By JULIE CRESWELL RALEIGH, N.C. — As darkness fell on a Friday evening over downtown Raleigh, N.C., Michael Lyons, a paramedic supervisor for Wake County Emergency Medical Services, slowly approached the tall, lanky man who was swaying back and forth in a gentle rhythm. In answer to Mr. Lyons’s questions, the man, wearing a red shirt that dwarfed his thin frame, said he was bipolar, schizophrenic and homeless. He was looking for help because he did not think his prescribed medication was working. In the past, paramedics would have taken the man to the closest hospital emergency room — most likely the nearby WakeMed Health and Hospitals, one of the largest centers in the region. But instead, under a pilot program, paramedics ushered him through the doors of Holly Hill Hospital, a commercial psychiatric facility. “He doesn’t have a medical complaint, he’s just a mental health patient living on the street who is looking for some help,” said Mr. Lyons, pulling his van back into traffic. “The good news is that he’s not going to an E.R. That’s saving the hospital money and getting the patient to the most appropriate place for him,” he added. The experiment in Raleigh is being closely watched by other cities desperate to find a way to help mentally ill patients without admitting them to emergency rooms, where the cost of treatment is high — and unnecessary. While there is evidence that other types of health care costs might be declining slightly, the cost of emergency room care for the mentally ill shows no sign of ebbing. Nationally, more than 6.4 million visits to emergency rooms in 2010, or about 5 percent of total visits, involved patients whose primary diagnosis was a mental health condition or substance abuse. That is up 28 percent from just four years earlier, according to the latest figures available from the Agency for Healthcare Research and Quality in Rockville, Md. By one federal estimate, spending by general hospitals to care for these patients is expected to nearly double to $38.5 billion in 2014, from $20.3 billion in 2003. © 2013 The New York Times Company

Keyword: Schizophrenia
Link ID: 19071 - Posted: 12.27.2013

By KEN BELSON Revelations in recent years that thousands of former football players might have severe brain trauma from injuries sustained on the field have set off a rush in the medical community to seize the potentially lucrative market for assessing brain damage. But experts say claims regarding the validity of these assessments are premature and perhaps unfounded. Most researchers believe that C.T.E., or chronic traumatic encephalopathy, the degenerative brain disease found in dozens of former N.F.L. players, can be diagnosed only posthumously by analyzing brain tissue. Researchers at U.C.L.A. have developed a test they assert might identify the condition in a living person by injecting a compound that clings to proteins in the brain and later appears in a PET scan. But some are skeptical. “There has really been so much hype surrounding C.T.E., so there is a real need for making sure the public knows that this type of science moves slowly and must move very carefully,” said Robert Stern, a professor of neurology and neurosurgery at Boston University School of Medicine and a founder of the Center for the Study of Traumatic Encephalopathy. He is part of a group that is developing a different biomarker to identify tau, the protein that is a hallmark of C.T.E. “My fear is the people out there who are so much in need, scared for their lives and desperate for information, it might give them false hope,” he said. The debate over the scientific validity of such brain exams was highlighted recently when Tony Dorsett, a Hall of Fame running back for the Dallas Cowboys, and several other prominent former players said they were found to have C.T.E. after taking the experimental test developed by U.C.L.A. Dorsett, 59, told CNN that “they came to find out I have C.T.E.” and that his memory lapses, short temper and moodiness were “all because of C.T.E.” Despite what was widely reported as a diagnosis, the experimental test is perhaps years from gaining federal approval. An antidote is even more remote because C.T.E. is a degenerative condition with no known cure. That is why neurologists, researchers and bioethicists question whether the doctors at U.C.L.A. and at TauMark, the company with the exclusive license to commercialize the test, may leave some former players and their families with false hopes or undue worry. © 2013 The New York Times Company

Keyword: Brain Injury/Concussion
Link ID: 19070 - Posted: 12.27.2013

By Sandra G. Boodman, Bebe Bahnsen remembers the night, alone in her small cottage on the Alabama coast, that she felt a strong urge to drink a can of drain cleaner. For years, antidepressants combined with talk therapy had enabled Bahnsen, whose first name is Beatrice, to function well, establishing a thriving public relations business in Washington followed by a career as a newspaper reporter. But those days had been supplanted by a prolonged suicidal depression that had proved impervious to electroshock treatments, periodic hospitalizations and a raft of psychiatric drugs. The phone call in which Bahnsen confided her desire to drink poison seemed to confirm the worst fears of one of her closest friends. “I figured, well, she was one of those people who just was not ever going to get better,” said Paddy Bowman, a folklore specialist who lives in Alexandria. Bahnsen, now 73, traces the beginning of her psychological slide to the mid-1990s, when she decided that, after two decades, she’d had enough of Washington. She moved back to her home state of Georgia and her life slowly began to unravel. She felt estranged from her large and devoted circle of friends, began having problems at work, and grew restless and increasingly depressed. “I felt as though I was on a large island and everyone was slowly moving away and I was there by myself,” Bahnsen recalled. For the first time in her life, she said, she was intermittently psychotic. Periodic suicide attempts, some involving overdoses of prescribed sleeping pills, landed her in a series of mental hospitals. In November 2006 she was hospitalized in Las Vegas, where she was then living with one of her sons. Doctors, baffled by her longstanding failure to improve, decided to take a closer look at her case. What they found resulted in an entirely different treatment, one that had a rapid and dramatic effect on her mental state. © 1996-2013 The Washington Post

Keyword: Depression; Alzheimers
Link ID: 19069 - Posted: 12.24.2013

By RICHARD A. FRIEDMAN, M.D. When will we ever get depression under control? Of all the major illnesses, mental or physical, depression has been one of the toughest to subdue. Despite the ubiquity of antidepressant drugs — there are now 26 to choose from — only a third of patients with major depression will experience a full remission after the first round of treatment, and successive treatments with different drugs will give some relief to just 20 to 25 percent more. About 30 percent of people with depression have some degree of treatment resistance. And the greater the degree of resistance, the more likely a future relapse, even if the patient continues taking the drug. Although we have learned much about depression — for example, the recent research showing that the successful treatment of insomnia in depressed patients essentially doubles their response to a drug like Prozac — we still don’t understand its fundamental cause. The old idea that the disease results from a deficiency of a single neurotransmitter like serotonin or dopamine is clearly simplistic and wrong. Maybe psychiatrists and neuroscientists have something to learn from the successful hunt for the Higgs boson. Of course a debilitating disease has nothing in common with a subatomic particle, except that both are mysterious and elusive. But it was those very qualities that inspired international teams of physicists to work together for years until they finally identified the boson last year. Among biomedical scientists, who compete for the same research dollars and want to be first across the finish line with an important finding, such cooperation is hardly the norm. But there are signs that this is changing. Not long ago, I sat in at a meeting of the Hope for Depression Research Foundation. Audrey Gruss, the knowledgeable and energetic philanthropist who started the foundation, has corralled a group of senior basic and clinical neuroscientists to look for solutions. (It is not the first to try a collaborative approach; others are being sponsored by the MacArthur Foundation and the Pritzker Consortium.) Copyright 2013 The New York Times Company

Keyword: Depression
Link ID: 19068 - Posted: 12.24.2013

By Regina Harrell and Pulse, I am a primary-care doctor who makes house calls in and around Tuscaloosa, Ala. Today my rounds start at a house located down a dirt road a few miles outside town. Gingerly, I cross the front walk; Mrs. Edgars told me that she killed a rattlesnake in her flowerbed last year. She is at the door, expecting my visit. Mr. Edgars sits on the couch, unable to recall that I am his doctor, or even that I am a doctor, but happy to see me nonetheless. We chat about the spring garden and the rain, then we move on to Mr. Edgars’s arthritis. Earlier on in his dementia, he wandered the woods, and his wife was afraid he would get lost and die, although the entire family agreed that this was how he would want it. Now, in a strange twist, his knee arthritis has worsened enough that it has curtailed his wanderings. I suspect that Mrs. Edgars is undertreating the pain to decrease the chance that he’ll wander off again. We talk about how anxious he grows whenever she’s out of his sight and how one of his children comes to sit with him so that she can run errands. She shows me a quilt remnant found in a log cabin on their property; it likely belonged to her husband’s grandfather, making the rough-edged fabric about a century old. I leave carrying a parting gift from her — a jar of homegrown pickled okra. When I get back to the office, I turn on the computer to write a progress note in Mr. Edgars’s electronic health record, or EHR. In addition to recording the details of our visit, I must try to meet the new federal criteria for “meaningful use,” criteria that have been adopted by my office with threats that I won’t get paid for my work if I don’t. © 1996-2013 The Washington Post

Keyword: Alzheimers
Link ID: 19067 - Posted: 12.24.2013

By Melissa Hogenboom Science reporter, BBC News An analysis of a Neanderthal's fossilised hyoid bone - a horseshoe-shaped structure in the neck - suggests the species had the ability to speak. This has been suspected since the 1989 discovery of a Neanderthal hyoid that looks just like a modern human's. But now computer modelling of how it works has shown this bone was also used in a very similar way. Writing in journal Plos One, scientists say its study is "highly suggestive" of complex speech in Neanderthals. The hyoid bone is crucial for speaking as it supports the root of the tongue. In non-human primates, it is not placed in the right position to vocalise like humans. An international team of researchers analysed a fossil Neanderthal throat bone using 3D x-ray imaging and mechanical modelling. This model allowed the group to see how the hyoid behaved in relation to the other surrounding bones. Stephen Wroe, from the University of New England, Armidale, NSW, Australia, said: "We would argue that this is a very significant step forward. It shows that the Kebara 2 hyoid doesn't just look like those of modern humans - it was used in a very similar way." He told BBC News that it not only changed our understanding of Neanderthals, but also of ourselves. "Many would argue that our capacity for speech and language is among the most fundamental of characteristics that make us human. If Neanderthals also had language then they were truly human, too." BBC © 2013

Keyword: Evolution; Language
Link ID: 19066 - Posted: 12.24.2013

Helen Shen The ability to erase memory may jump from the realm of film fantasy (such as Eternal Sunshine of the Spotless Mind, shown here) to reality. In the film Eternal Sunshine of the Spotless Mind, unhappy lovers undergo an experimental brain treatment to erase all memories of each other from their minds. No such fix exists for real-life couples, but researchers report today in Nature Neuroscience that a targeted medical intervention helps to reduce specific negative memories in patients who are depressed1. "This is one time I would say that science is better than art," says Karim Nader, a neuroscientist at McGill University in Montreal, Canada, who was not involved in the research. "It's a very clever study." The technique, called electroconvulsive (ECT) or electroshock therapy, induces seizures by passing current into the brain through electrode pads placed on the scalp. Despite its sometimes negative reputation, ECT is an effective last-resort treatment for severe depression, and is used today in combination with anaesthesia and muscle relaxants. Marijn Kroes, a neuroscientist at Radboud University Nijmegen in the Netherlands, and his colleagues found that by strategically timing ECT bursts, they could target and disrupt patients' memory of a disturbing episode. A matter of time The strategy relies on a theory called memory reconsolidation, which proposes that memories are taken out of 'mental storage' each time they are accessed and 're-written' over time back onto the brain's circuits. Results from animal studies and limited evidence in humans suggest that during reconsolidation, memories are vulnerable to alteration or even erasure2–4. © 2013 Nature Publishing Group

Keyword: Learning & Memory; Stress
Link ID: 19065 - Posted: 12.23.2013

By MICHAEL LUO and MIKE McINTIRE Last April, workers at Middlesex Hospital in Connecticut called the police to report that a psychiatric patient named Mark Russo had threatened to shoot his mother if officers tried to take the 18 rifles and shotguns he kept at her house. Mr. Russo, who was off his medication for paranoid schizophrenia, also talked about the recent elementary school massacre in Newtown and told a nurse that he “could take a chair and kill you or bash your head in between the eyes,” court records show. The police seized the firearms, as well as seven high-capacity magazines, but Mr. Russo, 55, was eventually allowed to return to the trailer in Middletown where he lives alone. In an interview there recently, he denied that he had schizophrenia but said he was taking his medication now — though only “the smallest dose,” because he is forced to. His hospitalization, he explained, stemmed from a misunderstanding: Seeking a message from God on whether to dissociate himself from his family, he had stabbed a basketball and waited for it to reinflate itself. When it did, he told relatives they would not be seeing him again, prompting them to call the police. As for his guns, Mr. Russo is scheduled to get them back in the spring, as mandated by Connecticut law. “I don’t think they ever should have been taken out of my house,” he said. “I plan to get all my guns and ammo and knives back in April.” The Russo case highlights a central, unresolved issue in the debate over balancing public safety and the Second Amendment right to bear arms: just how powerless law enforcement can be when it comes to keeping firearms out of the hands of people who are mentally ill. Connecticut’s law giving the police broad leeway to seize and hold guns for up to a year is actually relatively strict. Most states simply adhere to the federal standard, banning gun possession only after someone is involuntarily committed to a psychiatric facility or designated as mentally ill or incompetent after a court proceeding or other formal legal process. Relatively few with mental health issues, even serious ones, reach this point. © 2013 The New York Times Company

Keyword: Aggression; Schizophrenia
Link ID: 19064 - Posted: 12.23.2013

By Elijah Wolfson Of the many ills that can befall the human body, brain damage is one of the most devastating – and confusing. When a person suffers from a traumatic brain injury that leaves him or her in an uncommunicative state, doctors and loved ones face one of medical science’s most confounding questions: How do we know when a person is still there? When is a body just a body? Those question only get more complicated with the startling news that the brains of some patients in a vegetative state appear to recognize familiar faces. The implications are mind-boggling. Brain death – when there is zero brain function – is both a medical and legal term, and it is, quite literally, death. But when there is some brain function left, the lines blur rather quickly. A brain-damaged patient may live for months and even years, in limbo: her eyes may open and she may sleep and wake up in what appears to be a normal cycle, but she has no meaningful interactions and shows no awareness of her surroundings – or herself. She is in what the medical community calls a “persistent vegetative state,” awake but unaware. It’s unlikely that she will ever recover, and if she does, she will probably face severe physical and neurological impairments. Not what most of us call living. Someone in a vegetative state raises an essential moral and ethical question and an often bitter debate: How much should we do to keep a body on autopilot going? The debate has intensified in recent years, as a few studies have found striking examples of vegetative patients who seem to be able, on some level, to communicate. “With changing paradigms of imaging and other techniques,” Dr. Karen Hirsch, a neurologist and neurosurgeon at the Stanford University Medical Center, told Newsweek, “we are learning that maybe some of these people do have some awareness.” © 2013 IBT MEDIA INC

Keyword: Consciousness
Link ID: 19063 - Posted: 12.23.2013

By Alexandra Sifferlin It’s always been conventional wisdom that girls reach maturity more quickly than boys, but now scientists have provided some proof. In new research published in the journal Cerebral Cortex, an international group of researchers led by a team from Newcastle University in England found that girls’ brains march through the reorganization and pruning typical of normal brain development earlier than boys’ brains. In the study, in which 121 people between ages 4 to 40 were scanned using MRIs, the scientists documented the ebb and flow of new neural connections, and found that some brain fibers that bridged far-flung regions of the brain tended to remain stable, while shorter connections, many of which were redundant, were edited away. And the entire reorganization seemed to occur sooner in girls’ brains than in boys’ brains. Females also tended to have more connections across the two hemispheres of the brain. The researchers believe that the earlier reorganization in girls makes the brain work more efficiently, and therefore reach a more mature state for processing the environment. What drives the gender-based difference in timing isn’t clear from the current study, but the results suggest that may be a question worth investigating. © 2013 Time Inc.

Keyword: Development of the Brain; Sexual Behavior
Link ID: 19062 - Posted: 12.23.2013

By Gary Stix Is sleep good for everything? Scientists hate giving unqualified answers. But the more sleep researchers look, the more the answer seems to be tending toward a resounding affirmative. The slumbering brain plays an essential role in learning and memory, one of the findings that sleep researchers have reinforced repeatedly in recent years. But that’s not all. There’s a growing recognition that sleep appears to be involved in regulating basic metabolic processes and even in mental health. Robert Stickgold, a leading sleep researcher based at Harvard Medical School, gives a précis here of the current state of sommeil as it relates to memory, schizophrenia, depression, diabetes—and he even explains what naps are good for. How far have we come in understanding sleep? Although we understood the function of every other basic drive 2,000 years ago, we are still struggling to figure out what the biological functions of sleep are. One of the clearest messages now is that for every two hours humans spend awake during the day, the brain needs an hour offline to process the information it takes in and figure out what to save and what to dump and how to file and what it all means. So what is sleep for? Memories are processed during sleep. But sleep doesn’t have just one function. It’s a little bit like listening to tongue researchers arguing about whether the function of the tongue has to do with taste or speech. And you want to say: ‘Guys, c’mon, it’s both.’ There’s very good evidence now that sleep, besides helping memory, has a role in immune and endocrine functions. There’s a lot of talk about to what extent the obesity epidemic is actually a consequence of too little sleep. © 2013 Scientific American

Keyword: Sleep; Obesity
Link ID: 19061 - Posted: 12.21.2013

Don’t worry about watching all those cat videos on the Internet. You’re not wasting time when you are at your computer—you’re honing your fine-motor skills. A study of people’s ability to translate training that involves clicking and twiddling a computer mouse reveals that the brain can apply that expertise to other fine-motor tasks requiring the hands. We know that computers are altering the way that people think. For example, using the Internet changes the way that you remember information. But what about use of the computer itself? You probably got to this story by using a computer mouse, for example, and that is a bizarre task compared with the activities that we’ve encountered in our evolutionary history. You made tiny movements of your hand in a horizontal plane to cause tiny movements of a cursor in a completely disconnected vertical plane. But with daily practice—the average computer user makes more than 1000 mouse clicks per day—you have become such an expert that you don’t even think about this amazing feat of dexterity. Scientists would love to know if that practice affects other aspects of your brain’s control of your body. The problem is finding people with no computer experience. So Konrad Kording, a psychologist at Northwestern University’s Rehabilitation Institute of Chicago in Illinois, and his former postdoc Kunlin Wei, now at Peking University in Beijing, turned to migrant Chinese workers. The country’s vast population covers the whole socioeconomic spectrum, from elite computer hackers to agricultural laborers whose lifestyles have changed little over the past century. The country’s economic boom is bringing people in waves from the countryside to cities in search of employment. © 2013 American Association for the Advancement of Science

Keyword: Learning & Memory
Link ID: 19060 - Posted: 12.21.2013

By JAN HOFFMAN Just in time to protect patients from the dangers of holiday cheer, a new scholarly review from a British medical journal describes many harmful effects wrought by laughter. Among the alarms it sounds: The force of laughing can dislocate jaws, prompt asthma attacks, cause headaches, make hernias protrude. It can provoke cardiac arrhythmia, syncope or even emphysema (this last, according to a clinical lecturer in 1892). Laughter can trigger the rare but possibly grievous Pilgaard-Dahl and Boerhaave’s syndromes (see explanation below). And ponder, briefly, the mortifying impact of sustained laughter on the urinary tract (detailed in a 1982 The Lancet paper entitled “Giggle Incontinence”). At the very least, the new review could be considered an affirmation for the perpetually dour. If 2013 was the year of the worried well, the authors imply that 2014 is poised to be the year of the humorless healthy. The analysis, “Laughter and MIRTH (Methodical Investigation of Risibility, Therapeutic and Harmful),” was drawn from about 5,000 studies. It appears in BMJ, formerly known as The British Medical Journal, which for more than 30 years has traditionally featured rigorously researched but lighthearted articles in its Christmas issue. A deputy editor, Dr. Tony Delamothe, said that the MIRTH study was indeed peer-reviewed — presumably by a doctor with a carefully managed sense or humor (or humour). This year, companion studies in the issue include “Were James Bond’s drinks shaken because of alcohol induced tremor?” , “The survival time of chocolates on hospital wards: covert observational study,” and “Operating room safety: the 10 point plan to safe flinging” (among the cautions: “Before flinging, identify your target and the area beyond it” and “Never fling an instrument straight up into the air”). Copyright 2013 The New York Times Company

Keyword: Emotions
Link ID: 19059 - Posted: 12.21.2013

By Felicity Muth This might seem perplexing to some, but I’ve just spent two days listening to talks and meeting with people who all work on social insects. And it was great. I was at Royal Holloway, University of London, where the IUSSI meeting was taking place. The IUSSI is the ‘International Union for the Study of Social Insects’, although they seem to let people in who work on social spiders too (a nice inclusive attitude if you ask me). This meeting was specifically for researchers who are in the UK and North-West Europe, of which there are a surprisingly large number. The talks were really good, sharing a lot of the recent research that’s happened using social insects, and I thought I’d share my highlight of first day’s events here. One of my favourite talks from the first day was from Elli Leadbeater who spoke about work carried out primarily by Erika Dawson. I’ve written before about ‘social learning’ in monkeys and whales, where one animal can learn something from observing another animal, normally of the same species. Dawson and her colleagues were looking specifically at whether there is actually anything ‘social’ about ‘social learning’, or whether it can be explained with the same mechanism as other types of learning. In the simplest form of learning, associative learning, an animal learns to associate a particular stimulus (for example a particular colour, smell or sound) with a reward (usually food). The classic example of this was Pavlov’s dogs, who learned to associate the sound of a metronome with food. When Pavlov then sounded the metronome, the dogs salivated even when there was no food present. © 2013 Scientific American

Keyword: Learning & Memory
Link ID: 19058 - Posted: 12.21.2013

By Deborah Kotz / Globe Staff Anyone who hears about the tragic death of a 13-year-old California girl after a routine tonsil-removal surgery has to feel for the grieving parents who don’t want her removed from life support. The McMaths refuse to believe that their daughter Jahi, who was declared brain dead more than a week ago, is truly dead because machines are keeping her other organs alive. “How could you not let me have my kid for Christmas?” said Nailah Winkfield, McMath’s mother, in an interview with local reporters. “And this is Children’s Hospital, supposed to be so compassionate, so loving, and I asked, can my daughter just live a few more days? Because she is living.” McMath was declared brain dead more than a week ago, and her family has been fighting with hospital staff at Children’s Hospital & Research Center in Oakland to keep her body in a viable state and have her provided with nutrition via a feeding tube. “To me, it just looks like she’s at peace and she’s resting,” said Jahi’s uncle Omari Sealey, “and when she’s done going through the traumatic stuff that her body’s going through right now, and she feels well enough, she’ll wake up.” But McMath is dead—as horrible as that is for her family to fathom—and leaving her body attached to machines is akin to allowing a corpse remain in a hospital bed without a proper burial. Perhaps hospitals should stop calling such care “life support” since it’s not actually supporting any living person, just a body. “This case is so sad it is almost beyond description,” wrote Arthur Caplan, head of the division of medical ethics at NYU Langone Medical Center in a blog he posted Thursday on the NBC News website. “But that fact should not be a reason to take the view that we don’t know what to do when someone is pronounced brain dead. Brain dead is dead.” © 2013 Boston Globe Media Partners, LLC

Keyword: Consciousness
Link ID: 19057 - Posted: 12.21.2013

// by Megan Gannon, Live Science News Editor Bonobos have a reputation among the great apes as "hippie chimps," and new research hints that high levels of a key thyroid hormone may play a role in keeping the animals' aggression in check. Found in the lowland forests of the Democratic Republic of the Congo, bonobos (Pan troglodytes) are closely related to chimpanzees (Pan troglodytes) but the two diverge in behavior. Bonobos seem to diffuse social tension with an impressive repertoire of sex acts rather than physical fights. Males in particular show low levels of aggression — they even maintain platonic friendships with females and stick by their mothers into adulthood. The life of male chimpanzees, meanwhile, revolves around climbing the social ladder (or at least hanging onto their current rung), and navigating cooperative and aggressive relationships with other males. [8 Humanlike Behaviors of Primates] Scientists recently found another big difference between the two Pan species: A key thyroid hormone decreases at a much later age in bonobos compared with chimps. For their study, scientists took urine samples from about 100 chimpanzees and 96 bonobos living in zoos. The researchers specifically looked at the apes' levels of triiodothyronine (T3), a hormone in the thyroid gland that is crucial for development in all vertebrates (animals with backbones). © 2013 Discovery Communications, LLC

Keyword: Hormones & Behavior; Aggression
Link ID: 19056 - Posted: 12.21.2013

Ed Yong As the H1N1 swine flu pandemic swept the world in 2009, China saw a spike in cases of narcolepsy — a mysterious disorder that involves sudden, uncontrollable sleepiness. Meanwhile, in Europe, around 1 in 15,000 children who were given Pandemrix — a now-defunct flu vaccine that contained fragments of the pandemic virus — also developed narcolepsy, a chronic disease. Immunologist Elizabeth Mellins and narcolepsy researcher Emmanuel Mignot at Stanford University School of Medicine in California and their collaborators have now partly solved the mystery behind these events, while also confirming a longstanding hypothesis that narcolepsy is an autoimmune disease, in which the immune system attacks healthy cells. Narcolepsy is mostly caused by the gradual loss of neurons that produce hypocretin, a hormone that keeps us awake. Many scientists had suspected that the immune system was responsible, but the Stanford team has found the first direct evidence: a special group of CD4+ T cells (a type of immune cell) that targets hypocretin and is found only in people with narcolepsy. “Up till now, the idea that narcolepsy was an autoimmune disorder was a very compelling hypothesis, but this is the first direct evidence of autoimmunity,” says Mellins. “I think these cells are a smoking gun.” The study is published today in Science Translational Medicine1. Thomas Scammell, a neurologist at Harvard Medical School in Boston, Massachusetts, says that the results are welcome after “years of modest disappointment”, marked by many failures to find antibodies made by a person's body against their own hypocretin. “It’s one of the biggest things to happen in the narcolepsy field for some time.” It is not clear why some people make these T cells and others do not, but genetics may play a part. In earlier work2, Mignot showed that 98% of people with narcolepsy have a variant of the gene HLA that is found in only 25% of the general population. © 2013 Nature Publishing Group

Keyword: Narcolepsy; Neuroimmunology
Link ID: 19055 - Posted: 12.19.2013

by Ashley Yeager With a little help from implanted electrodes, Parkinson's patients make fewer driving errors, at least on a computer. When steering a simulator, patients with active brain stimulators averaged 3.8 driving errors, compared with 7.5 for healthy people and 11.4 for those with Parkinson's disease who did not have implants. The Parkinson’s patients’ driving skills were also more accurate when receiving deep brain stimulation than when taking levodopa, a common treatment for the disease, researchers report December 18 in Neurology. © Society for Science & the Public 2000 - 2013

Keyword: Parkinsons
Link ID: 19054 - Posted: 12.19.2013

Amanda Mascarelli In children with certain gene variants, symptoms similar to common learning disabilities could be omens of serious psychiatric conditions. People who carry high-risk genetic variants for schizophrenia and autism have impairments reminiscent of disorders such as dyslexia, even when they do not yet have a mental illness, a new study has found. The findings offer a window into the brain changes that precede severe mental illness and hold promise for early intervention and even prevention, researchers say. Rare genetic alterations called copy number variants (CNVs), in which certain segments of the genome have an abnormal number of copies, play an important part in psychiatric disorders: Individuals who carry certain CNVs have a several-fold increased risk of developing schizophrenia or autism1. But previous studies were based on individuals who already have a psychiatric disorder, and until now, no one had looked at what effects these CNVs have in the general population. In a study published today in Nature2, researchers report that people with these variants but no diagnosis of autism or a mental illness still show subtle brain changes and impairments in cognitive function. “In psychiatry we always have the problem that disorders are defined by symptoms that patients experience or tell us about, or that we observe,” says study co-author Andreas Meyer-Lindenberg, a psychiatrist and the director the Central Institute of Mental Health in Mannheim, Germany, affiliated with the University of Heidelberg. This work, on the other hand, provides a glimpse into the biological underpinnings of people who are at risk of psychiatric disorders, he says. The team searched a genealogical database of more than 100,000 Icelanders, focusing on 26 genetic variants that have been shown to increase the risk of schizophrenia or autism. They found that 1,178 people in the database, or 1.16% of the sample, carried one or more of these CNVs. © 2013 Nature Publishing Group

Keyword: Schizophrenia; Autism
Link ID: 19053 - Posted: 12.19.2013

By GRETCHEN REYNOLDS A remarkable recent experiment allowed scientists to see inside the skull and brain of animals that had just experienced a concussion, providing sobering new evidence of how damaging even minor brain impacts can be. While the results, which were published in Nature, are worrisome, they also hint at the possibility of treating concussions and lessening their harm. Concussions occur when the brain bounces against the skull after someone’s head is bumped or jolted. Such injuries are fairly common in contact sports, like football and hockey, and there is growing concern that repeated concussions might contribute to lingering problems with thinking or memory. This concern was heightened this week by reports that the brain of the late major league baseball player Ryan Freel showed symptoms of chronic traumatic encephalopathy, a degenerative condition. He reportedly had been hit in the head multiple times during his career. But scientists did not know exactly what happens at a molecular level inside the brain during and after a concussion. The living brain is notoriously difficult to study, since it shelters behind the thick, bony skull and other protective barriers. In some earlier studies, scientists had removed portions of lab animals’ skulls to view what happened to their brains during subsequent impacts. But removing part of the skull causes its own tissue damage and physiological response, muddying any findings about how the brain is affected by concussions. So scientists at the National Institute of Neurological Disorders and Stroke, a division of the National Institutes of Health, decided to develop a less destructive means of seeing inside skulls and came up with the deceptively simple method of shaving away microscopic layers of a lab mouse’s skull, thinning it to the point that powerful microscopic lenses could see through it, even as the skull remained essentially intact. Copyright 2013 The New York Times Company

Keyword: Brain Injury/Concussion
Link ID: 19052 - Posted: 12.18.2013