Most Recent Links

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Featured Article

'Language Gene' Has a Partner

Few genes have made the headlines as much as FOXP2. The first gene associated with language disorders , it was later implicated in the evolution of human speech. Girls make more of the FOXP2 protein, which may help explain their precociousness in learning to talk. Now, neuroscientists have figured out how one of its molecular partners helps Foxp2 exert its effects.

The findings may eventually lead to new therapies for inherited speech disorders, says Richard Huganir, the neurobiologist at Johns Hopkins University School of Medicine in Baltimore, Maryland, who led the work. Foxp2 controls the activity of a gene called Srpx2, he notes, which helps some of the brain's nerve cells beef up their connections to other nerve cells. By establishing what SRPX2 does, researchers can look for defective copies of it in people suffering from problems talking or learning to talk.

Until 2001, scientists were not sure how genes influenced language. Then Simon Fisher, a neurogeneticist now at the Max Planck Institute for Psycholinguistics in Nijmegen, the Netherlands, and his colleagues fingered FOXP2 as the culprit in a family with several members who had trouble with pronunciation, putting words together, and understanding speech. These people cannot move their tongue and lips precisely enough to talk clearly, so even family members often can?t figure out what they are saying. It “opened a molecular window on the neural basis of speech and language,” Fisher says.

Photo credit: Yoichi Araki, Ph.D.


Links 1 - 20 of 22025

By Daniel Engber In the spring of 2013, a 63-year-old social psychologist in Wurzburg, Germany, made a bold suggestion in a private email chain. For months, several dozen of his colleagues had been squabbling over how to double-check the scientific literature on “social priming,” the idea that even very subtle cues—the height of a chair, the temperature of a cup of coffee, the color of a printed word—can influence someone’s behavior or judgment. Now the skeptics in the group wanted volunteers: Who among the priming experts and believers would help them with a large-scale replication effort, in which a major finding would be tested in many different labs at once? Who—if anyone—would agree to put his research to this daunting test? The experts were reluctant to step forward. In recent months their field had fallen into scandal and uncertainty: An influential scholar had been outed as a fraud; certain bedrock studies—even so-called “instant classics”—had seemed to shrivel under scrutiny. But the rigidity of the replication process felt a bit like bullying. After all, their work on social priming was delicate by definition: It relied on lab manipulations that had been precisely calibrated to elicit tiny changes in behavior. Even slight adjustments to their setups, or small mistakes made by those with less experience, could set the data all askew. So let’s say another lab—or several other labs—tried and failed to copy their experiments. What would that really prove? Would it lead anyone to change their minds about the science?

Keyword: Emotions
Link ID: 22609 - Posted: 08.29.2016

Doctors describe 16-year-old Sebastian DeLeon as a walking miracle — he is only the fourth person in the U.S. to survive an infection from the so-called brain-eating amoeba. Infection from Naegleria fowleri is extremely rare but almost always fatal. Between 1962 and 2015, there were only 138 known infections due to the organism, according to the Centers for Disease Control and Prevention. Just three people survived. This summer, two young people, one in Florida and one in North Carolina, became infected after water recreation. Only one had a happy ending. DeLeon is a 16-year-old camp counselor. The Florida Department of Health thinks he got the infection while swimming in unsanitary water on private property in South Florida before his family came to visit Orlando's theme parks. So many things had to go right for DeLeon to survive. On a Friday, he had a bad headache. The next day, his parents decided this was way more than just a migraine and took him to the emergency room at Florida Hospital for Children. Doctors persuaded the family to do a spinal tap to rule out meningitis, even though he didn't have a stiff neck, the telltale symptom. Sheila Black, the lab coordinator, looked at the sample and assumed she saw white blood cells. But then she took a second, longer look. "We are all detectives," Black said. "We literally had to look at this and study it for a while and watch for the movement because the amoeba can look like a white cell. So unless you're actually visually looking for this and looking for the movement, you're going to miss it." © 2016 npr

Keyword: Miscellaneous
Link ID: 22608 - Posted: 08.29.2016

By KATE MURPHY We’ve all seen them, those colorful images that show how our brains “light up” when we’re in love, playing a video game, craving chocolate, etc. Created using functional magnetic resonance imaging, or fM.R.I., these pictures are the basis of tens of thousands of scientific papers, the backdrop to TED talks and supporting evidence in best-selling books that tell us how to maintain healthy relationships, make decisions, market products and lose weight. But a study published last month in the Proceedings of the National Academy of Sciences uncovered flaws in the software researchers rely on to analyze fM.R.I. data. The glitch can cause false positives — suggesting brain activity where there is none — up to 70 percent of the time. This cued a chorus of “I told you so!” from critics who have long said fM.R.I. is nothing more than high-tech phrenology. Brain-imaging researchers protested that the software problems were not as bad nor as widespread as the study suggested. The dust-up has caused considerable angst in the fM.R.I. community, about not only the reliability of their pretty pictures but also how limited funding and the pressure to publish splashy results might have allowed such a mistake to go unnoticed for so long. The remedial measures some in the field are now proposing could be a model for the wider scientific community, which, despite breathtaking technological advances, often produces findings that don’t hold up over time. “We have entered an era where the kinds of data and the analyses that people run have gotten incredibly complicated,” said Martin Sereno, the chairman of the cognitive neuroimaging department at the University of California, San Diego. “So you have researchers using sophisticated software programs that they probably don’t understand but are generally accepted and everyone uses.” © 2016 The New York Times Company

Keyword: Brain imaging
Link ID: 22607 - Posted: 08.29.2016

By Usha Lee McFarling @ushamcfarling LOS ANGELES — A team of physicians and neuroscientists on Wednesday reported the successful use of ultrasound waves to “jump start” the brain of a 25-year-old man recovering from coma — and plan to launch a much broader test of the technique, in hopes of finding a way to help at least some of the tens of thousands of patients in vegetative states. The team, based at the University of California, Los Angeles, cautions that the evidence so far is thin: They have no way to know for sure whether the ultrasound stimulation made the difference for their young patient, or whether he spontaneously recovered by coincidence shortly after the therapy. But the region of the brain they targeted with the ultrasound — the thalamus — has previously been shown to be important in restoring consciousness. In 2007, a 38-year-old man who had been minimally conscious for six years regained some functions after electrodes were implanted in his brain to stimulate the thalamus. The ultrasound technique is a “good idea” that merits further study, said Dr. Nicholas Schiff, a pioneer in the field of using brain stimulation to restore consciousness who conducted the 2007 study. “It’s intriguing and it’s an interesting possibility,” said Schiff, a neuroscientist at Weill Cornell Medicine. The UCLA procedure used an experimental device, about the size of a teacup saucer, to focus ultrasonic waves on the thalamus, two walnut-sized bulbs in the center of the brain that serve as a critical hub for information flow and help regulate consciousness and sleep.

Keyword: Consciousness
Link ID: 22606 - Posted: 08.27.2016

Laura Sanders Scientists have identified the “refrigerator” nerve cells that hum along in the brains of mice and keep the body cool. These cells kick on to drastically cool mice’s bodies and may prevent high fevers, scientists report online August 25 in Science. The results “are totally new and very important,” says physiologist Andrej Romanovsky of the Barrow Neurological Institute in Phoenix. "The implications are far-reaching." By illuminating how bodies stay at the right temperature, the discovery may offer insights into the relationship between body temperature and metabolism. Scientists had good reasons to think that nerve cells controlling body temperature are tucked into the hypothalamus, a small patch of neural tissue in the middle of the brain. Temperature fluctuations in a part of the hypothalamus called the preoptic area prompt the body to get back to baseline by conserving or throwing off heat. But the actual identify of the heat sensors remained mysterious. The new study reveals the cells to be those that possess a protein called TRPM2. “Overall, this is a major discovery in the field of thermoregulation,” says Shaun Morrison of Oregon Health & Science University in Portland. Jan Siemens, a neurobiologist at the University of Heidelberg in Germany, and colleagues tested an array of molecules called TRP channels, proteins that sit on cell membranes and help sense a variety of stimuli, including painful tear gas and cool menthol. In tests of nerve cells in lab dishes, one candidate, the protein TRPM2, seemed to respond to heat. |© Society for Science & the Public 2000 - 201

Keyword: Pain & Touch
Link ID: 22605 - Posted: 08.27.2016

By Amy Ellis Nutt Before iPhones and thumb drives, before Google docs and gigabytes of RAM, memory was more art than artifact. It wasn’t a tool or a byproduct of being human. It was essential to our character and therefore a powerful theme in both myth and literature. At the end of Book 2 of the “Divine Comedy,” with Paradise nearly in reach, Dante is dipped into the River Lethe, where the sins of the self are washed away in the waters of forgetfulness. To be truly cleansed of his memories, however, Dante must also drink from the river of oblivion. Only then will he be truly purified and the memories of his good deeds restored to him. Before we can truly remember, according to Dante, we must forget. In “Patient H.M.: A Story of Memory, Madness, and Family Secrets,” author Luke Dittrich seems to be saying that before we can forgive, we must remember. The terrible irony is that H.M., the real-life character around whom Dittrich’s book revolves, had no memory at all. In prose both elegant and intimate, and often thrilling, “Patient H.M.” is an important book about the wages not of sin but of science. It is deeply reported and surprisingly emotional, at times poignant, at others shocking. H.M., arguably the single most important research subject in the history of neuroscience, was once Henry Molaison, an ordinary New England boy. When Henry was 9 years old, he was hit by a bicyclist as he walked across the street in his home town, Hartford, Conn. © 1996-2016 The Washington Post

Keyword: Learning & Memory
Link ID: 22604 - Posted: 08.27.2016

By Kas Roussy, In a room at Sunnybrook Health Sciences Centre in Toronto, Brian Smith gives one last hug to his wife, Noreen. "You're doing really well, sweetheart," he says to her. Doctors have finished prepping the 76-year-old patient. She's clad in a blue hospital gown, her head has been shaved and metallic headgear is attached to her skull. Google's latest a spoon that steadies tremors New technology could help seniors stay independent longer She's ready to be wheeled into an MRI room, where she'll undergo a procedure that her doctors believe will revolutionize the way brain diseases are treated. Before that happens, Noreen leans into her husband for a kiss. "Best buddy," she whispers. Noreen Smith is among the three per cent of the Canadian population who suffer from a nervous system disorder called essential tremor. It causes uncontrollable shaking, most often in a person's hands. Smith noticed the first signs when she was 33. "It started developing in my dominant hand, which is my right hand," she said the day before her medical procedure from her home in Bobcaygeon, Ont. She went to a specialist who delivered the diagnosis: essential tremor. Media placeholder Smith ‘really, really excited’ about treatment’s potential0:48 Just as shocking was what he said next, alluding to a high-profile actor who had the condition. "This particular person wasn't terribly helpful because he said: 'Do you happen to know Katharine Hepburn? I'm going to give you some medication, and you can go home and get used to the idea that eventually you're going to end up looking like Katharine Hepburn.' I was devastated," says Smith. Medication helped for the first few years. But Smith's tremor was still severe and like others who suffer from this disorder, the shaking worsened with simple movements or everyday tasks like applying makeup or pouring a glass of water. ©2016 CBC/Radio-Canada.

Keyword: Movement Disorders
Link ID: 22603 - Posted: 08.25.2016

By Christie Aschwanden The Olympic stadium was quiet on Wednesday morning, and spectators in the sparsely filled stands seemed to pay little notice to South African runner Caster Semenya as she cruised to an easy win in her first-round heat of the 800 meters. But on Saturday evening, when Semenya will contest the 800-meter final, she’ll have the world’s eyes on her. “There is no more certain gold medal in the Rio Olympics than Semenya,” wrote Ross Tucker, an exercise scientist in South Africa, on his blog, The Science of Sport. “She could trip and fall, anywhere in the first lap, lose 20m, and still win the race.” If she does indeed dominate, some sports fans will be cheering Semenya, while others will be less inclined to celebrate, believing that she has an unfair advantage over her rivals. Semenya made headlines in 2009 amid rumors that track’s governing body, the International Association of Athletics Federations, had required her to undergo tests to confirm that she was female. Media accounts have reported that she has hyperandrogenism, a condition that causes higher-than-average testosterone levels — an allegation that neither Semenya nor the IAAF has publicly confirmed. Semenya’s case is the latest saga in sport’s checkered history of sex testing, a task that is purportedly aimed at creating an even playing field but — as I’ve discussed previously — raises serious questions about how athletics organizations treat women. Her muscular build, deep voice and remarkable results had raised suspicions among some of Semenya’s rivals about whether she was really a woman. “Just look at her,” said Mariya Savinova, a Russian runner now tangled in her country’s doping scandal.

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 22601 - Posted: 08.25.2016

By Sara Chodosh When a single neuron fires, it is an isolated chemical blip. When many fire together, they form a thought. How the brain bridges the gap between these two tiers of neural activity remains a great mystery, but a new kind of technology is edging us closer to solving it. The glowing splash of cyan in the photo above comes from a type of biosensor that can detect the release of very small amounts of neurotransmitters, the signaling molecules that brain cells use to communicate. These sensors, called CNiFERs (pronounced “sniffers”), for cell-based neurotransmitter fluorescent engineered reporters, are enabling scientists to examine the brain in action and up close. This newfound ability, developed as part of the White House BRAIN Initiative, could further our understanding of how brain function arises from the complex interplay of individual neurons, including how complex behaviors like addiction develop. Neuroscientist Paul Slesinger at Icahn School of Medicine at Mount Sinai, one of the senior researchers who spearheaded this research, presented the sensors Monday at the American Chemical Society’s 252nd National Meeting & Exposition. Current technologies have proved either too broad or too specific to track how tiny amounts of neurotransmitters in and around many cells might contribute to the transmission of a thought. Scientists have used functional magnetic resonance imaging to look at blood flow as a surrogate for brain activity over fairly long periods of time or have employed tracers to follow the release of a particular neurotransmitter from a small set of neurons for a few seconds. But CNiFERs make for a happy medium; they allow researchers to monitor multiple neurotransmitters in many cells over significant periods of time. © 2016 Scientific American

Keyword: Brain imaging
Link ID: 22600 - Posted: 08.25.2016

James Hamblin Like ​The Atlantic? Subscribe to ​the Daily​, our free weekday email newsletter. Elite tennis players have an uncanny ability to clear their heads after making errors. They constantly move on and start fresh for the next point. They can’t afford to dwell on mistakes. Peter Strick is not a professional tennis player. He’s a distinguished professor and chair of the department of neurobiology at the University of Pittsburgh Brain Institute. He’s the sort of person to dwell on mistakes, however small. “My kids would tell me, dad, you ought to take up pilates. Do some yoga,” he said. “But I’d say, as far as I’m concerned, there's no scientific evidence that this is going to help me.” Still, the meticulous skeptic espoused more of a tennis approach to dealing with stressful situations: Just teach yourself to move on. Of course there is evidence that ties practicing yoga to good health, but not the sort that convinced Strick. Studies show correlations between the two, but he needed a physiological mechanism to explain the relationship. Vague conjecture that yoga “decreases stress” wasn’t sufficient. How? Simply by distracting the mind? The stress response in humans is facilitated by the adrenal glands, which sit on top of our kidneys and spit adrenaline into our blood whenever we’re in need of fight or flight. That stress response is crucial in dire circumstances. But little of modern life truly requires it (especially among academic scientists). Most of the time, our stress responses are operating as a sort of background hum, keeping us on edge. Turn that off, and we relax. © 2016 by The Atlantic Monthly Group

Keyword: Stress
Link ID: 22599 - Posted: 08.25.2016

By Alice Callahan As new parents, Penn State researcher Doug Teti and his wife were co-sleepers, sharing their bed at night with all three of their children, now grown. So when Dr. Teti, a professor of human development and family studies, embarked on an usual study of co-sleeping, bringing cameras into the bedrooms of 139 Pennsylvania couples, he did not expect to see co-sleeping associated with family stress. But to his surprise, many of the parents in the study who co-slept with their children beyond 6 months of age, a group he called “persistent co-sleepers,” did show signs of stress, particularly the mothers. Dr. Teti emphasized that the research isn’t an indictment against co-sleeping, but does suggest that a number of factors, including cultural pressures and an unsupportive spouse, can make longer-term co-sleeping a more stressful experience for some families. “Co-sleeping is simply a practice, just like solitary sleep is a practice,” he said. “It is important for parents to be on the same page about whatever practices with their children they choose to put into effect.” The study, published this month in the journal Developmental Psychology, was unusual in that it tracked 139 couples, mostly married or living together, who generously allowed researchers to peek into their bedrooms with video cameras, recording nighttime interactions with their new babies at five time points in the first year of life. Co-sleeping — defined in this study as room-sharing or bed-sharing, often a mix of the two — was surprisingly common in early infancy. Nearly 75 percent of the parents co-slept with infants early on, and about half were still co-sleeping three months after the birth. But once the babies reached 6 months of age, only one in four babies continued to share a bed or a room with their parents. © 2016 The New York Times Company

Keyword: Sleep
Link ID: 22598 - Posted: 08.25.2016

Laura Sanders Brain scientists Eric Jonas and Konrad Kording had grown skeptical. They weren’t convinced that the sophisticated, big data experiments of neuroscience were actually accomplishing anything. So they devised a devilish experiment. Instead of studying the brain of a person, or a mouse, or even a lowly worm, the two used advanced neuroscience methods to scrutinize the inner workings of another information processor — a computer chip. The unorthodox experimental subject, the MOS 6502, is the same chip that dazzled early tech junkies and kids alike in the 1980s by powering Donkey Kong, Space Invaders and Pitfall, as well as the Apple I and II computers. Of course, these experiments were rigged. The scientists already knew everything about how the 6502 works. “The beauty of the microprocessor is that unlike anything in biology, we understand it on every level,” says Jonas, of the University of California, Berkeley. A barrel-hurling gorilla is the enemy in Donkey Kong, a video game powered by the MOS 6502 microprocessor. Along with Space Invaders and Pitfall, this game served as the “behavior” in a recent experiment. Using a simulation of MOS 6502, Jonas and Kording, of Northwestern University in Chicago, studied the behavior of electricity-moving transistors, along with aspects of the chip’s connections and its output, to reveal how it handles information. Since they already knew what the outcomes should be, they were actually testing the methods. By the end of their experiments, Jonas and Kording had discovered almost nothing. |© Society for Science & the Public 2000 - 2016

Keyword: Brain imaging
Link ID: 22597 - Posted: 08.24.2016

Neuroscience News Researchers have identified a brain mechanism that could be a drug target to help prevent tolerance and addiction to opioid pain medication, such as morphine, according to a study by Georgia State University and Emory University. The findings, published in the Nature journal Neuropsychopharmacology in August, show for the first time that morphine tolerance is due to an inflammatory response produced in the brain. This brain inflammation is caused by the release of cytokines, chemical messengers in the body that trigger an immune response, similar to a viral infection. Researchers’ results show blocking a particular cytokine eliminated morphine tolerance, and they were able to reduce the dose of morphine required to alleviate pain by half. “These results have important clinical implications for the treatment of pain and also addiction,” said Lori Eidson, lead author and a graduate student in the laboratory of Dr. Anne Murphy in the Neuroscience Institute of Georgia State. “Until now, the precise underlying mechanism for opioid tolerance and its prevention have remained unknown.” Over 67 percent of the United States population will experience chronic pain at some point in their lives. Morphine is the primary drug used to manage severe and chronic pain, with 3 to 4 percent of adults in the U.S. receiving long-term opioid therapy. However, tolerance to morphine, defined as a decrease in pain relief over time, significantly impedes treatment for about 60 percent of patients. Long-term treatment with opioids is associated with increased risk of abuse, dependence and fatal overdoses.

Keyword: Drug Abuse; Pain & Touch
Link ID: 22596 - Posted: 08.24.2016

Nicola Davis Children who suffer a traumatic brain injury, including mild concussion from a blow to the head, are less likely to do well at school and are at increased risk of early death, researchers have revealed. As adults they are also more likely to receive a disability pension, have failed to gain secondary school qualifications and nearly twice as likely to have been hospitalised for psychiatric reasons. The team analysed data from more than a million people born between 1973 and 1985, finding that around 9% had been diagnosed with at least one traumatic brain injury before the age of 25. More than 75% of these were mild injuries. The researchers compared the outcomes for these individuals with those of others who had not experienced a head injury, as well as carrying out a second comparison, where possible, with siblings who had not been injured. Once factors such as age and sex were taken into account, the team found that those diagnosed with a traumatic brain injury have an increased risk of experiencing a number of health and social problems. Those who had suffered a traumatic brain injury were 76% more likely to receive a disability pension, 58% more likely to have failed to gain secondary school qualifications and nearly twice as likely to have been hospitalised for psychiatric reasons, compared to those who had sustained no injury. When the researchers looked at patients who had siblings that had not sustained a traumatic brain injury, they found similar - although smaller - effects, suggesting that genetics could also play a role. © 2016 Guardian News and Media Limited

Keyword: Brain Injury/Concussion; Development of the Brain
Link ID: 22595 - Posted: 08.24.2016

By PAM BELLUCK The images tell a heartbreaking story: Zika’s calamitous attack on the brains of babies — as seen from the inside. A study of brain scans and ultrasound pictures of 45 Brazilian babies whose mothers were infected with Zika in pregnancy shows that the virus can inflict serious damage to many different parts of the fetal brain beyond microcephaly, the condition of unusually small heads that has become the sinister signature of Zika. The images, published Tuesday in the journal Radiology, also suggest a grim possibility: Because some of the damage was seen in brain areas that continue to develop after birth, it may be that babies born without obvious impairment will experience problems as they grow. “It really brings to the forefront the importance of truly understanding the impact of Zika virus and the fact that we need to follow children who not only are exposed to Zika in pregnancy, but even those who don’t appear to have any complications at birth,” said Dr. Catherine Y. Spong, chief of the pregnancy and perinatology branch of the Eunice Kennedy Shriver National Institute of Child Health and Human Development, who was not involved in the study. Most of the babies in the study were born with microcephaly, although three were not. Each also suffered other impairments, almost all of which emerge earlier than microcephaly because a smaller head is really a consequence of brain that has failed to develop fully or has been damaged along the way, experts said. “The brain that should be there is not there,” said Dr. Deborah Levine, an author of the study and a professor of radiology at Harvard Medical School in Boston. “The abnormalities that we see in the brain suggest a very early disruption of the brain development process.” © 2016 The New York Times Company

Keyword: Development of the Brain
Link ID: 22594 - Posted: 08.24.2016

Ian Sample Science editor For Jules Verne it was the friend who keeps us waiting. For Edgar Allan Poe so many little slices of death. But though the reason we spend a third of our lives asleep has so far resisted scientific explanation, research into the impact of sleepless nights on brain function has shed fresh light on the mystery - and also offered intriguing clues to potential treatments for depression. In a study published on Tuesday, researchers show for the first time that sleep resets the steady build-up of connectivity in the human brain which takes place in our waking hours. The process appears to be crucial for our brains to remember and learn so we can adapt to the world around us. The loss of a single night’s sleep was enough to block the brain’s natural reset mechanism, the scientists found. Deprived of rest, the brain’s neurons seemingly became over-connected and so muddled with electrical activity that new memories could not be properly laid down. Lack of sleep alters brain chemicals to bring on cannabis-style 'munchies' But Christoph Nissen, a psychiatrist who led the study at the University of Freiburg, is also excited about the potential for helping people with mental health disorders. One radical treatment for major depression is therapeutic sleep deprivation, which Nissen believes works through changing the patient’s brain connectivity. The new research offers a deeper understanding of the phenomenon which could be adapted to produce more practical treatments. © 2016 Guardian News and Media Limited

Keyword: Sleep; Learning & Memory
Link ID: 22593 - Posted: 08.24.2016

by Laura Sanders When someone uses the phrase “sleeping like a baby,” it’s obvious that they don’t really know how babies sleep. Many babies, especially newborns, are lousy sleepers, waking up every few hours to rustle around, cry and eat. For creatures who sleep up to 18 hours per 24-hour period, newborns are exhausting. That means that bone-tired parents are often desperate to get their babies to sleep so they can rest too. A study published in the September Pediatrics captured this nightly struggle in the homes of 162 Pennsylvanian families. And the results revealed something disturbing: Despite knowing that they were being videotaped, many parents didn’t put their babies into a safe sleeping spot. The risk of sleep-related infant deaths, including those caused by strangulation or sudden infant death syndrome, goes up when babies are put in unsafe sleeping positions or near suffocation hazards. Babies should be on their back on a firm mattress free of any objects. But that wasn’t the case for the majority of babies in the study, says Ian Paul, a pediatrician at Penn State. As a parent to three, Paul is sympathetic to the difficulties of soothing babies to sleep. “The first few months are really exhausting,” he says. But as a pediatrician, he also sees the risks of ignoring safe sleep guidelines. “Parents need to realize that these risks are real and might happen to them.” The videos taken for the study revealed that at 1 month of age, nearly all of the babies were put onto a sleep surface that had a loose or ill-advised item. |© Society for Science & the Public 2000 - 2016

Keyword: Sleep; Development of the Brain
Link ID: 22592 - Posted: 08.24.2016

By Roni Caryn Rabin We’ve all heard about the power of positive thinking. But will it help me sleep? My problem isn’t falling asleep – it’s staying asleep. This particular form of torture has been dubbed “sleep-maintenance” insomnia. Call me a high-functioning sufferer: I’m usually O.K. once I’ve had my morning coffee. But I worry about the long-term health ramifications of losing sleep. Now several medical organizations have endorsed a treatment known as cognitive behavioral therapy for insomnia or C.B.T.-I. In May the American College of Physicians advised its members that C.B.T.-I. was the first treatment they should offer patients with insomnia. I wanted to try it, but there is a shortage of trained therapists with expertise in C.B.T.-I. I didn’t want to wait for an appointment; I just wanted to solve the problem. So I decided to try an online sleep program. Convincing data that internet-based programs are effective is piling up, and a recent review of clinical trials reported that insomniacs improved their sleep as much after online C.B.T.-I. programs as they did after face-to-face C.B.T.-I. counseling. Internet programs are likely to be cheaper than most therapists, too. I downloaded a five-week course called Conquering Insomnia for $40. Another online C.B.T. program called SHUTi charges $135 for 16 weeks of access to a program, which includes a series of six sessions and follow-up for 10 weeks. Both programs provide individualized feedback on your weekly sleep logs. The developers of these programs say they want them to be accessible to as many people as possible. One in 10 people suffer from insomnia. “The number of clinicians nationally who know how to do C.B.T. for insomnia is a couple of thousand. We need 100,000,” said Dr. Gregg Jacobs, a sleep medicine specialist and assistant professor of psychiatry at the University of Massachusetts Medical School who developed the Conquering Insomnia program. “There are tens of millions of people out there who have insomnia.” © 2016 The New York Times Company

Keyword: Sleep
Link ID: 22591 - Posted: 08.24.2016

By NICHOLAS ST. FLEUR Neuroscientists have developed a way to turn an entire mouse, including its muscles and internal organs, transparent while illuminating the nerve paths that run throughout its body. The process, called uDisco, provides an alternate way for researchers to study an organism’s nervous system without having to slice into sections of its organs or tissues. It allows researchers to use a microscope to trace neurons from the rodent’s brain and spinal cord all the way to its fingers and toes. “When I saw images on the microscope that my students were obtaining, I was like ‘Wow, this is mind blowing,’” said Ali Ertürk, a neuroscientist from the Ludwig Maximilians University of Munich in Germany and an author of the paper. “We can map the neural connectivity in the whole mouse in 3D.” They published their technique Monday in the journal Nature Methods. So far, the technique has been conducted only in mice and rats, but the scientists think it could one day be used to map the human brain. They also said it could be particularly useful for studying the effects of mental disorders like Alzheimer’s disease or schizophrenia. Dr. Ertürk and his colleagues study neurodegenerative disorders, and are particularly interested in diseases that occur from traumatic brain injuries. Researchers often study these diseases by examining thin slices of brain tissue under a microscope. “That is not a good way to study neurons because if you slice the brain, you slice the network,” Dr. Ertürk said. “The best way to look at it is to look at the entire organism, not only the brain lesion but beyond that. We need to see the whole picture.” To do this, Dr. Ertürk and his team developed a two-step process that renders a rodent transparent while keeping its internal organs structurally sound. The mice they used were dead and had been tagged with a special fluorescent protein to make specific parts of their anatomy glow. © 2016 The New York Times Company

Keyword: Brain imaging
Link ID: 22590 - Posted: 08.23.2016

Scientists and clinicians have long dreamed of helping the injured brain repair itself by creating new neurons, and an innovative NIH-funded study published today in Nature Medicine may bring this goal much closer to reality. A team of researchers has developed a therapeutic technique that dramatically increases the production of nerve cells in mice with stroke-induced brain damage. The therapy relies on the combination of two methods that show promise as treatments for stroke-induced neurological injury. The first consists of surgically grafting human neural stem cells into the damaged area, where they mature into neurons and other brain cells. The second involves administering a compound called 3K3A-APC, which the scientists have shown helps neural stem cells grown in a petri dish develop into neurons. However, it was unclear what effect the molecule, derived from a human protein called activated protein-C (APC), would have in live animals. A month after their strokes, mice that had received both the stem cells and 3K3A-APC performed significantly better on tests of motor and sensory functions compared to mice that received neither or only one of the treatments. In addition, many more of the stem cells survived and matured into neurons in the mice given 3K3A-APC. “This USC-led animal study could pave the way for a potential breakthrough in how we treat people who have experienced a stroke,” added Jim Koenig, Ph.D., a program director at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS), which funded the research. “If the therapy works in humans, it could markedly accelerate the recovery of these patients.”

Keyword: Stroke; Stem Cells
Link ID: 22589 - Posted: 08.23.2016