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

Keyword: Consciousness
Link ID: 22606 - Posted: 08.27.2016

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

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

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

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

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

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

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

Keyword: Stress
Link ID: 22599 - Posted: 08.25.2016

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

Keyword: Sleep
Link ID: 22598 - Posted: 08.25.2016

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

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

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

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

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

Keyword: Sleep
Link ID: 22591 - Posted: 08.24.2016

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

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

By Clare Wilson Taking a daily vitamin or mineral supplement is widely seen as a common-sense way of looking after yourself – a kind of insurance, like wearing a seat belt. But evidence is growing that it might not be such a healthy habit after all. The latest finding is that calcium supplements, taken by many women after the menopause to strengthen their bones, are linked to dementia. Among women who have had a stroke, taking calcium was associated with a seven-fold rise in the number who went on to have dementia. Calcium was also linked with a smaller, non-statistically significant, rise in dementia in women who had not had a stroke. The finding emerged from a study that was not a randomised trial, so it is not the most robust type of medical evidence. The researchers merely counted dementia cases in people who had chosen whether to take calcium, and so the data could be biased. But the results are striking and come on the heels of a previous study that was a randomised trial, which found a link between calcium supplements and a modestly higher risk of heart attacks – suggesting that caution over calcium is indeed warranted. If future research confirms the association with dementia, women would face a horrible dilemma: should they continue to take calcium, staving off bone weakness that can lead to fatal hip fractures, while running an increased risk of one of the most dreaded illness of ageing? So what’s going on? Team member Silke Kern at the Sahlgrenska Academy Institute of Neuroscience and Physiology in Gothenburg, Sweden, says that taking a calcium pill triggers a rapid surge in the mineral’s levels in the blood, one that you wouldn’t get from calcium in food. © Copyright Reed Business Information Ltd.

Keyword: Alzheimers
Link ID: 22588 - Posted: 08.23.2016

By GINA KOLATA Shena Pearson nearly froze in her seat, terrified, as she stared at a power-point slide. She was at her first meeting of an epilepsy foundation, seeking help for her 12-year-old son Trysten, when a neurologist flashed the slide about something called Sudep. It stands for sudden unexpected death in epilepsy. Her son’s neurologist had never mentioned it. “Oh dear God, my child is at risk, seriously at risk,” Ms. Pearson thought to herself. Sudden death in epilepsy is a little-known and seldom-mentioned phenomenon, but now, after a push by advocates, the federal government has begun a concerted program to understand it. Yet a question remains: When, if ever, should patients be warned? In a way, the extreme reticence of many neurologists to mention sudden unexpected death to epilepsy patients harks back to the days when doctors and families often did not tell people they had cancer — too terrifying. But today, patients learn not just about cancer but about many other potentially fatal conditions, like an inoperable brain aneurysm that could burst at any time and kill a person. So the quiet about the epilepsy death risk appears to be an anomaly. Sudep’s name pretty much explains what it is: Someone with epilepsy — unprovoked seizures, which are electrical surges in the brain — dies, and there is no apparent cause. Often a person with epilepsy goes to bed and is found in the morning, unresponsive. In some cases, there is indirect evidence of a seizure, like urine on the sheets, bloodshot eyes or a severely bitten tongue, leading to the suggestion that preventing seizures as much as possible with medications could lower patients’ risks. But so much about the syndrome remains unknown. © 2016 The New York Times Company

Keyword: Epilepsy
Link ID: 22587 - Posted: 08.23.2016

By Daniel Barron After prepping for the day’s cases, “Mike Brennan,” a 63-year-old cardiology technician, sat down for his morning coffee and paper. On the front page, he discovered something troubling: he could no longer read. No matter how long he stared at a word, its meaning was lost on him. With a history of smoking and hypertension, he worried that he might have had a stroke. So, leaving his coffee, he walked himself down the hall to the emergency department, where neurologists performed a battery of tests to tease out what had happened. Mike still recognized individual letters and, with great difficulty, could sound out small words. But even some simple vocabulary presented problems, for example, he read “desk” as “dish” or “flame” as “thame.” Function words such as prepositions and pronouns gave him particular trouble. Mike couldn’t read, but there was nothing wrong with his eyes. Words heard were no problem. He could recognize colors, faces, and objects. He could speak, move, think and even write normally. Mike had “pure alexia,” meaning he could not read but showed no other impairments. An M.R.I. scan of Mike’s brain revealed a pea-sized stroke in his left inferior occipitotemporal cortex, a region on the brain’s surface just behind the left ear. © 2016 Scientific American

Keyword: Language
Link ID: 22586 - Posted: 08.23.2016

By Lydia Pyne | On August 3, 1908, the first near-complete Neanderthal skeleton was discovered in a cave near the village of La Chapelle-aux-Saints in south central France, during a survey of the region’s Paleolithic archaeological sites. For decades prior, prehistorians had collected bits and pieces of curious but not-quite-human fossils from museums and excavations alike—the odd skull here, a scrap of tooth there. In 1863, the mélange of bones was finally given its own species designation, Homo neanderthalensis. Forty-five years later, the La Chapelle discovery was the first Neanderthal specimen found in an original archaeological context and the first to be expertly excavated and carefully studied. Because the body was arranged in a flexed, fetal position and carefully placed in the floor of the cave, excavators argued that fossil—nicknamed the Old Man—had been purposefully buried by his Neanderthal contemporaries. More than any other single individual, the Old Man of La Chapelle has shaped the way that science and popular culture have thought about Neanderthals. But why? What is it about this Neanderthal’s story that is so special? In short, the Old Man was the right fossil found at the right time. He was—and still is—offered as a key bit of evidence in debates about evolution and human origins. He quickly became a scientific touchstone, an archetype for how science and popular culture create celebrity fossils. I explore the stories of similarly spectacular paleoanthropological finds in my new book Seven Skeletons: The Evolution of the World’s Most Famous Human Fossils. © 1986-2016 The Scientist

Keyword: Evolution
Link ID: 22585 - Posted: 08.23.2016

Laura Sanders Fractions of a second after food hits the mouth, a specialized group of energizing nerve cells in mice shuts down. After the eating stops, the nerve cells spring back into action, scientists report August 18 in Current Biology. This quick response to eating offers researchers new clues about how the brain drives appetite and may also provide insight into narcolepsy. These nerve cells have intrigued scientists for years. They produce a molecule called orexin (also known as hypocretin), thought to have a role in appetite. But their bigger claim to fame came when scientists found that these cells were largely missing from the brains of people with narcolepsy. People with narcolepsy are more likely to be overweight than other people, and this new study may help explain why, says neuroscientist Jerome Siegel of UCLA. These cells may have more subtle roles in regulating food intake in people without narcolepsy, he adds. Results from earlier studies hinted that orexin-producing nerve cells are appetite stimulators. But the new results suggest the opposite. These cells actually work to keep extra weight off. “Orexin cells are a natural obesity defense mechanism,” says study coauthor Denis Burdakov of the Francis Crick Institute in London. “If they are lost, animals and humans gain weight.” Mice were allowed to eat normally while researchers eavesdropped on the behavior of their orexin nerve cells. Within milliseconds of eating, orexin nerve cells shut down and stopped sending signals. |© Society for Science & the Public 2000 - 2016

Keyword: Obesity
Link ID: 22583 - Posted: 08.22.2016

By Andrea Anderson When we bed down in a new locale, our sleep often suffers. A recent study finds that this so-called first-night effect may be the result of partial wakefulness in one side of the brain—as if the brain is keeping watch. Researchers at Brown University and the Georgia Institute of Technology used neuroimaging and a brain wave–tracking approach called polysomnography to record activity in four brain networks in 11 individuals as they slept on two nights about a week apart. The subjects nodded off at their normal bedtimes, and their brain was scanned for about two hours—the length of a sleep cycle. As participants slept, right hemisphere regions showed consistent slow-wave activity regardless of the night. Yet average slow-wave activity was shallower in their left hemisphere during the first night—an asymmetry that was enhanced in those who took longer to fall asleep. The results, published in May in Current Biology, suggest systems in one side of the brain remain active as people venture into unfamiliar sleep situations—an apparent survival strategy reminiscent of the unihemispheric sleep reported in certain animals. Because the results represent just one sleep cycle, however, it is unclear whether the left side of the brain is always tasked with maintaining attentiveness, explains the study's senior author Yuka Sasaki, a cognitive, linguistic and psychological sciences researcher at Brown. It is possible the right hemisphere takes over guard dog duties at some point in the night. © 2016 Scientific American

Keyword: Sleep
Link ID: 22580 - Posted: 08.22.2016

By Diana Kwon When glial cells were discovered in the 1800s, they were thought to be passive, supporting structures—the “glue”—as their Greek name implies—that holds neurons together in the brain and throughout the nervous system. In recent years, however, neuroscientists have discovered that far from being passive, these small cells play an astonishing variety of roles in both the development and functioning of the brain. Some of the latest discoveries suggest that glia play complex roles in regulating appetite and metabolism, making them a possible target for treating obesity. Signs that glia might play such roles were first identified in the 1980s. Neuroscientist Pierre Magistretti and his colleagues found evidence that neurotransmitters could promote the release of glucose reserves stored in astrocytes, a star-shaped type of glial cell. Other studies revealed that obesity leads to increased activation of glial cells in the hypothalamus—the key area of the brain for controlling metabolic processes. This was despite the fact that, for a long time, “neurons were considered the only players in the control of energy metabolism,” says Cristina García-Cáceres, a neurobiologist at the Helmholtz Diabetes Center in Germany. Two recent studies add new evidence that glia play a key role in metabolism. In one study, published last week in Cell, García-Cáceres, together with Matthias Tschöp, the director of the Helmholtz Diabetes Center and colleagues, reported that insulin acts on astrocytes to regulate sugar intake in the brain. © 2016 Scientific American,

Keyword: Obesity; Glia
Link ID: 22578 - Posted: 08.20.2016

Researchers may have discovered a method of detecting changes in the eye which could identify Parkinson's disease before its symptoms develop. Scientists at University College London (UCL) say their early animal tests could lead to a cheap and non-invasive way to spot the disease. Parkinson's affects 1 in 500 people and is the second most common neurodegenerative disease worldwide. The charity Parkinson's UK welcomed the research as a "significant step". The researchers examined rats and found that changes could be seen at the back of their eyes before visible symptoms occurred. Professor Francesca Cordeiro who led the research said it was a "potentially revolutionary breakthrough in the early diagnosis and treatment of one of the world's most debilitating diseases". "These tests mean we might be able to intervene much earlier and more effectively treat people with this devastating condition." Symptoms of Parkinson's include tremors and muscle stiffness, slowness of movement and a reduced quality of life. These symptoms usually only emerge after brain cells have been damaged. But there is currently no brain scan, or blood test, that can definitively diagnose Parkinson's disease. Parkinson's does not directly cause people to die, but symptoms do get worse over time. © 2016 BBC

Keyword: Parkinsons
Link ID: 22577 - Posted: 08.20.2016

Meghan Rosen Zika may harm grown-up brains. The virus, which can cause brain damage in infants infected in the womb, kills stem cells and stunts their numbers in the brains of adult mice, researchers report August 18 in Cell Stem Cell. Though scientists have considered Zika primarily a threat to unborn babies, the new findings suggest that the virus may cause unknown — and potentially long-term — damage to adults as well. In adults, Zika has been linked to Guillain-Barré syndrome, a rare neurological disorder (SN: 4/2/16, p. 29). But for most people, infection is typically mild: a headache, fever and rash lasting up to a week, or no symptoms at all. In pregnant women, though, the virus can lodge in the brain of a fetus and kill off newly developing cells (SN: 4/13/16). If Zika targets newborn brain cells, adults may be at risk, too, reasoned neuroscientist Joseph Gleeson of Rockefeller University in New York City and colleagues. Parts of the forebrain and the hippocampus, which plays a crucial role in learning and memory, continue to generate nerve cells in adult brains. In mice infected with Zika, the virus hit these brain regions hard. Nerve cells died and the regions generated one-fifth to one-half as many new cells compared with those of uninfected mice. The results might not translate to humans; the mice were genetically engineered to have weak immune systems, making them susceptible to Zika. But Zika could potentially harm immunocompromised people and perhaps even healthy people in a similar way, the authors write. © Society for Science & the Public 2000 - 2016.

Keyword: Development of the Brain
Link ID: 22575 - Posted: 08.20.2016

By Jef Akst ANDRZEJ KRAUZEAs a psychiatrist at Western University in London, Ontario, Lena Palaniyappan regularly sees patients with schizophrenia, the chronic mental disorder that drastically affects how a person thinks, feels, and behaves. The disorder can be devastating, often involving hallucinations and delusions. But one thing Palaniyappan and other mental health professionals have noticed is that, unlike those with degenerative neurological disorders such as Alzheimer’s disease, Huntington’s, or Parkinson’s, sometimes schizophrenia patients eventually start to improve. “In the clinic we do actually see patients with schizophrenia having a very relentless progress in early years,” Palaniyappan says. “But a lot of them do get better over the years, or they don’t progress as [quickly].” So far, most research has focused on the neurological decline associated with schizophrenia—typically involving a loss of brain tissue. Palaniyappan and his colleagues wondered whether there might be “something happening in the brain [that] helps them come to a state of stability.” To get at this question, he and his colleagues performed MRI scans to assess the cortical thickness of 98 schizophrenia patients at various stages of illness. Sure enough, the researchers noted that, while patients who were less than two years removed from their diagnosis had significantly thinner tissue than healthy controls, those patients who’d had the disease for longer tended to show less deviation in some brain regions, suggesting some sort of cortical amelioration (Psychol Med, doi:10.1017/S0033291716000994, 2016). “Some brain regions are regaining or normalizing while other brain regions continue to show deficits,” Palaniyappan says. © 1986-2016 The Scientist

Keyword: Schizophrenia; Regeneration
Link ID: 22572 - Posted: 08.18.2016