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It can start with flashing lights, a tingling sensation and a feeling of unease, followed by excruciating pain. Migraines can be triggered by lack of food or too much stress but their underlying cause has remained a mystery. Now researchers have found that a migraine may be triggered by a protein deep in the brain that stimulates the neurons controlling facial sensations. The discovery creates a potential new target for safer migraine medicines and adds weight to the theory that neurons, not blood vessels, are responsible for migraine attacks. “Where a migraine starts is a key question,” says Debbie Hay at the University of Auckland in New Zealand. “There has been a great deal of debate around the mechanisms of migraine. If we can pin this down, we may have better chances of preventing it.” To investigate, Simon Akerman at New York University and Peter Goadsby at Kings College London, UK, studied two neuropeptides released by neurons thought to play a role in the pain associated with migraine. These protein-like molecules, called VIP and PACAP, first raised suspicion after they were found to be elevated in blood drained from the brains of people having a migraine attack. When researchers administered these peptides to volunteers, they found that they could cause a headache or migraine about two hours later. Both peptides widen blood vessels, which was thought to be significant in migraine. In fact, the only drugs specifically developed for migraine that are in use today – triptans – were designed to shrink blood vessels in the brain. As a result, they cannot be used by people with cardiovascular disorders. © Copyright Reed Business Information Ltd.
Keyword: Pain & Touch
Link ID: 21489 - Posted: 10.08.2015
By Gretchen Reynolds We’ve probably all heard someone exclaim, “Ah, my endorphins are kicking in!” at the end of a good run. Endorphins are famous for supposedly producing “runner’s high,” that fleeting sense of calm and euphoria that engulfs many of us after a satisfying workout. But in fact, endorphins may be unfairly hogging the credit for making workouts enjoyable, according to an enlightening new experiment with animals. The findings suggest that endorphins have little to do with runner’s high. Instead, that euphoric feeling may be the product of a completely different but oddly familiar substance — the body’s own endocannabinoids, the chemicals that, like the cannabinoids in marijuana, lighten mood. Endorphins first became a household word in the 1980s, when researchers found that blood levels increased after prolonged exercise. This finding made sense. Exercise can cause discomfort or pain, and endorphins are the body’s self-produced opiates, with pain-relieving properties much like morphine. From that discovery, it was a short step to believing that endorphins must also produce the pleasurable mental sensations that many people feel after exercise. But there is a substantial problem with that idea, and it involves the substantial-ness of endorphins. They are large molecules, too big to pass through the blood-brain barrier. They might staunch pain in the muscles, but they wouldn’t have effects directly inside the brain, where any high would originate. So for the past decade or so, scientists have been looking for other substances that might be involved in making exercisers feel high, which led them, perhaps unsurprisingly, to endocannabinoids. © 2015 The New York Times Company
Keyword: Drug Abuse
Link ID: 21488 - Posted: 10.08.2015
By Somer Bishop Subtle, significant. In a nutshell, these two words capture the symptoms of many girls with autism. Like many in my field, I’ve seen this subtlety firsthand. One 6-year-old girl I met several years ago seemed, at first, to have good social skills. She responded appropriately when I introduced myself, complimented my outfit, and politely answered all of my questions. It was only when I saw her again a few days later that I understood her family’s concerns: She made nearly identical overtures, as if our interaction were part of a play she had rehearsed. I also met a teenage girl with autism who was highly intelligent. Because she could not relate to the other girls at her high school, she began interacting exclusively with boys, whose social behaviors she found easier to imitate. She even went through a period of wanting to become a boy, reasoning that she might have more success navigating the social world as a male. The past several years have seen an explosion of studies aimed at backing up these one-off observations about how autism presents differently in girls than in boys. This is a welcome development, as understanding the unique presentation of autism in girls will help us to better identify and treat the disorder. Consistently recognizing autism in girls can be challenging, however. This is not only because girls with autism are as diverse as any other group of individuals with the disorder but also because most autism screening and diagnostic tools were developed based primarily on observations of behaviors in boys. © 2015 The Slate Group LLC.
by Sarah Schwartz People with multiple sclerosis who got less sun exposure and had higher body mass as young adults developed the disease sooner than those who spent more time in the sun and were a normal weight, a new study finds. In a study of over 1,100 Danish people with MS — a nervous system condition that causes muscle weakness and pain — patients who were overweight at age 20 developed multiple sclerosis an average of 1.5 years sooner than patients of normal weight. And subjects who reported spending time in the sun every summer’s day during adolescence developed the disease 1.8 years later, on average, than patients who got less sun exposure, Danish researchers report online October 7 in Neurology. The results echo earlier work that found a link between adolescent obesity and risk of MS. And sun exposure may increase patients’ levels of vitamin D, which has been shown to protect against the disease, the researchers say. © Society for Science & the Public 2000 - 2015
By Jessica Schmerler Many studies trumpet the positive effects of oxytocin. The hormone facilitates bonding, increases trust and promotes altruism. Such findings earned oxytocin its famous nickname, the “love hormone.” But more recent research has shown oxytocin has a darker side, too: it can increase aggression, risk taking and prejudice. A new analysis of this large body of work reveals that oxytocin's effects on our brain and behavior actually look a lot like another substance that can cut both ways: alcohol. As such, the hormone might point to new treatments for addiction. Researchers led by Ian Mitchell, a psychologist at the University of Birmingham in England, conducted the meta-analysis, which reveals that both oxytocin and alcohol reduce fear, anxiety and stress while increasing trust, generosity and altruism. Yet both also increase aggression, risk taking and “in-group” bias—favoring people similar to ourselves at the expense of others, according to the paper published in August in Neuroscience and Biobehavioral Reviews. The scientists posit that these similarities probably exist because oxytocin and alcohol act at different points in the same chemical pathway in the brain. Oxytocin stimulates release of the neurotransmitter GABA, which tends to reduce neural activity. Alcohol binds to GABA receptors and ramps up GABA activity. Oxytocin and alcohol therefore both have the general effect of tamping down brain activity—perhaps explaining why they both lower inhibitions. © 2015 Scientific American
Jo Marchant Most new painkiller drugs fail in clinical trials — but a growing placebo response may be to blame. Drug companies have a problem: they are finding it ever harder to get painkillers through clinical trials. But this isn't necessarily because the drugs are getting worse. An extensive analysis of trial data1 has found that responses to sham treatments have become stronger over time, making it harder to prove a drug’s advantage over placebo. The change in reponse to placebo treatments for pain, discovered by researchers in Canada, holds true only for US clinical trials. “We were absolutely floored when we found out,” says Jeffrey Mogil, who directs the pain-genetics lab at McGill University in Montreal and led the analysis. Simply being in a US trial and receiving sham treatment now seems to relieve pain almost as effectively as many promising new drugs. Mogil thinks that as US trials get longer, larger and more expensive, they may be enhancing participants’ expectations of their effectiveness. Stronger placebo responses have already been reported for trials of antidepressants and antipsychotics2, 3, triggering debate over whether growing placebo effects are seen in pain trials too. To find out, Mogil and his colleagues examined 84 clinical trials of drugs for the treatment of chronic neuropathic pain (pain which affects the nervous system) published between 1990 and 2013. © 2015 Nature Publishing Group,
Keyword: Pain & Touch
Link ID: 21484 - Posted: 10.07.2015
By Nicholas Bakalar There may be a link between later bedtimes and weight gain, new research suggests. Researchers studied 3,342 adolescents starting in 1996, following them through 2009. At three points over the years, all reported their normal bedtimes, as well as information on fast food consumption, exercise and television time. The scientists calculated body mass index at each interview. After controlling for age, sex, race, ethnicity and socioeconomic status, the researchers found that each hour later bedtime during the school or workweek was associated with about a two-point increase in B.M.I. The effect was apparent even among people who got a full eight hours of sleep, and neither TV time nor exercise contributed to the effect. But fast food consumption did. The study, in the October issue of Sleep, raises questions, said the lead author, Lauren D. Asarnow, a graduate student at the University of California, Berkeley. “First, what is driving this relationship?” she said. “Is it metabolic changes that happen when you stay up late? And second, if we change sleep patterns, can we change eating behavior and the course of weight change?” The scientists acknowledge that their study had limitations. Their sleep data depended on self-reports, and they did not have complete diet information. Also, they had no data on waist circumference, which, unlike B.M.I., can help distinguish between lean muscle and abdominal fat. © 2015 The New York Times Company
Laura Sanders Scribes usually have pretty good handwriting. That’s not the case for one prolific 13th century writer known to scholars only as the Tremulous Hand of Worcester. Now scientists suggest the writer suffered from a neurological condition called essential tremor. Neurologist Jane Alty and historical handwriting researcher Deborah Thorpe, both of the University of York in England, made the retrospective diagnosis August 31 in Brain after studying the spidery wiggles that pervade the scribe’s writing. Essential tremor can cause shaking of the hands, head and voice and is distinct from other tremor-causing conditions such as Parkinson’s disease. Here, the anonymous writer’s peculiar script is evident (lighter portion of text) in an early Middle English version of the Nicene Creed, a summary of the Christian faith. Buried in the manuscript are clues that helped the researchers conclude that essential tremor plagued the Tremulous Hand. The Tremulous Hand of Worcester’s writing appeared in more than 20 books, including the Nicene Creed, a summary of the Christian faith. The writer’s distinctive script is the lighter portion of the text, about a third of the way down the page. Several clues led researchers to diagnose the scribe with essential tremor (see following images). © Society for Science & the Public 2000 - 2015.
Keyword: Movement Disorders
Link ID: 21482 - Posted: 10.07.2015
By Virginia Morell How homing pigeons find their way home has long mystified scientists. Experiments have shown they rely on smells to create a mental map of their route and on the sun or Earth’s magnetic fields to navigate. But they also use vision, memorizing roads, railway lines, and rivers. To understand just how important pigeons’ visual memories are for homing, scientists trained 12 birds to fly to their home lofts while wearing patches covering one eye (as in the photo above). Each bird wore a GPS logging device and made 18 flights with the left or right eye blocked, followed by another 18 trips with the opposite eye covered. Unlike mammals, birds lack a key neural structure—the corpus callosum—that allows both hemispheres of the brain to access what an animal sees. The experiments revealed that this missing neural structure affects the pigeons’ homing abilities, the scientists report in today’s the Proceedings of the Royal Society B. Pigeons that learned their way home with a blocked left eye couldn’t repeat the same journey when they wore a patch over their right eye, and vice versa. Instead, they flew slightly off course, following more of a curve than a straight line. The new work proves that vision, too, plays a key role in how pigeons find their way home. © 2015 American Association for the Advancement of Science.
Susan Milius Bachelor prairie voles can’t tell females of their species apart. Yet the clueless fellows can change, forming pair-bonds for life with the opposite sex and even distinguishing between two female strangers. Bachelors aren’t blind or stupid; they recognize individual males among their fellow short-tailed Microtus ochrogaster rodents scurrying through old fields in the center of North America. And males are certainly interested in the interchangeable females. In lab tests, bachelors claw and bite at cage dividers between the sexes, says Alexander Ophir of Cornell University. Conquering the divide and mating with a female after just six hours of her company can form a lifelong pair-bond between voles. Only about 5 percent of mammal species live this socially monogamous lifestyle, and the voles have played starring roles in studies of the neurobiology of bonding. (Social monogamists, including both voles and some Homo sapiens, don’t entirely forgo extra-pair encounters.) A pair-bonded couple can crowd three litters of young into their roughly six to nine months of life in the wild, Ophir says. One aid to speeding through family life: Females can get pregnant as soon as they give birth. “You sometimes see pups being delivered as males are trying to copulate with the female,” he says. Pair-bonding requires recognizing at least one female. “It’s all well and good to fall in love, but if you don’t know who you fell in love with, it’s worthless,” Ophir says. And paired-up voles can go further. Tests show they notice the difference between two females they have never mated with, Ophir and former student Tomica Blocker report in the October Animal Behaviour. © Society for Science & the Public 2000 - 2015
By Miriam E. Tucker Before he got sick, Whitney Dafoe was an award-winning photographer and a world traveler. He’d helped build a nunnery in India, ridden a motorcycle in the Himalayas and visited all 50 American states. He also worked on Barack Obama’s 2008 presidential campaign, and although he was already ill by January 2009, pushed himself to travel to Washington from his California home to photograph the inauguration. But now, at 31, Whitney lies in bed in a darkened room in his parents’ home, unable to talk, walk or eat. He is fed intravenously and is barely able to tolerate light, sounds or being touched. His parents and the medical personnel who see him wear plain clothing when they enter his room because bright colors, shapes or any kind of print make him feel even worse, as does any movement that he’s not expecting. “It’s hard to explain how fragile he is,” says his mother, Janet Dafoe. This isn’t the picture that people imagine when they hear “chronic fatigue syndrome,” which is often viewed by the public and the health-care community as a trivial or primarily psychological complaint. In a February report, the Institute of Medicine gave the illness a new name — systemic exertion intolerance disease. Many patients have long criticized the name “chronic fatigue syndrome” for not reflecting the seriousness of the illness. The new name, some say, is not much of an improvement. Some patients call it by an older name, “myalgic encephalomyelitis.” Most official documents refer to it with a compromise term, “myalgic encephalomyelitis/chronic fatigue syndrome,” or ME/CFS.
Link ID: 21479 - Posted: 10.06.2015
By Erika Hayasaki For 40 years, Joel Dreyer was a respected psychiatrist who oversaw a clinic for troubled children, belonged to an exclusive country club, and doted on his four daughters and nine grandchildren. Then, suddenly, he became a major drug dealer. Why? In the 1980s, psychiatrist Joel Dreyer was a fixture on Detroit’s WXYZ Channel 7. His commercials promoting his treatment center, InnerVisions, which he named after the Stevie Wonder album, sometimes ran up to five times a day. In one ad, Dreyer blocks a bartender from serving a mug of beer to a patron and says, “Don’t let your marriage or your job suffer from alcohol or drugs.” In another, Dreyer, in a navy pinstriped suit with a white pocket square, looks into the camera, his expression concerned and sympathetic. “Don’t you want to talk to someone who will listen?” he asks. “Someone who won’t pass judgment? Someone who cares? Come talk to me.” InnerVisions, which was based in Southfield, a suburb northwest of Detroit, had a staff of 80 physicians, psychologists, and therapists and took up two floors of a high-rise. It had made Dreyer not only a public figure but also wealthy. He maintained a side career as an expert witness. Attorneys called on him because he was smart, charming, and persuasive. Dreyer mostly testified for the defense, and with each high-profile case, his celebrity grew. Between the clinic, trial work, and his private practice, he was earning as much as $450,000 a year. Dreyer loved to be the center of attention. He would sometimes ride to work on a motorcycle in a bejeweled Elvis outfit to entertain his colleagues.
By Kimberly G. Noble What if we could draw a line from key areas of a low-income child’s brain to a policy intervention that would dramatically reduce his or her chances of staying in poverty, dropping out of school and entering the criminal justice or social welfare system? Wouldn’t we want to make that policy prescription as widely available as any vaccination against childhood disease? Thanks to remarkable advances in neuroscience and the social sciences, we are closing in on this possibility. In a study published this year in Nature Neuroscience, several co-authors and I found that family income is significantly correlated with children’s brain size — specifically, the surface area of the cerebral cortex, which is the outer layer of the brain that does most of the cognitive heavy lifting. Further, we found that increases in income were associated with the greatest increases in brain surface area among the poorest children. Not surprisingly, our findings made many people uncomfortable. Some feared the study would be used to reinforce the notion that people remain in poverty because they are less capable than those with higher incomes. As neuroscientists, we interpret the results very differently. We know that the brain is most malleable in the early years of life and that experiences during that time have lifelong effects on the mind. Work by social scientists such as Sendhil Mullainathan at Harvard University and Eldar Shafir at Princeton University has shown that poverty depletes parents’ cognitive resources, leaving less capacity for making everyday decisions about parenting. These parents are also at far greater risk for depression and anxiety — poverty’s “mental tax.” All of this has important implications for children.
Archy de Berker and Sven Bestmann A great deal of excitement has been generated in recent weeks by a review paper examining the literature on the drug modafinil, which concluded that “modafinil may well deserve the title of the first well-validated pharmaceutical ‘nootropic’ [cognitive enhancing] agent”. Coverage in the Guardian, Telegraph, British Medical Journal, and the Independent all called attention to the work, with a press release from Oxford University trumpeting “Review of ‘smart drug’ shows modafinil does enhance cognition”. The paper in question is a well-written summary of the recent literature (although though it probably underestimates side effects, as pointed out in the British Medical Journal). A deeper problem is that reviews do not “show” anything. Reviews can be educational and informative, but that’s not the same as using all of the available data to test whether something works or not. Two different scientists can write reviews on the same topic and come to completely different conclusions. You can think of reviews as a watercolour painting of current knowledge. We sometimes forget that this is a far cry from a technical drawing, each element measured, quantified, and bearing a strict resemblance to reality. Scientists, and the public, trying to figure out what works face a tricky problem: there will often be many papers on a given topic, offering a variety of sometimes conflicting conclusions. Fortunately, we have a well-developed toolkit for assessing the state of the current literature and drawing conclusions from it. This procedure is called meta-analysis; it combines the available sources of data (e.g., published studies), and is extensively used to assess the efficacy of medical interventions. Initiatives such as the Cochrane Collaboration use meta-analyses to synthesize available evidence into a consensus on what works and what doesn’t. © 2015 Guardian News and Media Limited
By ANDREW POLLACK What could become the first gene therapy to win approval in the United States moved closer to market on Monday, when its developer announced that the medicine had succeeded in a late-stage clinical trial in treating an inherited eye disease that can cause blindness. The developer, Spark Therapeutics, said the treatment had allowed people with certain so-called inherited retinal dystrophies to more easily maneuver in dimmer light than they could before. The company said it planned to apply to the Food and Drug Administration next year for approval to sell the product. “We saw substantial restoration of vision in patients who were progressing toward complete blindness,” Dr. Albert M. Maguire, a professor of ophthalmology at the University of Pennsylvania and a lead researcher in the study, said in a news release being issued by Spark. Dr. Katherine High, Spark’s president and chief scientific officer, said this was the first successful randomized, controlled trial for any gene therapy aimed at an inherited disease. “I’ve been working in gene therapy for most of my career,” she said. “It’s been a long time coming, and I’m delighted.” Besides encouraging the once beleaguered field of gene therapy, the results — if interpreted positively by investors — could help lift biotechnology stocks, which have been battered recently by concerns over a backlash against high drug prices. Still, much remains unknown. Spark did not provide the actual trial data, saying only that the treatment achieved the main goal of the study as well as two out of three of its secondary goals. It is also unclear what the F.D.A. will deem sufficient for approval of the product. Spark’s stock had slumped in the last two months as it changed how it would measure the results of the trial. © 2015 The New York Times Company
Link ID: 21475 - Posted: 10.05.2015
Gareth Cook talks to Douwe Draaisma Much has been written on the wonders of human memory: its astounding feats of recall, the way memories shape our identities and are shaped by them, memory as a literary theme and a historical one. But what of forgetting? This is the topic of a new book by Douwe Draaisma, author of The Nostalgia Factory: Memory, Time and Ageing (Yale University Press, 2013; 176 pages) and a professor of the history of psychology at the University of Groningen in the Netherlands. In Forgetting: Myths, Perils and Compensations (Yale University Press, 2015; 288 pages), Draaisma considers dreaming, amnesia, dementia and all the ways in which our minds—and lives—are shaped by memory’s opposite. He answered questions from contributing editor Gareth Cook. What is your earliest memory, and why, do you suppose, have you not forgotten it? Quite a few early memories in the Netherlands involve bicycles; mine is no exception. I was two and a half years old when my aunts walked my mother to the train station. They had taken a bike to transport her bags. I was sitting on the back of the bike. Suddenly the whole procession came to a halt when my foot got caught between the spokes of a wheel. I am pretty sure this memory is accurate because I had to see a doctor, and there is a dated medical record. It is a brief, snapshotlike memory, black-and-white. I do not remember any pain, but I do remember the consternation among my mom and her sisters. Looking back on this memory from a professional perspective, I would say that it has the flashlike character typical for first memories from before age three; “later” first memories are usually a bit longer and more elaborate. © 2015 Scientific American
Keyword: Learning & Memory
Link ID: 21474 - Posted: 10.05.2015
Carl Zimmer In recent years, a peculiar sort of public performance has taken place periodically on the sidewalks of Seattle. It begins with a woman named Kaeli N. Swift sprinkling peanuts and cheese puffs on the ground. Crows swoop in to feed on the snacks. While Ms. Swift observes the birds from a distance, notebook in hand, another person walks up to the birds, wearing a latex mask and a sign that reads “UW CROW STUDY.” In the accomplice’s hands is a taxidermied crow, presented like a tray of hors d’oeuvres. This performance is not surreal street theater, but an experiment designed to explore a deep biological question: What do crows understand about death? Ms. Swift has been running this experiment as part of her doctoral research at the University of Washington, under the guidance of John M. Marzluff, a biologist. Dr. Marzluff and other experts on crow behavior have long been intrigued by the way the birds seem to congregate noisily around dead comrades. Dr. Marzluff has witnessed these gatherings many times himself, and has heard similar stories from other people. “Whenever I give a talk about crows, there’s always someone who says, ‘Well, what about this?’ ” he said. Dr. Marzluff and Ms. Swift decided to bring some scientific rigor to these stories. They wanted to determine whether a dead crow really does trigger a distinctive response from living crows and, if so, what the purpose of the large, noisy gatherings might be. To run the experiment, Ms. Swift began by delivering food to a particular spot each day, so that the crows learned to congregate there to eat. Then one of her volunteers would approach the feast with a dead crow, and Ms. Swift observed how the birds reacted. © 2015 The New York Times Company
By Margaret M. McCarthy “We have raised our children in a gender-neutral household since the day they were born, and we never allowed any sort of weapons, not even a water pistol,” a young mother told me emphatically from the microphone in the lecture hall where I’d just given a talk on the differences between male and female brains. “But the other day my seven-year-old son bit his peanut butter and jelly sandwich into the shape of a gun and started shooting his little sister with it!” The audience laughed appreciatively; everyone had a similar story. “What did we do wrong?” she pleaded. This story is a common refrain I hear when discussing my research on sex differences in the brain. There is no single correct answer when it comes to human behavior. Some researchers would insist that there is nothing parents can do to suppress the innate tendencies of boys to gravitate to guns and trucks while girls prefer dolls and tea sets. Others would disagree, arguing that there is no inherent biological difference between the brains of boys and girls. Rather, it is the parents’ own implicit biases and those of society at large that influence their children to behave in gender-typical ways. In the end, my response is that sex differences in the brain are more than some would like and less than others believe. Just how large those differences are, however, is the crux of an ongoing debate in science. And how much a brain’s function can be attributed to biology versus cultural expectations is a challenging question to answer. Confounding the issue is the concept of gender, a purely human construct that can itself influence brain development. Gender refers to both personal and societal perceptions of one’s sex, and embodies all the complexities of cultural expectations, inherent biases, and predetermined norms of behavior, each of which differs for boys and girls and can affect the young brain. © 1986-2015 The Scientist
Keyword: Sexual Behavior
Link ID: 21472 - Posted: 10.03.2015
By Emily Underwood WASHINGTON, D.C.—As part of President Barack Obama’s high-profile initiative to study the brain, the Kavli Foundation and several university partners today announced $100 million in new funding for neuroscience research, including three new institutes at universities in Maryland, New York, and California. Each of the institutes will receive a $20 million endowment, provided equally by their universities and the foundation, along with start-up funding to pursue projects in areas such as brain plasticity and tool development. The new funding, geared at providing stable support for high-risk, interdisciplinary research, exceeds the original commitment of $40 million that the Kavli Foundation made to the national Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative, when it was first launched by President Obama in 2013. The funds are also unrestricted, allowing each institute to determine which projects to pursue. “That’s the most precious money any scientist can have,” Robert Conn, president and CEO of The Kavli Foundation, noted at a meeting today on Capitol Hill. Neuroscientist Loren Frank, who will serve as co-director at the new institute at the University of California, San Francisco, says the funds will allow his lab to explore fundamental questions such as how the brain can maintain its function despite constant change, and to form interdisciplinary partnerships with labs such as the Lawrence Livermore National Laboratory. The other two sites creating new institutes are Johns Hopkins University in Baltimore, Maryland, and Rockefeller University in New York City. In addition, Kavli announced a $40 million boost for four of its existing neuroscience institutes, located at Yale University, UC San Diego, Columbia University, and the Norwegian University of Science and Technology. © 2015 American Association for the Advancement of Science.
Keyword: Brain imaging
Link ID: 21471 - Posted: 10.03.2015
By Steve Mirsky Harvard neuroscientist Beth Stevens, talking about glia cells, which make up more than half the human brain. This week Stevens got a MacArthur Fellowship, the so-called genius grant, for her studies of glia. “These cells are incredibly responsive to damage or injury. They can protect our brain by, for example, clearing bacteria or debris in the brain in the case of injury and disease… “Until about 10 years ago, almost all of the research devoted to these cells was in these contexts. We discovered that there was another role for these cells in the normal healthy brain, in particular during development… “So a synapse is the junction of communication between two neurons, it’s how neurons talk to each other…we’re actually born with an excess of synaptic connections…and through this normal developmental process called pruning, a large number of these extra synapses get permanently removed or eliminated while others get strengthened and maintained. These microglial cells were in fact engulfing or eating these extra synapses. So these cells are necessary to do this and now of course we’re trying to better understand how it is that they know which synapse to prune and which synapse to leave alone. “A hallmark of many neurodegenerative diseases, including Alzheimer’s disease, is the early loss of synaptic connections or synapses…And what’s most striking about this is, it’s thought that the synapse loss happens years before you see signs of cognitive impairment or pathology. © 2015 Scientific American