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'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 20157

Nicholette Zeliadt, One afternoon in October 2012, a communication therapist from Manchester visited the home of Laura and her three children. Laura sat down at a small white table in a dimly lit room to feed her 10-month-old daughter, Bethany, while the therapist set up a video camera to record the pair’s every movement. (Names of research participants have been changed to protect privacy.) Bethany sat quietly in her high chair, nibbling on macaroni and cheese. She picked up a slimy noodle with her tiny fingers, looked up at Laura and thrust out her hand. “Oh, Mommy’s going to have some, yum,” Laura said. “Clever girl!” Bethany beamed a toothy grin at her mother and let out a brief squeal of laughter, and then turned her head to peer out the window as a bus rumbled by. “Oh, you can hear the bus,” Laura said. “Can you say ‘bus?’” “Bah!” Bethany exclaimed. “Yeah, bus!” Laura said. This ordinary domestic moment, immortalized in the video, is part of the first rigorous test of a longstanding idea: that the everyday interactions between caregiver and child can shape the course of autism1. The dynamic exchanges with a caregiver are a crucial part of any child’s development. As Bethany and her mother chatter away, responding to each other’s glances and comments, for example, the little girl is learning how to combine gestures and words to communicate her thoughts. In a child with autism, however, this ‘social feedback loop’ might go awry. An infant who avoids making eye contact, pays little attention to faces and doesn’t respond to his or her name gives parents few opportunities to engage. The resulting lack of social interaction may reinforce the baby’s withdrawal, funneling into a negative feedback loop that intensifies mild symptoms into a full-blown disorder. © 2015 Guardian News and Media Limited

Keyword: Autism
Link ID: 20733 - Posted: 03.30.2015

|By Roni Jacobson As intangible as they may seem, memories have a firm biological basis. According to textbook neuroscience, they form when neighboring brain cells send chemical communications across the synapses, or junctions, that connect them. Each time a memory is recalled, the connection is reactivated and strengthened. The idea that synapses store memories has dominated neuroscience for more than a century, but a new study by scientists at the University of California, Los Angeles, may fundamentally upend it: instead memories may reside inside brain cells. If supported, the work could have major implications for the treatment of post-traumatic stress disorder (PTSD), a condition marked by painfully vivid and intrusive memories. More than a decade ago scientists began investigating the drug propranolol for the treatment of PTSD. Propranolol was thought to prevent memories from forming by blocking production of proteins required for long-term storage. Unfortunately, the research quickly hit a snag. Unless administered immediately after the traumatic event, the treatment was ineffective. Lately researchers have been crafting a work-around: evidence suggests that when someone recalls a memory, the reactivated connection is not only strengthened but becomes temporarily susceptible to change, a process called memory reconsolidation. Administering propranolol (and perhaps also therapy, electrical stimulation and certain other drugs) during this window can enable scientists to block reconsolidation, wiping out the synapse on the spot. The possibility of purging recollections caught the eye of David Glanzman, a neurobiologist at U.C.L.A., who set out to study the process in Aplysia, a sluglike mollusk commonly used in neuroscience research. Glanzman and his team zapped Aplysia with mild electric shocks, creating a memory of the event expressed as new synapses in the brain. The scientists then transferred neurons from the mollusk into a petri dish and chemically triggered the memory of the shocks in them, quickly followed by a dose of propranolol. © 2015 Scientific American

Keyword: Learning & Memory; Stress
Link ID: 20732 - Posted: 03.30.2015

By Victoria Gill Science reporter, BBC News Researchers in Denmark have revealed how porpoises finely adjust the beams of sound they use to hunt. The animals hunt with clicks and buzzes - detecting the echoes from their prey. This study showed them switching from a narrow to a wide beam of sound - "like adjusting a flashlight" - as they homed in on a fish. Researchers think that other whales and dolphins may use the same technique to trap a fish in their beam of sound in the final phase of an attack. This could help prevent porpoises, whales and dolphins' prey from evading their capture. By revealing these acoustic secrets in detail, researchers are hoping to develop ways to prevent porpoises, and other toothed whales, from becoming trapped in fishing nets. The study, published in the journal eLife, was led by Danuta Wisniewska of Aarhus University. She and her colleagues worked with harbour porpoises in a semi-natural enclosure on the coast of Denmark. "The facility is quite exceptional, " explained Dr Wisniewska. "The animals still have access to the seafloor and are only separated from the harbour by a net. Fish are able to come in, so they're still hunting." In this unique environment, the researchers were able to fit the porpoises with sound-detecting tags, and to place an array of microphones to pick up sound around their enclosure. The team carried out a series of these experiments to work out where the sound energy the porpoises produced was being directed In one experiment, researchers dropped fish into the water to tempt the porpoises to hunt. As echolocating porpoises, whales and dolphins hunt, they switch from an exploratory clicking to a more intense, high frequency buzz - to elicit a continuous echo from the fish they are pursuing. Their beam can be envisaged a cone of sound, said Dr Wisniewska, comparing it to the cone-shaped beam of light from a torch. © 2015 BBC.

Keyword: Hearing
Link ID: 20731 - Posted: 03.30.2015

Just like the human brain itself, the European Commission’s billion-euro Human Brain Project (HBP) defies easy explanation. Launched 18 months ago, the massive project is complex and, to most observers, confusing. Many people—both scientists and non-scientists—have thus accepted a description of the project that emerged from its leaders and its publicity machine: the aim of simulating the entire human brain in a supercomputer and so find cures for psychiatric and neurological disorders. Like many simplistic explanations of the brain, that characterization of the project provoked a backlash from neuroscientists. This climaxed in a full-scale uprising last summer, when hundreds of researchers signed a critical open letter to the commission (www.neurofuture.eu). Autocratic management, they complained, was running the project off its scientific course and exaggerating its clinical reach. An independent committee was established to investigate and mediate on the dispute. Last week it published its report. This time, the main points were easier for outsiders to decipher. The rebellious neuroscientists who made the complaints were correct. The brain project is failing and must be fixed. The committee’s criticisms endorse more or less all the concerns of the scientists. The project fails not only in its governance, the report says, but also in its scientific plan—particularly the core aim, the simulation of the entire brain that critics had long dismissed as unrealistic. © 2015 Scientific American

Keyword: Brain imaging
Link ID: 20730 - Posted: 03.30.2015

Founded by two men in Akron, Ohio, in 1935, Alcoholics Anonymous has since spread around the world as a leading community-based method of overcoming alcohol dependence and abuse. Many people swear by the 12-step method, which has become the basis of programs to treat the abuse of drugs, gambling, eating disorders and other compulsive behaviors. But not everyone's a fan. In a recent critique of AA, author Gabrielle Glaser writes in the April issue of The Atlantic that, "Nowhere in the field of medicine is treatment less grounded in modern science." Glaser, whose 2013 book, Her Best-Kept Secret, explores what she calls "the epidemic of female drinking" in the U.S., says recent research on the brain suggests that the abstinence advocated by AA isn't the only solution — or even the best for many people. Cognitive therapy combined with the medication naltrexone, Glaser says, can help ease cravings and has been shown in some studies to help some problem drinkers learn to drink moderately without quitting. Glaser's magazine story has drawn fire from defenders of AA, including Huffington Post writer Tommy Rosen, who calls himself "a person in long-term recovery (23 years) who overcame severe drug addiction and alcoholism in great part due to the 12 Steps." Glaser's article, Rosen writes, is "painfully one-sided." Therapist and psychology reporter Robi Ludwig told Glaser and the host of MSNBC's program All in With Chris Hayes last week that she thinks it's "very dangerous to put out the idea that AA doesn't work. Does it work for everybody? No. There's not going to be one form of treatment that works for everybody." © 2015 NPR

Keyword: Drug Abuse
Link ID: 20729 - Posted: 03.28.2015

Patrick Fuller is a neuroscientist at Harvard Medical School's esteemed Division of Sleep Medicine. What have you found in your research on the "neurocircuit basis" that supports sleep? In specific reference to our recent work on the brainstem slow-wave-sleep promoter "center," we showed that this region of the brain is first connected (synaptically) to an important wake-promoting region of the brainstem that in turn is connected with important wake-promoting circuitry of the forebrain, which itself connects to the cerebral cortex. Essentially, we provided a circuit "wiring diagram" by which activation of brainstem sleep-promoting neurons might produce "whole brain" sleep. The reason I emphasize the word "neurocircuit" in our work is because I believe that in order to understand how the brain accomplishes virtually anything, one must first understand the functional cellular and synaptic "scaffolding" from which brain phenomena emerge. Tell me about how circadian regulation affects our sleep and wakeful consciousness. So it all starts (and ends!) with a little biological clock in our brain. The so-called "master" circadian clock is actually a collection of neurons located in a small region of the hypothalamus, itself a very small structure. (In humans, the hypothalamus is about the size of an almond.) This clock is remarkable for many reasons, perhaps most notably that no other region of the brain can assume its function if/when it is damaged. The clock's fundamental role is to keep us "synchronized" with the Earth's light-dark cycle as well as keep our body's internal rhythms synchronized with one another. And we now know that proper external and internal synchronization is fundamental to our physical and mental well-being. ©2015 TheHuffingtonPost.com, Inc.

Keyword: Sleep
Link ID: 20728 - Posted: 03.28.2015

By Nicholas Bakalar Air pollution — even for just one day — significantly increases the risk of stroke, a large review of studies has found. Researchers pooled data from 103 studies involving 6.2 million stroke hospitalizations and deaths in 28 countries. The analysis, published online in BMJ, found that all types of pollution except ozone were associated with increased risk for stroke, and the higher the level of pollution, the more strokes there were. Daily increases in pollution from nitrogen dioxide, sulfur dioxide, carbon monoxide and particulate matter were associated with corresponding increases in strokes and hospital admissions. The strongest associations were apparent on the day of exposure, but increases in particulate matter had longer-lasting effects. The exact reason for the effect is unclear, but studies have shown that air pollution can constrict blood vessels, increase blood pressure and increase the risk for blood clots. Other research has tied air pollution to a higher risk of heart attacks, stroke and other ills. The lead author, Dr. Anoop Shah, a lecturer in cardiology at the University of Edinburgh, said that there was little an individual can do when air pollution spikes. “If you’re elderly, or have co-morbid conditions, you should stay inside,” he said. But policies leading to cleaner air would have the greatest impact, he said. “It’s a question of getting cities and countries to change.” © 2015 The New York Times Company

Keyword: Stroke; Neurotoxins
Link ID: 20727 - Posted: 03.28.2015

By Virginia Morell Children and parrot and songbird chicks share a rare talent: They can mimic the sounds that adults of their species make. Now, researchers have discovered this vocal learning skill in baby Egyptian fruit bats (Rousettus aegyptiacus, pictured), a highly social species found from Africa to Pakistan. Only a handful of other mammals, including cetaceans and certain insectivorous bats, are vocal learners. The adult fruit bats have a rich vocal repertoire of mouselike squeaks and chatter (listen to a recording here), and the scientists suspected the bat pups had to learn these sounds. To find out, they placed baby bats with their mothers in isolation chambers for 5 months and made video and audio recordings of each pair. Lacking any other adults to vocalize to, the mothers were silent, and their babies made only isolation calls and babbling sounds, the researchers report today in Science Advances. As a control, the team raised another group of bat pups with their mothers and fathers, who chattered to each other. Soon, the control pups’ babbling gave way to specific sounds that matched those of their mothers. But the isolated pups quickly overcame the vocal gap after the scientists united both sets of bats—suggesting that unlike many songbird species (and more like humans), the fruit bats don’t have a limited period for vocal learning. Although the bats’ vocal learning is simple compared with that of humans, it could provide a useful model for understanding the evolution of language, the scientists say. © 2015 American Association for the Advancement of Science

Keyword: Hearing; Development of the Brain
Link ID: 20726 - Posted: 03.28.2015

Jon Hamilton A biotech company and two scientists hope to change that. On Wednesday, Avalanche Biotechnologies in Menlo Park and the University of Washington in Seattle announced a licensing agreement to develop the first treatment for colorblindness. The deal brings together a gene therapy technique developed by Avalanche with the expertise of vision researchers at the University of Washington. "Our goal is to be treating colorblindness in clinical trials in patients in the next one to two years," says Thomas Chalberg, the founder and CEO of Avalanche. Dalton the squirrel monkey during the color vision test. i Dalton the squirrel monkey during the color vision test. Courtesy of Neitz Laboratory The agreement has its roots in a scientific breakthrough that occurred six years ago. That's when two vision researchers at the University of Washington used gene therapy to cure a common form of colorblindness in squirrel monkeys. "This opened the possibility of ultimately getting this to cure colorblindness in humans," says Jay Neitz, who runs the Color Vision Lab at UW along with his wife, Maureen Neitz. The couple knew that transferring their success from monkey to man would be a challenge. But they were determined, says Maureen Neitz. "We've spent our entire careers writing NIH grants where we say our goal is to improve human health." © 2015 NPR

Keyword: Vision
Link ID: 20725 - Posted: 03.26.2015

Carl Zimmer Scientists in Iceland have produced an unprecedented snapshot of a nation’s genetic makeup, discovering a host of previously unknown gene mutations that may play roles in ailments as diverse as Alzheimer’s disease, heart disease and gallstones. “This is amazing work, there’s no question about it,” said Daniel G. MacArthur, a geneticist at Massachusetts General Hospital who was not involved in the research. “They’ve now managed to get more genetic data on a much larger chunk of the population than in any other country in the world.” In a series of papers published on Wednesday in the journal Nature Genetics, researchers at Decode, an Icelandic genetics firm owned by Amgen, described sequencing the genomes — the complete DNA — of 2,636 Icelanders, the largest collection ever analyzed in a single human population. With this trove of genetic information, the scientists were able to accurately infer the genomes of more than 100,000 other Icelanders, or almost a third of the entire country. “From the technical point of view, these papers are a tour-de-force,” said David Reich, a geneticist at Harvard Medical School who was not involved in the research. While some diseases, like cystic fibrosis, are caused by a single genetic mutation, the most common ones are not. Instead, mutations to a number of different genes can each raise the risk of getting, say, heart disease or breast cancer. Discovering these mutations can shed light on these diseases and point to potential treatments. But many of them are rare, making it necessary to search large groups of people to find them. The wealth of data created in Iceland may enable scientists to begin doing that. In their new study, the researchers at Decode present several such revealing mutations. For example, they found eight people in Iceland who shared a mutation on a gene called MYL4. Medical records showed that they also have early onset atrial fibrillation, a type of irregular heartbeat. © 2015 The New York Times Company

Keyword: Genes & Behavior; Alzheimers
Link ID: 20724 - Posted: 03.26.2015

Hannah Devlin, science correspondent Scientists have raised the alert about an antibiotic routinely prescribed for chest infections, after linking it to an increased risk of epilepsy and cerebral palsy in children whose mothers took the drug during pregnancy. Children of mothers who had taken macrolide antibiotics were found to be almost twice as likely to be affected by the conditions, prompting scientists to call for a review of their use during pregnancy. The study authors urged pregnant women not to stop taking prescribed antibiotics, however. The potential adverse effects are rare and, as yet, unproven, while infections during pregnancy are a well-established cause of health problems in babies. Professor Ruth Gilbert, a clinical epidemiologist who led the research at University College London, said: “The main message is for medicines regulators and whether they need to issue a warning about these drugs. For women, if you’ve got a bacterial infection, it’s more important to get on and treat it.” The study tracked the children of nearly 65,000 women who had been prescribed a variety of antibiotics for illnesses during pregnancy, including chest and throat infections and cystitis. There was no evidence that most antibiotics (including penicillin, which made up 67% of prescriptions), led to an increased risk of the baby developing cerebral palsy or epilepsy. However, when the antibiotics were compared head-to-head, the potential adverse effect of macrolide drugs emerged. Around 10 in 1,000 children whose mothers were given the drug had developed the conditions by the age of seven, compared to 6 in 1,000 children, for those who had other types of antibiotic. © 2015 Guardian News and Media Limited

Keyword: Development of the Brain; Epilepsy
Link ID: 20723 - Posted: 03.26.2015

By BONNIE ROCHMAN Reasons Why I Shouldn’t Have to Go Tonight: If I wanted to talk about it, I would. / It’s my body. / It’s a waste of time. / It’s a waste of money. / I know what I need to know. / It sounds pretty stupid to me. PLEASE DON’T MAKE ME GO. I DON’T WANT TO GO. The plea came from Leah Likin, a fifth grader. It was addressed to her mother, who had registered both of them for a two-part course on puberty called “For Girls Only.” The missive, which included additional objections, failed: Mother took daughter anyway. But Leah had plenty of company, peers who shared her resistance, their arms crossed, their eyes downcast. Last year, the course, which is split into sessions for preteen boys and girls and held mostly in and around Seattle, and also in the Bay Area, pulled in 14,000 attendees. They heard about it from their pediatricians, or through word of mouth. The creator of the course, Julie Metzger, has been trying for nearly three decades to turn what’s so often at best a blush-inducing experience — the “facts of life” talk — into a candid dialogue between parents and children. In the mid-1980s, she was a graduate student at the University of Washington School of Nursing when she reviewed survey data on how women had learned about menarche, or the onset of menstruation, for her master’s thesis. Most reported getting information from gym class or their mothers. “You can picture those conversations lasting from 10 seconds to 10 hours,” Metzger says. “And I thought, Wouldn’t it be interesting if you actually had a class where you sit with your parents and hear these things from someone? What if that class were fun and funny and interactive?” Metzger, who is 56 and vigorous, with flushed cheeks and blue eyes, says she has always been comfortable talking about sexuality; her father was a urologist, her mother a nurse. “Hand me a microphone,” she says. “I get so into this topic that I can make myself cry in front of the class, and it’s real.” © 2015 The New York Times Company

Keyword: Sexual Behavior
Link ID: 20722 - Posted: 03.26.2015

Jon Hamilton Doctors are much more likely to level with patients who have cancer than patients who have Alzheimer's, according to a report released this week by the Alzheimer's Association. The report found that just 45 percent of Medicare patients who'd been diagnosed with Alzheimer's said they were informed of the diagnosis by their doctor. By contrast, more than 90 percent of Medicare patients with cancer said they were told by their doctor. "What we found is really shocking," says Beth Kallmyer, vice president of constituent services for the Alzheimer's Association. "This is reminiscent of what happened in the 1960s and 1970s with cancer," she says. "But that's changed now, and it really needs to change for Alzheimer's as well." For years, the association's help line has been receiving complaints from family members who say that doctors are reluctant to reveal an Alzheimer's diagnosis, Kallmyer says. So the association decided to investigate by studying medical records and survey results from Medicare recipients. To make sure that Alzheimer's patients hadn't simply forgotten what a doctor said, the group also looked at Medicare survey responses from family members and other caregivers. The result wasn't much better: Just 53 percent said a doctor told them of the patient's diagnosis. © 2015 NPR

Keyword: Alzheimers
Link ID: 20721 - Posted: 03.25.2015

By Rachel Feltman I'm not usually one for heartstring-tugging ads, but this collaboration between Valspar Paint and EnChroma, a company that makes color-boosting sunglasses for the color-blind, is pretty cool. And the coolest thing about the glasses in the above video is that they weren't designed to help the color-blind at all. Smithsonian Magazine reports that EnChroma Labs founder Don McPherson (a materials scientist) had originally engineered the glasses with surgeons in mind. The lenses contained rare earth iron and absorbed a ton of light to protect surgeons performing laser eye surgery. The boosted absorption also made colors pop more vibrantly, allowing them to more easily distinguish among different tissues during surgery. But the stellar eye protection and vibrant colors meant that many surgeons wanted to wear them outside the operating room. McPherson himself started using them as regular sunglasses. And when a color-blind friend tried them on, he was amazed: He could distinguish orange traffic cones from the grass and pavement around them. He was perceiving color in a way he never had before. Now EnChroma sells the glasses (which have been specifically tailored for color blindness since the accidental discovery) for a few hundred bucks a pop. McPherson explains that all people have three photopigments in the eye, also known as cones, which are sensitive to blue, green and red. Blue operates fairly independently, while the red and green cones, in most humans, overlap, affecting the perception of certain colors. For example, if 10 photons landed on the red cone and 100 landed on the green cone, the object viewed would appear more green. Whereas if an equal number of photons landed on the red and green cones, the color perceived would be yellow.

Keyword: Vision
Link ID: 20720 - Posted: 03.25.2015

Alice Park We start to talk before we can read, so hearing words, and getting familiar with their sounds, is obviously a critical part of learning a language. But in order to read, and especially in order to read quickly, our brains have to “see” words as well. At least that’s what Maximilian Riesenhuber, a neuroscientist at Georgetown University Medical Center, and his colleagues found in an intriguing brain-mapping study published in the Journal of Neuroscience. The scientists recruited a small group of college students to learn a set of 150 nonsense words, and they imaged their brains before and after the training. Before they learned the words, their brains registered them as a jumble of symbols. But after they were trained to give them a meaning, the words looked more like familiar words they used every day, like car, cat or apple. The difference in way the brain treated the words involved “seeing” them rather than sounding them out. The closest analogy would be for adults learning a foreign language based on a completely different alphabet system. Students would have to first learn the new alphabet, assigning sounds to each symbol, and in order to read, they would have to sound out each letter to put words together. In a person’s native language, such reading occurs in an entirely different way.

Keyword: Language
Link ID: 20719 - Posted: 03.25.2015

By Harriet Brown If you’re one of the 45 million Americans who plan to go on a diet this year, I’ve got one word of advice for you: Don’t. You’ll likely lose weight in the short term, but your chance of keeping if off for five years or more is about the same as your chance of surviving metastatic lung cancer: 5 percent. And when you do gain back the weight, everyone will blame you. Including you. This isn’t breaking news; doctors know the holy trinity of obesity treatments—diet, exercise, and medication—don’t work. They know yo-yo dieting is linked to heart disease, insulin resistance, higher blood pressure, inflammation, and, ironically, long-term weight gain. Still, they push the same ineffective treatments, insisting they’ll make you not just thinner but healthier. In reality, 97 percent of dieters regain everything they lost and then some within three years. Obesity research fails to reflect this truth because it rarely follows people for more than 18 months. This makes most weight-loss studies disingenuous at best and downright deceptive at worst. One of the principles driving the $61 billion weight-loss industries is the notion that fat is inherently unhealthy and that it’s better, health-wise, to be thin, no matter what you have to do to get there. But a growing body of research is beginning to question this paradigm. Does obesity cause ill health, result from it, both, or neither? Does weight loss lead to a longer, healthier life for most people? Studies from the Centers for Disease Control and Prevention repeatedly find the lowest mortality rates among people whose body mass index puts them in the “overweight” and “mildly obese” categories.

Keyword: Obesity
Link ID: 20718 - Posted: 03.25.2015

Mo Costandi Two teams of scientists have developed new ways of stimulating neurons with nanoparticles, allowing them to activate brain cells remotely using light or magnetic fields. The new methods are quicker and far less invasive than other hi-tech methods available, so could be more suitable for potential new treatments for human diseases. Researchers have various methods for manipulating brain cell activity, arguably the most powerful being optogenetics, which enables them to switch specific brain cells on or off with unprecedented precision, and simultaneously record their behaviour, using pulses of light. This is very useful for probing neural circuits and behaviour, but involves first creating genetically engineered mice with light-sensitive neurons, and then inserting the optical fibres that deliver light into the brain, so there are major technical and ethical barriers to its use in humans. Nanomedicine could get around this. Francisco Bezanilla of the University of Chicago and his colleagues knew that gold nanoparticles can absorb light and convert it into heat, and several years ago they discovered that infrared light can make neurons fire nervous impulses by heating up their cell membranes. They therefore attached gold nanorods to three different molecules that recognise and bind to proteins in the cell membranes – the scorpion toxin Ts1, which binds to a sodium channel involved in producing nervous impulses, and antibodies that bind the P2X3 and the TRPV1 channels, both found in dorsal root ganglion (DRG) neurons, which transmit touch and pain information up the spinal cord and into the brain. © 2015 Guardian News and Media Limited

Keyword: Brain imaging
Link ID: 20717 - Posted: 03.25.2015

By Kate Baggaley Mutations on a gene necessary for keeping cells clean can cause Lou Gehrig’s disease, scientists report online March 24 in Nature Neuroscience. The gene is one of many that have been connected to the condition. In amyotrophic lateral sclerosis, also known as Lou Gehrig’s disease, nerve cells that control voluntary movement die, leading to paralysis. Scientists have previously identified mutations in 29 genes that are linked with ALS, but these genes account for less than one-third of all cases. To track down more genes, a team of European researchers looked at the protein-coding DNA of 252 ALS patients with a family history of the disease, as well as of 827 healthy people. The team discovered eight mutations on a gene called TBK1 that were associated with ALS. TBK1 normally codes for a protein that controls inflammation and cleans out damaged proteins from cells. “We do not know which of these two principle functions of TBK1 is the more relevant one” to ALS, says coauthor Jochen Weishaupt, a neurologist at Ulm University in Germany. In cells with one of the eight TBK1 mutations, the protein either is missing or lacks components that it needs to interact with other proteins, the researchers found. TBK1 mutations may explain 2 percent of ALS cases that run in families, which make up about 10 percent of all incidences of the disease, Weishaupt says. © Society for Science & the Public 2000 - 2015

Keyword: ALS-Lou Gehrig's Disease ; Genes & Behavior
Link ID: 20716 - Posted: 03.25.2015

By NICHOLAS BAKALAR Concussions are not as common in Major League Baseball as they are in professional football, but they happen often enough, with players getting hit by pitches, running into walls or catching a knee in the head sliding into a base. Catchers are particularly at risk — a foul tip off the mask will snap the neck back and give the brain a solid rattle. Collisions at the plate take a toll, too. Now, a study published in the American Journal of Sports Medicine suggests that position players in the majors who sustain concussions do not hit as effectively in their first weeks back after their injury. Under Major League Baseball rules, players can return after a concussion if they pass the concussion protocol — a series of interviews and tests of physical and mental functioning. But the new study found that even after passing the tests and having no apparent symptoms, hitters showed an initial decline when they returned to action. The study identified 66 position players who had concussions between 2007 and 2013, including some who never went on the disabled list. The study then compared their performance in the weeks before and after the injury. The gap was noticeable. In the two weeks before their injuries, the players hit .249 with a .315 on base percentage and a .393 slugging average. For the two weeks after the injury, their line was .227/.287/.347. Baseball instituted a seven-day disabled list in 2011, specifically to let players recover from concussions while allowing the team to maintain a full roster. But there is no set time that a player must stay out after a concussion. If he passes the protocol, he is cleared to play. © 2015 The New York Times Company

Keyword: Brain Injury/Concussion
Link ID: 20715 - Posted: 03.24.2015

By Gary Stix One of the most intriguing new areas of research in neuroscience has to do with the discovery that proteins involved with Alzheimer’s, Parkinson’s and other neurodegenerative illnesses can contort into the wrong shape. The misshapen molecules can spread throughout the brain in a manner akin to prion diseases—the most notorious of which is variant Creutzfeldt-Jakob disease, better known as Mad Cow. Misfolded proteins can lead to a buildup of cellular gunk that then causes damage inside or outside cells. If the process of misfolding observed in Alzheimer’s and Parkinson’s is similar to the one in Mad Cow, the next question is whether these misshapen proteins are transmissible from one organism to another. Last month, an article appeared in Acta Neuropathologica Communications from researchers at the Centre for Biological Threats and Special Pathogens at the Robert Koch-Institut in Berlin that raised questions about whether medical instruments need to be decontaminated if they come into contact with post-mortem brain tissue from Alzheimer’s or Parkinson’s patients. The case for putting in place such prophylaxis is rooted in lab studies that show that injecting deposits of these proteins into an animal brain can initiate a “seeding” process in which one protein causes another to misfold. “Whether those harmful effects can be also caused by transmitted protein particles in humans who express mutated or normal alpha-synuclein, A-beta or tau is still unknown,” the article says. But then it goes on: “…the ability to decontaminate medical instruments from aggregated A-beta, tau and alpha-synuclein may potentially add to patient safety.” © 2015 Scientific American

Keyword: Prions; Alzheimers
Link ID: 20714 - Posted: 03.24.2015