent of serious harm in clinical study reports, which are detailed documents sent to regulatory authorities such as the U.S. Food and Drug Administration and the European Medicines Agency (EMA) when applying for approval of a new drug. The researchers examined reports from 70 double-blind, placebo-controlled trials of two common categories of antidepressants—selective serotonin reuptake inhibitors (SSRIs) and serotonin and norepinephrine reuptake inhibitors (SNRIs)—and found that the occurrence of suicidal thoughts and aggressive behavior doubled in children and adolescents who used these drugs. The investigators discovered that some of the most revealing information was buried in appendices where individual patient outcomes are listed. For example, they found clear instances of suicidal thinking that had been passed off as “emotional lability” or “worsening depression” in the report itself. This information, however, was available for only 32 out of the 70 trials. “We found that a lot of the appendices were often only available on request to the authorities, and the authorities had never requested them,” says Tarang Sharma, a Ph.D. student at Cochrane and lead author of the study. “I'm actually kind of scared about how bad the actual situation would be if we had the complete data.” © 2016 Scientific American
By JOHN BRANCH When the N.F.L. agreed in 2012 to donate tens of millions of dollars to concussion research overseen by the National Institutes of Health, it was widely seen as a positive turning point in football’s long history of playing down the long-term effects of brain injuries on players. At the time, the league said that it would have no influence over how the money was used. But the league and its head, neck and spine committee worked to improperly influence the government research, trying to steer the study toward a doctor with ties to the league, according to a study conducted by a congressional committee and released on Monday. “Our investigation has shown that while the N.F.L. had been publicly proclaiming its role as funder and accelerator of important research, it was privately attempting to influence that research,” the study concluded. “The N.F.L. attempted to use its ‘unrestricted gift’ as leverage to steer funding away from one of its critics.” The N.F.L., in a statement, said it rejected the accusations laid out in the study, which was conducted by Democratic members of the House Committee on Energy and Commerce. “There is no dispute that there were concerns raised about both the nature of the study in question and possible conflicts of interest,” the league said. “These concerns were raised for review and consideration through the appropriate channels.” It is the latest in a long history of instances in which the N.F.L. has been found to mismanage concussion research, dating to the league’s first exploration of the crisis when it used deeply flawed data to produce a series of studies. In this case, some of the characters are the same, including Dr. Elliot Pellman, who led the league’s concussion committee for years before he was discredited for his questionable credentials and his role as a longtime denier of the effects of concussions on players. © 2016 The New York Times Company
Keyword: Brain Injury/Concussion
Link ID: 22241 - Posted: 05.24.2016