Chapter 5. The Sensorimotor System
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By Eric Hand That many animals sense and respond to Earth’s magnetic field is no longer in doubt, and people, too, may have a magnetic sense. But how this sixth sense might work remains a mystery. Some researchers say it relies on an iron mineral, magnetite; others invoke a protein in the retina called cryptochrome. Magnetite has turned up in bird beaks and fish noses and even in the human brain, as Joe Kirschvink of the California Institute for Technology in Pasadena reported in 1992, and it is extremely sensitive to magnetic fields. As a result, Kirschvink and other fans say, it can tell an animal not only which way it is heading (compass sense) but also where it is. “A compass cannot explain how a sea turtle can migrate all the way around the ocean and return to the same specific stretch of beach where it started out,” says neurobiologist Kenneth Lohmann of the University of North Carolina, Chapel Hill. A compass sense is enough for an animal to figure out latitude, based on changes in the inclination of magnetic field lines (flat at the equator, plunging into the earth at the poles). But longitude requires detecting subtle variations in field strength from place to place—an extra map or signpost sense that magnetite could supply, Lohmann says. Except in bacteria, however, no one has seen magnetite crystals serving as a magnetic sensor. The crystals could be something else—say, waste products of iron metabolism, or a way for the body to sequester carcinogenic heavy metals. In the early 2000s, scientists found magnetite-bearing cells in the beaks of pigeons. But a follow-up study found that the supposed magnetoreceptors were in fact scavenger immune cells that had nothing to do with the neural system. And because there is no unique stain or marker for magnetite, false sightings are easy to make. © 2016 American Association for the Advancement of Science
Keyword: Pain & Touch
Link ID: 22357 - Posted: 06.24.2016
By Eric Hand Birds do it. Bees do it. But the human subject, standing here in a hoodie—can he do it? Joe Kirschvink is determined to find out. For decades, he has shown how critters across the animal kingdom navigate using magnetoreception, or a sense of Earth’s magnetic field. Now, the geophysicist at the California Institute of Technology (Caltech) in Pasadena is testing humans to see if they too have this subconscious sixth sense. Kirschvink is pretty sure they do. But he has to prove it. He takes out his iPhone and waves it over Keisuke Matsuda, a neuroengineering graduate student from the University of Tokyo. On this day in October, he is Kirschvink’s guinea pig. A magnetometer app on the phone would detect magnetic dust on Matsuda—or any hidden magnets that might foil the experiment. “I want to make sure we don’t have a cheater,” Kirschvink jokes. They are two floors underground at Caltech, in a clean room with magnetically shielded walls. In a corner, a liquid helium pump throbs and hisses, cooling a superconducting instrument that Kirschvink has used to measure tiny magnetic fields in everything from bird beaks to martian meteorites. On a lab bench lie knives—made of ceramic and soaked in acid to eliminate magnetic contamination—with which he has sliced up human brains in search of magnetic particles. Matsuda looks a little nervous, but he will not be going under the knife. With a syringe, a technician injects electrolyte gel onto Matsuda’s scalp through a skullcap studded with electrodes. He is about to be exposed to custom magnetic fields generated by an array of electrical coils, while an electroencephalogram (EEG) machine records his brain waves. © 2016 American Association for the Advancement of Science.
Keyword: Pain & Touch
Link ID: 22356 - Posted: 06.24.2016
Jon Hamilton Researchers have identified a substance in muscles that helps explain the connection between a fit body and a sharp mind. When muscles work, they release a protein that appears to generate new cells and connections in a part of the brain that is critical to memory, a team reports Thursday in the journal Cell Metabolism. The finding "provides another piece to the puzzle," says Henriette van Praag, an author of the study and an investigator in brain science at the National Institute on Aging. Previous research, she says, had revealed factors in the brain itself that responded to exercise. The discovery came after van Praag and a team of researchers decided to "cast a wide net" in searching for factors that could explain the well-known link between fitness and memory. They began by looking for substances produced by muscle cells in response to exercise. That search turned up cathepsin B, a protein best known for its association with cell death and some diseases. Experiments showed that blood levels of cathepsin B rose in mice that spent a lot of time on their exercise wheels. What's more, as levels of the protein rose, the mice did better on a memory test in which they had to swim to a platform hidden just beneath the surface of a small pool. The team also found evidence that, in mice, cathepsin B was causing the growth of new cells and connections in the hippocampus, an area of the brain that is central to memory. But the researchers needed to know whether the substance worked the same way in other species. So they tested monkeys, and found that exercise did, indeed, raise circulating levels of cathepsin in the blood. © 2016 npr
By BARRY MEIER and ABBY GOODNOUGH A few months ago, Douglas Scott, a property manager in Jacksonville, Fla., was taking large doses of narcotic drugs, or opioids, to deal with the pain of back and spine injuries from two recent car accidents. The pills helped ease his pain, but they also caused him to withdraw from his wife, his two children and social life. “Finally, my wife said, ‘You do something about this or we’re going to have to make some changes around here,’” said Mr. Scott, 43. Today, Mr. Scott is no longer taking narcotics and feels better. Shortly after his wife’s ultimatum, he entered a local clinic where patients are weaned off opioids and spend up to five weeks going through six hours of training each day in alternative pain management techniques such as physical therapy, relaxation exercises and behavior modification. Mr. Scott’s story highlights one patient’s success. Yet it also underscores the difficulties that the Obama administration and public health officials face in reducing the widespread use of painkillers like OxyContin and Percocet. The use and abuse of the drugs has led to a national epidemic of overdose deaths, addiction and poor patient outcomes. In recent months, federal agencies and state health officials have urged doctors to first treat pain without using opioids, and some have announced plans to restrict how many pain pills a doctor can prescribe. But getting the millions of people with chronic pain to turn to alternative treatments is a daunting task, one that must overcome inconsistent insurance coverage as well as some resistance from patients and their doctors, who know the ease and effectiveness of pain medications. “We are all culpable,” said Dr. David Deitz, a former insurance industry executive and a consultant on pain treatment issues. “I don’t care whether you are a doctor, an insurer or a patient.” © 2016 The New York Times Compan
Keyword: Pain & Touch
Link ID: 22352 - Posted: 06.23.2016
Megan Scudellari Shinya Yamanaka looked up in surprise at the postdoc who had spoken. “We have colonies,” Kazutoshi Takahashi said again. Yamanaka jumped from his desk and followed Takahashi to their tissue-culture room, at Kyoto University in Japan. Under a microscope, they saw tiny clusters of cells — the culmination of five years of work and an achievement that Yamanaka hadn't even been sure was possible. Two weeks earlier, Takahashi had taken skin cells from adult mice and infected them with a virus designed to introduce 24 carefully chosen genes. Now, the cells had been transformed. They looked and behaved like embryonic stem (ES) cells — 'pluripotent' cells, with the ability to develop into skin, nerve, muscle or practically any other cell type. Yamanaka gazed at the cellular alchemy before him. “At that moment, I thought, 'This must be some kind of mistake',” he recalls. He asked Takahashi to perform the experiment again — and again. Each time, it worked. Over the next two months, Takahashi narrowed down the genes to just four that were needed to wind back the developmental clock. In June 2006, Yamanaka presented the results to a stunned room of scientists at the annual meeting of the International Society for Stem Cell Research in Toronto, Canada. He called the cells 'ES-like cells', but would later refer to them as induced pluripotent stem cells, or iPS cells. “Many people just didn't believe it,” says Rudolf Jaenisch, a biologist at the Massachusetts Institute of Technology in Cambridge, who was in the room. But Jaenisch knew and trusted Yamanaka's work, and thought it was “ingenious”. © 2016 Macmillan Publishers Limited,
By Teal Burrell Sociability may be skin deep. The social impairments and high anxiety seen in people with autism or related disorders may be partly due to a disruption in the nerves of the skin that sense touch, a new study in mice suggests. Autism spectrum disorders are primarily thought of as disorders of the brain, generally characterized by repetitive behaviors and deficits in communication skills and social interaction. But a majority of people with autism spectrum disorders also have an altered tactile sense; they are often hypersensitive to light touch and can be overwhelmed by certain textures. “They tend to be very wary of social touch [like a hug or handshake], or if they go outside and feel a gust of wind, it can be very unnerving,” says neuroscientist Lauren Orefice from Harvard Medical School in Boston. An appreciation for this sensory aspect of autism has grown in recent years. The newest version of psychiatry’s bible, the Diagnostic and Statistical Manual of Mental Disorders, includes the sensory abnormalities of autism as core features of the disease. “That was a big nod and a recognition that this is a really important aspect of autism,” says Kevin Pelphrey, a cognitive neuroscientist at The George Washington University in Washington, D.C., who was not involved in the work. The sensation of touch starts in the peripheral nervous system—in receptors at the surface of the skin—and travels along nerves that connect into the central nervous system. Whereas many autism researchers focus on the end of the pathway—the brain—Orefice and colleagues wondered about the first leg of the trip. So the group introduced mutations that silenced genes associated with autism spectrum disorders in mice, adding them in a way that restricted the effects to peripheral nerve cells, they report today in Cell. The team singled out the gene Mecp2, which encodes a protein that regulates the expression of genes that help forge connections between nerve cells. © 2016 American Association for the Advancement of Science
By ALAN COWELL LONDON — When Muhammad Ali died last week, the memories spooled back inevitably to the glory days of the man who called himself the Greatest, a champion whose life intertwined with America’s traumas of race, faith and war. It was a chronicle of valor asserted in the most public of arenas scrutinized by an audience that spanned the globe. But there was another narrative, just as striking to some admirers, of a private courage beyond his klieg-lit renown. For the minority afflicted by Parkinson’s disease, Ali’s 30-year struggle with the same illness magnified the broader status he built from his boxing prowess as a black man who embraced radical Islam, refused to fight in Vietnam, earned the opprobrium of the establishment and yet emerged as an icon. “It was his longest bout, and one that ultimately he could not win,” the reporter Patrick Sawer wrote in The Telegraph, referring to Ali’s illness. Yet the affliction “only served to increase the worldwide admiration he had gained before the disease robbed him of his powers.” As a global superstar, Ali touched many lands, and Britain felt a particular bond. Boxing fans recalled his far-flung bouts — the “Rumble in the Jungle” against George Foreman in Zaire, as the Democratic Republic of Congo was then called, in 1974; “The Thrilla in Manila” in the Philippines against Joe Frazier a year later. But in Britain, his two defeats in the 1960s of Henry Cooper, a much-loved British heavyweight who died in 2011, and his feisty appearances in prime-time television interviews left an indelible mark. © 2016 The New York Times Company
Link ID: 22308 - Posted: 06.11.2016
By Esther Landhuis About 100 times rarer than Parkinson’s, and often mistaken for it, progressive supranuclear palsy afflicts fewer than 20,000 people in the U.S.—and two thirds do not even know they have it. Yet this little-known brain disorder that killed comic actor Dudley Moore in 2002 is quietly becoming a gateway for research that could lead to powerful therapies for a range of intractable neurodegenerative conditions including Alzheimer’s and chronic traumatic encephalopathy, a disorder linked to concussions and head trauma. All these diseases share a common feature: abnormal buildup of a protein called tau in the brains of patients. Progressive supranuclear palsy has no cure and is hard to diagnose. Although doctors may have heard of the disease, many know little about it. It was not described in medical literature until 1964 but some experts believe one of the earliest accounts of the debilitating illness appeared in an 1857 short story by Charles Dickens and his friend Wilke Collins: “A cadaverous man of measured speech. A man who seemed as unable to wink, as if his eyelids had been nailed to his forehead. A man whose eyes—two spots of fire—had no more motion than if they had been connected with the back of his skull by screws driven through them, and riveted and bolted outside among his gray hair. He had come in and shut the door, and he now sat down. He did not bend himself to sit as other people do, but seemed to sink bolt upright, as if in water, until the chair stopped him.” © 2016 Scientific American
By ANNA FELS ONE of the most painful experiences of being a psychiatrist is having a patient for whom none of the available therapies or medications work. A while back, I was asked to do a consultation on just such a patient. This person had been a heroin addict in her early 20s. She had quit the opioid five years earlier, but her life was plagued with anxiety, apathy and self-doubt that prior treatments had not helped. At the end of the session, almost as an afterthought, she noted with irony that the only time in her adult life when she had been able to socialize easily and function at work was when she had been hooked on heroin. We are in the midst of a devastating and often lethal opioid epidemic, one of whose victims, we learned last week, was the pop star Prince. At such a time, it is hard to remember that there are multiple opioids naturally produced in our brains and required for our well-being. The neural circuitry utilizing these substances controls some of our most fundamental feelings of pain, stress and hopelessness, as well as pleasure and even euphoria. There is obviously a need for extreme caution, but research suggests that certain opioids may actually be useful in treating psychiatric diseases that have proved frustratingly unresponsive to current medications. It is the potentially addictive subset of opioids, whose natural ancestors were originally derived from poppies, that we associate with the word. These substances have been with us for most, if not all, of human civilization. Poppy seeds have been found at archaeological sites of Neolithic man. The Sumerians wrote about “the joy plant”; an Egyptian papyrus from the second millennium B.C. described the use of a product of poppies to stop the crying of children. Hippocrates suggested its use for female ailments, and a ninth-century Persian physician advocated the use of opium for melancholia. Millenniums later, during the American Civil War, the Union Army used 10 million opium pills to treat wounded soldiers. And then there were the two Opium Wars fought between China and Britain. Unquestionably, no other psychoactive substance has played such a central role in human affairs. © 2016 The New York Times Company
By DENISE GRADY Muhammad Ali, who died on Friday after a long struggle with Parkinson’s disease, was given the diagnosis in 1984 when he was 42. The world witnessed his gradual decline over the decades as tremors and stiffness set in, replacing his athletic stride with a shuffle, silencing his exuberant voice and freezing his face into an expressionless mask. What is Parkinson’s disease? It is a progressive, incurable deterioration of the part of the brain that produces a chemical needed to carry signals to the regions that control movement. How common is Parkinson’s? About one million people in the United States, and between seven million and 10 million worldwide, are thought to have Parkinson’s, according to the Parkinson’s Disease Foundation. What causes it? Was boxing a factor for Ali? The exact cause is not known. As with many disorders, experts suspect a combination of genes and environment, meaning that people with a particular genetic makeup may be predisposed to the disease if they are exposed to certain environmental factors. Head injuries, such as those sustained repeatedly in boxing, are among the possible risk factors listed by the National Parkinson Foundation. So is exposure to certain pesticides. These factors have both been suggested as possible contributors in Muhammad Ali’s case. Can Parkinson’s disease be treated? Medication can ease the symptoms for a time, but the disease continues to progress. In some cases, implanted devices called deep-brain stimulators can also help with symptoms. But Parkinson’s is not curable. © 2016 The New York Times Company
Link ID: 22284 - Posted: 06.06.2016
By JOHN ELIGON and SERGE F. KOVALESKI Prince, the music icon who struggled with debilitating hip pain during his career, died from an accidental overdose of self-administered fentanyl, a type of synthetic opiate, officials in Minnesota said Thursday. The news ended weeks of speculation about the sudden death of the musician, who had a reputation for clean living but who appears to have developed a dependency on medications to treat his pain. Authorities have yet to discuss how he came to be in possession of the fentanyl and whether it had been prescribed by a doctor. Officials had waited several weeks for the results of a toxicology test undertaken as part of an autopsy performed after he was found dead April 21 in an elevator at his estate. He was preparing to enroll in an opioid treatment program when he died at 57, according to the lawyer for a doctor who was planning to treat him. The Midwest Medical Examiner’s Office, which conducted the autopsy, declined to comment beyond releasing a copy of its findings. The Carver County Sheriff’s Office is continuing to investigate the death with help from the federal Drug Enforcement Administration. The sheriff’s office had said it was looking into whether opioid abuse was a factor, and a law enforcement official had said that painkillers were found on Prince when investigators arrived. “The M.E. report is one piece of the whole thing,” said Jason Kamerud, the county’s chief deputy sheriff. Fentanyl is a potent but dangerous painkiller, estimated to be more than 50 times more powerful than heroin, according to the Centers for Disease Control and Prevention. The report did not list how much fentanyl was found in Prince’s blood. Last year, federal officials issued an alert that said incidents and overdoses with fentanyl were “occurring at an alarming rate throughout the United States.” © 2016 The New York Times Company
By Gretchen Reynolds A weekly routine of yoga and meditation may strengthen thinking skills and help to stave off aging-related mental decline, according to a new study of older adults with early signs of memory problems. Most of us past the age of 40 are aware that our minds and, in particular, memories begin to sputter as the years pass. Familiar names and words no longer spring readily to mind, and car keys acquire the power to teleport into jacket pockets where we could not possibly have left them. Some weakening in mental function appears to be inevitable as we age. But emerging science suggests that we might be able to slow and mitigate the decline by how we live and, in particular, whether and how we move our bodies. Past studies have found that people who run, weight train, dance, practice tai chi, or regularly garden have a lower risk of developing dementia than people who are not physically active at all. There also is growing evidence that combining physical activity with meditation might intensify the benefits of both pursuits. In an interesting study that I wrote about recently, for example, people with depression who meditated before they went for a run showed greater improvements in their mood than people who did either of those activities alone. But many people do not have the physical capacity or taste for running or other similarly vigorous activities. So for the new study, which was published in April in the Journal of Alzheimer’s Disease, researchers at the University of California, Los Angeles, and other institutions decided to test whether yoga, a relatively mild, meditative activity, could alter people’s brains and fortify their ability to think. © 2016 The New York Times Company
Keyword: Learning & Memory
Link ID: 22270 - Posted: 06.01.2016
By Kelly Servick There’s an unfortunate irony for people who rely on morphine, oxycodone, and other opioid painkillers: The drug that’s supposed to offer you relief can actually make you more sensitive to pain over time. That effect, known as hyperalgesia, could render these medications gradually less effective for chronic pain, leading people to rely on higher and higher doses. A new study in rats—the first to look at the interaction between opioids and nerve injury for months after the pain-killing treatment was stopped—paints an especially grim picture. An opioid sets off a chain of immune signals in the spinal cord that amplifies pain rather than dulling it, even after the drug leaves the body, the researchers found. Yet drugs already under development might be able to reverse the effect. It’s no secret that powerful painkillers have a dark side. Overdose deaths from prescription opioids have roughly quadrupled over 2 decades, in near lockstep with increased prescribing. And many researchers see hyperalgesia as a part of that equation—a force that compels people to take more and more medication, while prolonging exposure to sometimes addictive drugs known to dangerously slow breathing at high doses. Separate from their pain-blocking interaction with receptors in the brain, opioids seem to reshape the nervous system to amplify pain signals, even after the original illness or injury subsides. Animals given opioids become more sensitive to pain, and people already taking opioids before a surgery tend to report more pain afterward. © 2016 American Association for the Advancement of Scienc
By Viviane Callier Bees don’t just recognize flowers by their color and scent; they can also pick up on their minute electric fields. Such fields—which form from the imbalance of charge between the ground and the atmosphere—are unique to each species, based on the plant’s distance from the ground and shape. Flowers use them as an additional way to advertise themselves to pollinators, but until now researchers had no idea how bees sensed these fields. In a new study, published online today in the Proceedings of the National Academy of Sciences, researchers used a laser vibrometer—a tiny machine that hits the bee hair with a laser—to measure how the hair on a bee’s body responds to a flower’s tiny electric field. As the hair moves because of the electric field, it changes the frequency of the laser light that hits it, allowing the vibrometer to keep track of the velocity of motion of the hair. When the bees buzzed within 10 centimeters of the flower, the electric field—like static electricity from a balloon—caused the bee’s hair to bend. This bending activates neurons at the base of bee hair sockets, which allows the insects to “sense” the field, the team found. Electric fields can only be sensed from a distance of 10 cm or so, so they’re not very useful for large animals like ourselves. But for small insects, this distance represents several body lengths, a relatively long distance. Because sensing such fields is useful to small animals, the team suspects this ability could be important to other insect species as well. © 2016 American Association for the Advancement of Science.
Keyword: Pain & Touch
Link ID: 22263 - Posted: 05.31.2016
by Bruce Bower For a landmark 1977 paper, psychologist Andrew Meltzoff stuck his tongue out at 2- to 3-week-old babies. Someone had to do it. After watching Meltzoff razz them for 15 seconds, babies often stuck out their own tongues within the next 2½ minutes. Newborns also tended to respond in kind when the young researcher opened his mouth wide, pushed out his lips like a duck and opened and closed the fingers of one hand. Meltzoff, now at the University of Washington in Seattle, and a colleague were the first to report that babies copy adults’ simple physical deeds within weeks of birth. Until then, most scientists assumed that imitation began at around 9 months of age. Newborns don’t care that imitation is the sincerest form of flattery. For them, it may be a key to interacting with (and figuring out) those large, smiley people who come to be known as mommy and daddy. And that’s job number one for tykes hoping to learn how to talk and hang out with a circle of friends. Meltzoff suspected that babies enter the world able to compare their own movements — even those they can feel but not see, such as a projecting tongue — to corresponding adult actions. Meltzoff’s report has inspired dozens of papers on infant imitation. Some have supported his results, some haven’t. A new report, published May 5 in Current Biology, falls in the latter group. The study of 106 Australian babies tracked from 1 to 9 weeks of age concludes that infants don’t imitate anyone. © Society for Science & the Public 2000 - 201
Keyword: Development of the Brain
Link ID: 22246 - Posted: 05.25.2016
By Ian Randall As if you needed another reason to hate the gym, it now turns out that exercise can exhaust not only your muscles, but also your eyes. Fear not, however, for coffee can perk them right up again. During strenuous exercise, our muscles tire as they run out of fuel and build up waste products. Muscle performance can also be affected by a phenomenon called “central fatigue,” in which an imbalance in the body’s chemical messengers prevents the central nervous system from directing muscle movements effectively. It was not known, however, whether central fatigue might also affect motor systems not directly involved in the exercise itself—such as those that move the eyes. To find out, researchers gave 11 volunteers a carbohydrate solution either with a moderate dose of caffeine—which is known to stimulate the central nervous system—or as a placebo without, during 3 hours of vigorous cycling. After exercising, the scientists tested the cyclists with eye-tracking cameras to see how well their brains could still control their visual system. The team found that exercise reduced the speed of rapid eye movements by about 8%, impeding their ability to capture new visual information. The caffeine—the equivalent of two strong cups of coffee—was sufficient to counteract this effect, with some cyclists even displaying increased eye movement speeds, the team reports today in Scientific Reports. So it might be a good idea to get someone else to drive you home after that marathon. © 2016 American Association for the Advancement of Science.
Link ID: 22243 - Posted: 05.25.2016
By Jessica Hamzelou People who experience migraines that are made worse by light might be better off seeing the world in green. While white, blue, red and amber light all increase migraine pain, low-intensity green light seems to reduce it. The team behind the finding hope that specially developed sunglasses that screen out all wavelengths of light except green could help migraineurs. Many people experience sensitivity to light during a migraine. Photophobia, as it is known, can leave migraineurs resorting to sunglasses in well-lit rooms, or seeking the comfort of darkness. The reaction is thought to be due to the brain’s wiring. In a brain region called the thalamus, neurons that transmit sensory information from our retinas cross over with other neurons that signal pain. As a result, during migraine, light can worsen pain and pain can cause visual disturbance, says Rami Burstein at Harvard University. But not all colours of light have the same effect. Six years ago, Burstein and his colleagues studied migraine in sufferers who are blind, either due to the loss of an eye or retina, or because of retinal damage. They found that people who had some remaining retinal cells had worse migraines when they were in brightly lit environments, and that blue light seemed to have the strongest impact. The finding caused a flurry of excitement, and the promotion of sunglasses that filter out blue light. © Copyright Reed Business Information Ltd.
By D. T. Max When a spinal cord is damaged, location is destiny: the higher the injury, the more severe the effects. The spine has thirty-three vertebrae, which are divided into five regions—the coccygeal, the sacral, the lumbar, the thoracic, and the cervical. The nerve-rich cord traverses nearly the entire length of the spine. The nerves at the bottom of the cord are well buried, and sometimes you can walk away from damage to these areas. In between are insults to the long middle region of the spine, which begins at the shoulders and ends at the midriff. These are the thoracic injuries. Although they don’t affect the upper body, they can still take away the ability to walk or feel below the waist, including autonomic function (bowel, bladder, and sexual control). Injuries to the cord in the cervical area—what is called “breaking your neck”—can be lethal or leave you paralyzed and unable to breathe without a ventilator. Doctors who treat spinal-cord-injury patients use a letter-and-number combination to identify the site of the damage. They talk of C3s (the cord as it passes through the third cervical vertebra) or T8s (the eighth thoracic vertebra). These morbid bingo-like codes help doctors instantly gauge the severity of a patient’s injury. Darek Fidyka, who is forty-one years old, is a T9. He was born and raised in Pradzew, a small farming town in central Poland, not far from Lodz. ... Several of the wounds punctured his lungs, and one nearly cut his spinal cord in half. As Fidyka lay on the ground, he felt his body change. “I can remember very vividly losing feeling in my legs, bit by bit,” he says. “It started in the upper part of the spine and was moving down slowly while I lay waiting for the ambulance to arrive.”
Link ID: 22230 - Posted: 05.19.2016
A bionic body is closer than you think By Dwayne Godwin, Jorge Cham Dwayne Godwin is a neuroscientist at the Wake Forest University School of Medicine. Jorge Cham draws the comic strip Piled Higher and Deeper at www.phdcomics.com. © 2016 Scientific American
Link ID: 22222 - Posted: 05.17.2016
Dara Mohammadi As the small motorboat chugs to a halt, three travellers, wind-beaten from the three-hour journey along the Atrato river, step on to the muddy banks of Bellavista, an otherwise inaccessible town in the heart of the heavily forested north-west of Colombia. They swing their hessian bags – stuffed with bedsheets, dried beans and cuddly toys – to their shoulders and clamber up a dusty path. Tucked inside the bag of one of the travellers, neuropsychologist Sonia Moreno, is the reason they are here: a wad of unfinished, hand-drawn charts of family trees. The people whose names are circled on the charts have Huntington’s disease, an incurable genetic brain disorder that usually starts between the ages of 35 and 45 years. It begins with personality changes that can make them aggressive, violent, uninhibited, anxious and depressed. The disease progresses slowly, robbing them first of the control of their body, which jerks and twists seemingly of its own will, and then their ability to walk, talk and think until, about 20 years after the symptoms first begin, they die. Their children, each of whom has a 50% chance of inheriting the disease, watch and wait to see if it will happen to them. It is in this way that the disease strangles families. With Moreno is Ignacio Muñoz-Sanjuan, vice president of translational biology at CHDI Foundation, a US nonprofit research organisation that aims to find ways to prevent or slow down the progression of the disease. The foundation spent $140m–$150m (£97m-£104m) on research last year, but Muñoz-Sanjuan is not here on official business. He’s here for Factor-H, an initiative he founded four years ago to help with the other end of the problem – poor families with Huntington’s struggling in Latin America. © 2016 Guardian News and Media Limited o