by Douglas Heaven Blind people could soon be able to read street signs using an implant that translates the alphabet into Braille and beams an image of the Braille directly to visual neurons at the back of the eye. The implant is a modified version of a class of devices called retinal prostheses, which are used to restore partial sight to people with retinitis pigmentosa. A degenerative eye disease that kills the photoreceptor cells in the retina, RP tends to affect people in early adulthood and can lead to blindness, but leaves intact the neurons that carry visual signals to the brain. Prostheses such as the Argus II, manufactured by Second Sight in Sylmar, California, convert video from a camera mounted on a pair of glasses into electronic signals "displayed" on a 10-by-6 grid of electrodes implanted over a person's retina. This gives users a pixellated view of the world, allowing them to distinguish light and dark regions and even detect features such as doorways. But deciphering letters and words with the prosthesis is slow because of its low resolution. To make this more practical, Thomas Lauritzen of Second Sight and colleagues have come up with a modified version of the Argus II that presents the user with Braille. Since Braille represents letters and numbers as dots in a 3-by-2 grid, it can be displayed using the electrode array of existing Argus implants. The modified implant was tried out on a Braille-reading volunteer who already uses the Argus II. Tested on single letters and words of up to four letters, transmitted in Braille to the retinal implant, he correctly identified the letters 89 per cent of the time and words 60 to 80 per cent of the time. © Copyright Reed Business Information Ltd.

Keyword: Vision; Robotics
Link ID: 17527 - Posted: 11.24.2012

Dan Jones As diagnoses of autism spectrum disorder rise, the need for effective therapies has increased in urgency. Today, a paper in Nature describes two ways of reversing autism-like symptoms in a new mouse model of the condition1. Autism spectrum disorder (ASD) affects up to 1 in 110 people. Although a few drugs have shown promise in mouse models, none is able to treat the core social deficits common to ASD in humans. A team of researchers led by Nahum Sonenberg of McGill University in Montreal, Quebec, created a new model of mouse autism, and then reversed its symptoms. They began by genetically engineering mice so that they lacked the gene Eif4ebp2. The 4E-BP2 protein that this produces suppresses the translation of certain messenger RNAs, so knocking out Eif4ebp2 allows the proteins that these mRNAs produce to be synthesized at above normal levels. Mice lacking Eif4ebp2 exhibit many autism-like symptoms, including poor social interaction, altered communication and repetitive behaviours. Sonenberg and his co-workers found that one group of proteins that proliferates in the absence of Eif4ebp2 is the neuroligins (NLGNs), which sit in the membrane of neurons and help to create and maintain the connections, or synapses, between nerve cells. When the authors examined mouse brain slices, they discovered that overproduction of NLGNs results in synapses that are prone to overstimulation, establishing a ‘hyperconnectivity’ that many researchers believe underlies the symptoms of ASD. © 2012 Nature Publishing Group

Keyword: Autism
Link ID: 17526 - Posted: 11.24.2012

Flora Graham, deputy editor, newscientist.com These glowing shapes aren't the ears of a rave-happy Vulcan - they're slices from a mouse's brain. The slice on the right is from a mouse that lacks a gene called Arl13b - the same gene whose mutation causes Joubert syndrome in humans. This is a rare neurological condition that is linked with autism-spectrum disorders and brain structure malformations. Without Arl13b, the nerve cells known as interneurons can't find the right destination in the cerebral cortex during the brain's development. Since the interneurons don't end up in the right places, they can't be wired up properly later on. This causes the disrupted brain development, typical of Joubert syndrome, visible in the image on the right. The researchers hope that their findings will lead to better treatments for people who have the syndrome. "Ultimately, if you're going to come up with therapeutic solutions, it's important to understand the biology of the disease," says Eva Anton of the University of North Carolina in Chapel Hill, who worked on the research, which was published in Developmental Cell last week. Journal reference: Developmental cell doi:10.1016/j.devcel.2012.09.019 © Copyright Reed Business Information Ltd

Keyword: Autism
Link ID: 17525 - Posted: 11.24.2012

By ALISSA QUART THIS fall, science writers have made sport of yet another instance of bad neuroscience. The culprit this time is Naomi Wolf; her new book, “Vagina,” has been roundly drubbed for misrepresenting the brain and neurochemicals like dopamine and oxytocin. Earlier in the year, Chris Mooney raised similar ire with the book “The Republican Brain,” which claims that Republicans are genetically different from — and, many readers deduced, lesser to — Democrats. “If Mooney’s argument sounds familiar to you, it should,” scoffed two science writers. “It’s called ‘eugenics,’ and it was based on the belief that some humans are genetically inferior.” Sharp words from disapproving science writers are but the tip of the hippocampus: today’s pop neuroscience, coarsened for mass audiences, is under a much larger attack. Meet the “neuro doubters.” The neuro doubter may like neuroscience but does not like what he or she considers its bastardization by glib, sometimes ill-informed, popularizers. A gaggle of energetic and amusing, mostly anonymous, neuroscience bloggers — including Neurocritic, Neuroskeptic, Neurobonkers and Mind Hacks — now regularly point out the lapses and folly contained in mainstream neuroscientific discourse. This group, for example, slammed a recent Newsweek article in which a neurosurgeon claimed to have discovered that “heaven is real” after his cortex “shut down.” Such journalism, these critics contend, is “shoddy,” nothing more than “simplified pop.” Additionally, publications from The Guardian to the New Statesman have published pieces blasting popular neuroscience-dependent writers like Jonah Lehrer and Malcolm Gladwell. The Oxford neuropsychologist Dorothy Bishop’s scolding lecture on the science of bad neuroscience was an online sensation last summer. © 2012 The New York Times Company

Keyword: Brain imaging
Link ID: 17524 - Posted: 11.24.2012

The search for genes predisposing people to depression has taken an unexpected twist, according to Canadian researchers who found a clue in an obesity gene. Studies on families and twins suggest depression has a genetic component, but for 15 years, scientists haven't been able to find genes associated with the illness. Researchers at McMaster University in Hamilton, Ont., took a different approach by testing how obesity genes may be linked with depression. "We found the first gene predisposing to depression with consistent results," said David Meyre, an associate professor in clinical epidemiology and biostatistics at McMaster and a Canada Research Chair in genetic epidemiology. In Monday's issue of the journal Molecular Psychiatry, Meyre and his co-authors reported that a variant of the FTO gene may be associated with a lower risk of depression independent of the gene's effect on obesity. The common perception is that obese people become depressed because of their appearance and poor self-esteem or discrimination. Another common thought is that those who are depressed are less likely to be physically active or follow healthy eating habits. Taking antidepressants can also lead to weight gain. But the genetic findings challenge that thinking, Meyre said, since those with the genetic mutation predisposing to obesity were protected from depression. "This suggests that the FTO gene may have a broader role than initially thought with an effect on depression and other common psychiatric disorders," the researchers wrote. © CBC 2012

Keyword: Obesity; Depression
Link ID: 17523 - Posted: 11.21.2012

By Simon J Makin “One hundred repetitions three nights a week for four years – sixty-two thousand four hundred repetitions make one truth.” These are the thoughts of Bernard Maxwell as he reflects on The World State’s sleep-teaching technique, hypnopaedia, in Aldous Huxley’s Brave New World, before concluding: “Idiots!” Huxley was using the idea to explore social conditioning and control in a dystopian future, rather than what we might call “useful” learning, but the promise of effortless learning while we sleep is an idea that refuses to go away, as evidenced by the continued existence of dubious sleep learning “courses”. The possibility was dismissed scientifically in the 1950s after an experiment showing that people who were played the answers to a list of questions while they slept could not recall any of them the next day, unless they had also shown electrical brain activity indicating they were waking up. But evidence is now growing that the sleeping brain can, in fact, be taught in certain, limited ways. The most striking demonstration of this comes from a recent study published in Nature Neuroscience, in which people learned to associate sounds with smells while they were asleep. Pleasant and unpleasant odours were paired with different sounds played to sleeping participants and their “sniff responses” were measured. Pleasant smells provoked stronger sniffs and when the sounds paired with these smells were later played alone they still provoked stronger sniffs than those that had been paired with unpleasant odours. This was true both while the participants were still asleep and after they awoke and, unsurprisingly, they had no awareness of having learned anything. This is a limited form of learning known as conditioning, famous since Pavlov and his dog, and it can’t be used for learning anything as complex as, say, language vocab. © 2012 Scientific American

Keyword: Sleep; Learning & Memory
Link ID: 17522 - Posted: 11.21.2012

By Linda Carroll It took almost two years for Nicole Delien’s family to find someone who could explain the mysterious illness that was making their little girl “sleep” for as long as 64 days. During those excruciating 21 months doctors diagnosed everything from West Nile to epilepsy. Some even suggested that Nicole’s parents might be drugging her or somehow manipulating her sleep – an accusation that led to a report to Child Protective Services. Finally, when the family was at their wits end, they found Dr. Michael Rancurello at Allegheny General Hospital in Pittsburgh, who diagnosed Nicole, 17, with an exceedingly rare disorder called Kleine-Levin Syndrome. Rancurello wasn’t an expert in the syndrome, but by chance he’d already treated several patients with the disorder that periodically sends patients into a strange state in which they alternate between long stretches of actual sleep and periods of semi conscious delirium. Nicole was 6 years old when contracted a virus that seems to have sparked her condition. “In the beginning we thought she had the flu because she had flu-like symptoms and a high fever,” Vicki Delien, Nicole’s mom, told TODAY’s Savannah Guthrie. “But then she just became, as the days progressed, more confused and lethargic. We didn’t know what was going on. “ © 2012 NBCNews.com

Keyword: Sleep; Genes & Behavior
Link ID: 17521 - Posted: 11.21.2012

By Ferris Jabr After Thanksgiving dinner, many people start to feel a little drowsy. Turkey typically gets the blame. It supposedly contains high levels of tryptophan, an amino acid that is sold in a purified form to help people fall asleep. But turkey contains about the same amount of tryptophan as chicken, beef and other meats. If Thanksgiving drowsiness is not about the main course, what is responsible? It may have more to do with the side dishes. To understand, we first need to digest a little food chemistry. To start, we get tryptophan and other essential amino acids from all the protein in our diet, not just from meat. These amino acids swim through the bloodstream, nourishing our cells. Brain cells convert tryptophan into a chemical called serotonin. This neurotransmitter helps regulate sleep and appetite and high levels of serotonin are associated with calm and relaxation. But tryptophan and other amino acids can’t access brain cells on their own—instead, teams of proteins transport amino acids across the blood-brain barrier. As it turns out, Thanksgiving side dishes probably make it easier for tryptophan to get inside the brain. © 2012 Scientific American,

Keyword: Sleep
Link ID: 17520 - Posted: 11.21.2012

By ANAHAD O'CONNOR A new study of elementary and middle school students has found that those who are the youngest in their grades score worse on standardized tests than their older classmates and are more likely to be prescribed stimulants for attention deficit hyperactivity disorder. The findings suggest that in a given grade, students born at the end of the calendar year may be at a distinct disadvantage. Those perceived as having academic or behavioral problems may in fact be lagging simply as a result of being forced to compete with classmates almost a full year older than them. For a child as young as 5, a span of one year can account for 20 percent of the child’s age, potentially making him or her appear significantly less mature than older classmates. The new study found that the lower the grade, the greater the disparity. For children in the fourth grade, the researchers found that those in the youngest third of their class had an 80 to 90 percent increased risk of scoring in the lowest decile on standardized tests. They were also 50 percent more likely than the oldest third of their classmates to be prescribed stimulants for A.D.H.D. The differences diminished somewhat over time, the researchers found, but continued at least through the seventh grade. The new study, published in the journal Pediatrics, used data from Iceland, where health and academic measures are tracked nationally and stimulant prescription rates are high and on par with rates in the United States. Previous studies carried out there and in other countries have shown similar patterns, even among college students. Copyright 2012 The New York Times Company

Keyword: ADHD; Development of the Brain
Link ID: 17519 - Posted: 11.21.2012

By David Pogue Okay, great: we can control Our phones with speech recognition and our television sets with gesture recognition. But those technologies don't work in all situations for all people. So I say, forget about those crude beginnings; what we really want is thought recognition. As I found out during research for a recent NOVA episode, it mostly appears that brain-computer interface (BCI) technology has not advanced very far just yet. For example, I tried to make a toy helicopter fly by thinking “up” as I wore a $300 commercial EEG headset. It barely worked. Such “mind-reading” caps are quick to put on and noninvasive. They listen, through your scalp, for the incredibly weak remnants of electrical signals from your brain activity. But they're lousy at figuring out where in your brain they originated. Furthermore, the headset software didn't even know that I was thinking “up.” I could just as easily have thought “goofy” or “shoelace” or “pickle”—whatever I had thought about during the 15-second training session. There are other noninvasive brain scanners—magnetoencephalography, positron-emission tomography and near-infrared spectroscopy, and so on—but each also has its trade-offs. Of course, you can implant sensors inside someone's skull for the best readings of all; immobilized patients have successfully manipulated computer cursors and robotic arms using this approach. Still, when it comes to controlling everyday electronics, brain surgery might be a tough sell. © 2012 Scientific American,

Keyword: Robotics
Link ID: 17518 - Posted: 11.21.2012

By GRETCHEN REYNOLDS Is playing football like falling in love? That question, which would perhaps not occur to most of us watching hours of the bruising game this holiday season, is the focus of a provocative and growing body of new science examining the role of oxytocin in competitive sports. Oxytocin is, famously, the “love hormone,” a brain peptide known to promote positive intersocial relations. It makes people like one another, especially in intimate relationships. New mothers are awash in oxytocin (which is involved in the labor process), and it is believed that the hormone promotes bonding between mother and infant. New-formed romantic couples also have augmented bloodstream levels of the peptide, many studies show. The original attraction between the lovers seems to prompt the release of oxytocin, and, in turn, its actions in the brain intensify and solidify the allure. Until recently, though, scientists had not considered whether a substance that promotes cuddliness and warm, intimate bonding might also play a role in competitive sports. But the idea makes sense, says Gert-Jan Pepping, a researcher at the Center for Human Movement Sciences at the University of Groningen in The Netherlands, and the author of a new review of oxytocin and competition. “Being part of a team involves emotions, as for instance when a team scores, and these emotions are associated with brain chemicals.” Copyright 2012 The New York Times Company

Keyword: Hormones & Behavior; Emotions
Link ID: 17517 - Posted: 11.21.2012

By David P. Barash Critics claim that evolutionary biology is, at best, guesswork. The reality is otherwise. Evolutionists have nailed down how an enormous number of previously unexplained phenomena—in anatomy, physiology, embryology, behavior—have evolved. There are still mysteries, however, and one of the most prominent is the origins of homosexuality. The mystery is simple enough. Its solution, however, has thus far eluded our best scientific minds. The sine qua non for any trait to have evolved is for it to correlate positively with reproductive success, or, more precisely, with success in projecting genes relevant to that trait into the future. So, if homosexuality is in any sense a product of evolution—and it clearly is, for reasons to be explained—then genetic factors associated with same-sex preference must enjoy some sort of reproductive advantage. The problem should be obvious: If homosexuals reproduce less than heterosexuals—and they do—then why has natural selection not operated against it? The paradox of homosexuality is especially pronounced for individuals whose homosexual preference is exclusive; that is, who have no inclination toward heterosexuality. But the mystery persists even for those who are bisexual, since it is mathematically provable that even a tiny difference in reproductive outcome can drive substantial evolutionary change. Copyright 2012.

Keyword: Sexual Behavior; Genes & Behavior
Link ID: 17516 - Posted: 11.21.2012

The Associated Press Chimpanzees going through a midlife crisis? It sounds like a setup for a joke. But there it is, in the title of a report published Monday in a scientific journal: "Evidence for a midlife crisis in great apes." So what do these apes do? Buy red Ferraris? Leave their mates for some cute young bonobos? Uh, no. "I believe no ape has ever purchased a sports car," said Andrew Oswald, an author of the study. But researchers report that captive chimps and orangutans do show the same low ebb in emotional well-being at midlife that some studies find in people. That suggests the human tendency toward midlife discontent may have been passed on through evolution, rather than resulting simply from the hassles of modern life, said Oswald, a professor of economics at the University of Warwick in England who presented his work Monday in the Proceedings of the National Academy of Sciences. A second study in the journal looks at a younger age group and finds that happiness in youth can lead to higher income a few years down the road. Several studies have concluded that happiness in human adults tends to follow a certain course between ages 20 and 70: It starts high and declines over the years to reach a low point in the late 40s, then turns around and rises to another peak at 70. On a graph, that's a U-shaped pattern. Some researchers question whether that trend is real, but to Oswald the mystery is what causes it. "This is one of the great patterns of human life. We're all going to slide along this U for good or ill," he said. "So what explains it?" © CBC 2012

Keyword: Emotions; Development of the Brain
Link ID: 17515 - Posted: 11.20.2012

By Alyssa A. Botelho When Jerry Berrier dreams, he hears and touches and smells and talks, but he doesn’t see. Blind since birth, he rarely remembers his dreams, however, because his sleep has been so poor. At 15, Berrier had both of his eyes removed and lost the little light perception he had as a child. Ever since, the Everett resident, now 60, has battled a vicious sleep cycle — a few days of sleep followed by weeks of hardly any. The bouts of sleeplessness come suddenly and subside without warning. When they hit, Berrier can’t sleep more than a couple hours a night, no matter how tired he is. Though physicians haven’t given him a formal diagnosis, scientists believe he suffers from a rare condition called non-24 sleep-wake disorder, or “non-24.” The chronic condition is characterized by a body clock that is out of synch with the 24-hour cycle of the Earth day. Non-24 can affect those with normal vision, but it especially plagues the totally blind who can’t perceive light, the strongest external signal that keeps the brain’s sleep-wake cycle aligned to the pattern of night and day. Of approximately 100,000 totally blind people in the United States, anywhere from 55 percent to 70 percent of them may suffer from non-24, according to Harvard neuroscientist Steven Lockley, one of the lead researchers in an ongoing clinical trial investigating sleep disorders in the blind. With 25 sites around the country, it’s the largest study of non-24 to date. Berrier is a participant in Boston. The toll of having an internal clock in competition with the 24-hour world can be high, adding another layer of challenge to life without sight. © 2012 NY Times Co.

Keyword: Sleep; Vision
Link ID: 17514 - Posted: 11.20.2012

By BENEDICT CAREY Hundreds of Iraq and Afghanistan veterans with post-traumatic stress have recently contacted a husband-and-wife team who work out of their home in suburban South Carolina to seek help. Many are desperate, pleading for treatment and willing to travel to get it. The soldiers have no interest in traditional talking cures or prescription drugs that have given them little relief. They are lining up to try an alternative: MDMA, better known as Ecstasy, a party drug that surfaced in the 1980s and ’90s that can induce pulses of euphoria and a radiating affection. Government regulators criminalized the drug in 1985, placing it on a list of prohibited substances that includes heroin and LSD. But in recent years, regulators have licensed a small number of labs to produce MDMA for research purposes. “I feel survivor’s guilt, both for coming back from Iraq alive and now for having had a chance to do this therapy,” said Anthony, a 25-year-old living near Charleston, S.C., who asked that his last name not be used because of the stigma of taking the drug. “I’m a different person because of it.” In a paper posted online Tuesday by the Journal of Psychopharmacology, Michael and Ann Mithoefer, the husband-and-wife team offering the treatment — which combines psychotherapy with a dose of MDMA — write that they found 15 of 21 people who recovered from severe post-traumatic stress in the therapy in the early 2000s reported minor to virtually no symptoms today. Many said they have received other kinds of therapy since then, but not with MDMA. The Mithoefers — he is a psychiatrist and she is a nurse — collaborated on the study with researchers at the Medical University of South Carolina and the nonprofit Multidisciplinary Association for Psychedelic Studies. © 2012 The New York Times Company

Keyword: Stress; Drug Abuse
Link ID: 17513 - Posted: 11.20.2012

By Scicurious Last week, Sci covered a paper on the nematode “version” of oxytocin, nematocin, and its role in learning behavior. We usually think of oxytocin-like peptides (including oxytocin and vasopressin), as being linked with emotion, trust, love, and of course, sex. But oxytocin also tends to get a lot of hype, especially as the “love”‘ or “trust” hormone. But it’s not that. It’s much more complicated than that. And understanding the evolution of oxytocin, and its very long history, allows us to understand HOW much more complicated than that. Because while nematodes have an oxytocin-like molecule that has roles in learning behavior…well it also has roles in mating. But I wouldn’t go do far as to call nematocin (oxytocin + nematode = nematocin!) the nematode love drug. Unless, of course, you believe nematodes have deep, passionate, trusting, and communicative one-night worm stands which commence upon immediate contact and end immediately after. Hey, you never know. This happens to be an interesting issue of Science, in which TWO papers were published, both identifying nematocin, at the same time. As they both call the new molecule nematocin, I have hopes that the two groups were happily collaborating with each other to further the interests of science (though I know that many times, when two groups find the name new, hot thing, it’s often a very bitter race to publish). So what is nematocin? Nematocin appears to be a chemical closely related to oxytocin and vasopressin, those much vaunted chemical in mammals which are making so much press for their role in our emotions and moral behavior. But oxytocin and vasopressin are both more complicated than emotion. Vasopressin, for example, plays a role in water balance. And it appears that the newly discovered nematocin in the nematode C. elegans may be similar, with more than one role in more than one system. © 2012 Scientific American

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 17512 - Posted: 11.20.2012

By Bruce Bower MINNEAPOLIS — Baboons use the order of regularly appearing letter pairs to tell words from nonwords, new evidence suggests. Psychologist Jonathan Grainger of the University of Aix-Marseille reported earlier this year that baboons can learn to tell real four-letter words from nonsense words (SN: 5/5/12, p. 5). But whether these animals detect signature letter combinations that enable their impressive word feats has been tough to demonstrate. Monkeys that previously learned to excel on this task are more likely to mistake nonwords created by reversing two letters of a word they already recognize as real, much as literate people do, Grainger reported November 16 at the Psychonomics Society annual meeting. “Letters played a role in baboons’ word knowledge,” Grainger concluded. “This is a starting point for determining how they discriminate words from nonwords.” Grainger’s team tested the six baboons in their original investigation. Some of the monkeys had previously learned to recognize many more words than others. In new trials, the best word identifiers made more errors than their less successful peers when shown nonwords that differed from known words by a reversed letter combination, such as WSAP instead of WASP and KTIE instead of KITE. Grainger’s team fed the same series of words and nonwords into a computer simulation of the experiment. The computer model best reproduced the animals’ learning curves when endowed with a capacity for tracking letter combinations. © Society for Science & the Public 2000 - 2012

Keyword: Language; Evolution
Link ID: 17511 - Posted: 11.20.2012

by Sid Perkins If you play sounds of many different frequencies at the same time, they combine to produce neutral "white noise." Neuroscientists say they have created an analogous generic scent by blending odors. Such "olfactory white" might rarely, if ever, be found in nature, but it could prove useful in research, other scientists say. Using just a few hundred types of biochemical receptors, each of which respond to just a few odorants, the human nose can distinguish thousands of different odors. Yet humans can't easily identify the individual components of a mixture, even when they can identify the odors alone, says Noam Sobel, a neuroscientist at the Weizmann Institute of Science in Rehovot, Israel. Now, he and his colleagues suggest, various blends made up of a large number of odors all begin to smell the same—even when the blends share no common components. For their study, the researchers used 86 nontoxic odorants that had a wide variety of chemical and physical properties such as molecular structure, molecular weight, and volatility. Those chemicals also spanned a perceptual scale from "pleasant" to "unpleasant" and another such scale on which scents were judged to range from "edible" to "poisonous." The researchers then diluted the chemicals so that their odors were equally intense. Finally, they created mixtures by dripping individual odorants onto separate regions of an absorptive pad in a jar, a technique that prevented the substances from reacting in liquid form to create new substances or odors. The odor blends contained anywhere from one to 43 of the chemicals, Sobel says. © 2010 American Association for the Advancement of Science

Keyword: Chemical Senses (Smell & Taste)
Link ID: 17510 - Posted: 11.20.2012

Scientists have reversed paralysis in dogs after injecting them with cells grown from the lining of their nose. The pets had all suffered spinal injuries which prevented them from using their back legs. The Cambridge University team is cautiously optimistic the technique could eventually have a role in the treatment of human patients. The study is the first to test the transplant in "real-life" injuries rather than laboratory animals. The only part of the body where nerve fibres continue to grow in adults is the olfactory system. Found in the at the back of the nasal cavity, olfactory ensheathing cells (OEC) surround the receptor neurons that both enable us to smell and convey these signals to the brain. The nerve cells need constant replacement which is promoted by the OECs. For decades scientists have thought OECs might be useful in spinal cord repair. Initial trials using OECs in humans have suggested the procedure is safe. In the study, funded by the Medical Research Council and published in the neurology journal Brain, the dogs had olfactory ensheathing cells from the lining of their nose removed. These were grown and expanded for several weeks in the laboratory. BBC © 2012

Keyword: Regeneration; Stem Cells
Link ID: 17509 - Posted: 11.19.2012

By Maggie Fox, NBC News Researchers trying to find a way to treat multiple sclerosis think they’ve come up with an approach that could not only help patients with MS, but those with a range of so-called autoimmune diseases, from type-1 diabetes to psoriasis, and perhaps even food allergies. So far it’s only worked in mice, but it has worked especially well. And while mice are different from humans in many ways, their immune systems are quite similar. “If this works, it is going to be absolutely fantastic,” said Bill Heetderks, who directs outside research at the National Institute of Biomedical Imaging and Bioengineering, part of the National Institutes of Health, which helped pay for the research. “Even if it doesn’t work, it’s going to be another step down the road.” In autoimmune disease, the body’s immune cells mistakenly attack and destroy healthy tissue. In MS, it’s the fatty protective sheath around the nerves; in type-1 or juvenile diabetes it’s cells in the pancreas that make insulin; in rheumatoid arthritis it’s tissue in the joint. Currently, the main treatment is to suppress the immune system, an approach that can leave patients vulnerable to infections and cancer. The new treatment re-educates the immune cells so they stop the attacks. The approach uses tiny little balls called nanoparticles made of the same material used to make surgical sutures that dissolve harmlessly in the body. They’re attached to little bits of the protein that the immune cells are attacking, the researchers report in Sunday’s issue of the journal Nature Biotechnology. © 2012 NBCNews.com

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 17508 - Posted: 11.19.2012