Chapter 5. The Sensorimotor System
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By Maia Szalavitz When a family member, spouse or other loved one develops an opioid addiction — whether to pain relievers like Vicodin or to heroin — few people know what to do. Faced with someone who appears to be driving heedlessly into the abyss, families often fight, freeze or flee, unable to figure out how to help. Families are sometimes overwhelmed with conflicting advice about what should come next. Much of the advice given by treatment groups and programs ignores what the data says in a similar way that anti-vaccination or climate skeptic websites ignore science. The addictions field is neither adequately regulated nor effectively overseen. There are no federal standards for counseling practices or rehab programs. In many states, becoming an addiction counselor doesn’t require a high school degree or any standardized training. “There’s nothing professional about it, and it’s not evidence-based,” said Dr. Mark Willenbring, the former director of treatment research at the National Institute on Alcohol Abuse and Alcoholism, who now runs a clinic that treats addictions. Consequently, families are often given guidance that bears no resemblance to what the research evidence shows — and patients are commonly subjected to treatment that is known to do harm. People who are treated as experts firmly proclaim that they know what they are doing, but often turn out to base their care entirely on their own personal and clinical experience, not data. “Celebrity Rehab with Dr. Drew,” which many people see as an example of the best care available, for instance, used an approach that is not known to be effective for opioid addiction. More than 13 percent of its participants died after treatment,1 mainly of overdoses that could potentially have been prevented with evidence-based care. Unethical practices such as taking kickbacks for patient referrals are also rampant.
By Diana Kwon Few things feel worse than not knowing when your next paycheck is coming. Economic insecurity has been shown to have a whole host of negative effects, including low self-esteem and impaired cognitive functioning. It turns out financial stress can also physically hurt, according to a paper published in February in Psychological Science. Eileen Chou, a public policy professor at the University of Virginia, and her collaborators began by analyzing a data set of 33,720 U.S. households and found that those with higher levels of unemployment were more likely to purchase over-the-counter painkillers. Then, using a series of experiments, the team discovered that simply thinking about the prospect of financial insecurity was enough to increase pain. For example, people reported feeling almost double the amount of physical pain in their body after recalling a financially unstable time in their life as compared with those who thought about a secure period. In another experiment, university students who were primed to feel anxious about future employment prospects removed their hand from an ice bucket more quickly (showing less pain tolerance) than those who were not. The researchers also found that economic insecurity reduced people's sense of control, which, in turn, increased feelings of pain. Chou and her colleagues suggest that because of this link between financial insecurity and decreased pain tolerance, the recent recession may have been a factor in fueling the prescription painkiller epidemic. Other experts are cautious about taking the findings that far. “I think the hypothesis [that financial stress causes pain] has a lot of merit, but it would be helpful to see additional rigorous evidence in a real-world environment,” says Heather Schofield, an economist at the University of Pennsylvania who was not involved in the study. © 2016 Scientific American,
By Sara Chodosh There has long been debate about a link between serious blows to the head and the development of neurodegenerative diseases later in life. Research has made cases for and against a relationship between traumatic brain injuries and neurological ailments such as Alzheimer’s, Parkinson’s and general dementia. Now the question is drawing ever more scrutiny as the alarming extent of these injuries becomes better known—and new research is finally casting some light on this murky and often quietly terrifying topic. A large-scale analysis of three separate studies published this week in JAMA Neurology found no association between unconsciousness-causing traumatic brain injuries (TBI) and Alzheimer’s disease or general dementia—but it did find a strong association between TBI and Parkinson’s disease. “I can’t decide if the positive or negative findings are more surprising,” says one of the study’s investigators, physician and Alzheimer’s researcher Paul Crane at the University of Washington. The positive association his team found between Parkinson’s and TBI was not entirely novel, but Crane says the magnitude of the link was unexpected. The researchers found the risk of Parkinson’s rose threefold for people whose head injuries had caused them to go unconscious for more than an hour. The more contentious finding is the lack of an association between TBI and Alzheimer’s. Prior research has been divided on whether there is a link, but many of the previous studies have been smaller in scale and conducted less-comprehensive analyses. “Although early studies suggested a clear link between TBI and an increased risk for Alzheimer’s disease, this has not been replicated,” explains Frances Corrigan at the University of Adelaide, who studies how TBI influences neurodegeneration. © 2016 Scientific American,
By Gretchen Reynolds To strengthen your mind, you may first want to exert your leg muscles, according to a sophisticated new experiment involving people, mice and monkeys. The study’s results suggest that long-term endurance exercise such as running can alter muscles in ways that then jump-start changes in the brain, helping to fortify learning and memory. I often have written about the benefits of exercise for the brain and, in particular, how, when lab rodents or other animals exercise, they create extra neurons in their brains, a process known as neurogenesis. These new cells then cluster in portions of the brain critical for thinking and recollection. Even more telling, other experiments have found that animals living in cages enlivened with colored toys, flavored varieties of water and other enrichments wind up showing greater neurogenesis than animals in drab, standard cages. But animals given access to running wheels, even if they don’t also have all of the toys and other party-cage extras, develop the most new brain cells of all. These experiments strongly suggest that while mental stimulation is important for brain health, physical stimulation is even more potent. But so far scientists have not teased out precisely how physical movement remakes the brain, although all agree that the process is bogglingly complex. Fascinated by that complexity, researchers at the National Institutes of Health recently began to wonder whether some of the necessary steps might be taking place far from the brain itself, and specifically, in the muscles, which are the body part most affected by exercise. Working muscles contract, burn fuel and pump out a wide variety of proteins and other substances. The N.I.H. researchers suspected that some of those substances migrated from the muscles into the bloodstream and then to the brain, where they most likely contributed to brain health. © 2016 The New York Times Company
Keyword: Learning & Memory
Link ID: 22429 - Posted: 07.13.2016
By Aviva Rutkin At first glance, she was elderly and delicate – a woman in her 90s with a declining memory. But then she sat down at the piano to play. “Everybody in the room was totally startled,” says Eleanor Selfridge-Field, who researches music and symbols at Stanford University. “She looked so frail. Once she sat down at the piano, she just wasn’t frail at all. She was full of verve.” Selfridge-Field met this woman, referred to as ME to preserve her privacy, at a Christmas party around eight years ago. ME, who is now aged 101, has vascular dementia: she rarely knows where she is, and doesn’t recognise people she has met in the last few decades. But she can play nearly 400 songs by ear – a trick that depends on tapping into a memory of previously stored musical imprints – and continues to learn new songs just by listening to them. She has even composed an original piece of her own. ME’s musical talent, despite her cognitive impairments, inspired Selfridge-Field to spend the last six years observing her, and she presented her observations today at the International Conference on Music Perception and Cognition in San Francisco, California. ME experienced a stroke-like attack when she was in her 80s, and a few years later was diagnosed with vascular dementia. She struggles most to remember events and encounters that are recent, and her memory is selective, focusing on specific periods – such as her childhood between the ages of 3 and 8. She can recognise people that she met before the age of about 75 to 80. She is never quite sure of her surroundings. © Copyright Reed Business Information Ltd.
Link ID: 22420 - Posted: 07.11.2016
Beatrice Alexandra Golomb, Statins can indeed produce neurological effects. These drugs are typically prescribed to lower cholesterol and thereby reduce the risk of heart attack and stroke. Between 2003 and 2012 roughly one in four Americans aged 40 and older were taking a cholesterol-lowering medication, according to the Centers for Disease Control and Prevention. But studies show that statins can influence our sleep and behavior—and perhaps even change the course of neurodegenerative conditions, including dementia. The most common adverse effects include muscle symptoms, fatigue and cognitive problems. A smaller proportion of patients report peripheral neuropathy—burning, numbness or tingling in their extremities—poor sleep, and greater irritability and aggression. Interestingly, statins can produce very different outcomes in different patients, depending on an individual's medical history, the statin and the dose. Studies show, for instance, that statins generally reduce the risk of ischemic strokes—which arise when a blocked artery or blood clot cuts off oxygen to a brain region—but can also increase the risk of hemorrhagic strokes, or bleeding into the brain. Statins also appear to increase or decrease aggression. In 2015 my colleagues and I observed that women taking statins, on average, showed increased aggression; men typically showed less, possibly because of reduced testosterone levels. Some men in our study did experience a marked increase in aggression, which was correlated with worsening sleep. © 2016 Scientific American
Andrew Orlowski Special Report If the fMRI brain-scanning fad is well and truly over, then many fashionable intellectual ideas look like collateral damage, too. What might generously be called the “British intelligentsia” – our chattering classes – fell particularly hard for the promise that “new discoveries in brain science” had revealed a new understanding of human behaviour, which shed new light on emotions, personality and decision making. But all they were looking at was statistical quirks. There was no science to speak of, the results of the experiments were effectively meaningless, and couldn’t support the (often contradictory) conclusions being touted. The fMRI machine was a very expensive way of legitimising an anecdote. This is an academic scandal that’s been waiting to explode for years, for plenty of warning signs were there. In 2005, Ed Vul, now a psychology professor at UCSD, and Hal Pashler – then and now at UCSD – were puzzled by a claim being made in a talk by a neuroscience researcher. He was explaining study that purported to report a high correlation between a test subject’s brain activity and the speed with which they left the room after the study. “It seemed unbelievable to us that activity in this specific brain area could account for so much of the variance in walking speed,” explained Vul. “Especially so, because the fMRI activity was measured some two hours before the walking happened. So either activity in this area directly controlled motor action with a delay of two hours — something we found hard to believe — or there was something fishy going on.” IT © 1998–2016
Keyword: Brain imaging
Link ID: 22410 - Posted: 07.08.2016
DAVID GREENE, HOST: Nearly one-quarter of all Americans reach for a bottle of acetaminophen every single week. Many of you might know this drug as Tylenol. It's a pain killer that can take the edge off a headache or treat you when you have a fever. It also might have another effect. And let's talk about this with NPR social science correspondent Shankar Vedantam. And, Shankar, straight out, is this going to make me not want to take Tylenol, what you're about to tell me? VEDANTAM: It might make you not want to take Tylenol when you're talking with me, David. GREENE: Oh, even more interesting. VEDANTAM: (Laughter) I was speaking with Dominik Mischkowski. He's currently a researcher at the National Institutes of Health. He recently conducted a couple of double blind experiments. These are experiments where the volunteers are given either sugar pills or Tylenol, but neither the volunteers nor the researchers know which volunteers are getting which pill. Mischkowski and his advisers at Ohio State University, Jennifer Crocker and Baldwin Way, they played loud noises for the volunteers. Not surprisingly, volunteers given Tylenol experienced less physical discomfort than volunteers given the placebo. © 2016 npr
Keyword: Pain & Touch
Link ID: 22403 - Posted: 07.07.2016
By Damian Garde, A boy in Pakistan became a local legend as a street performer in recent years by traversing hot coals and lancing his arms with knives without so much as a wince. A thousand miles away, in China, lived a family wracked by excruciating bouts of inexplicable pain, passed down generation after generation. Scientists eventually determined what the boy and the family had in common: mutations in a gene that functions like an on-off switch for agony. Now, a bevy of biotech companies, including Genentech and Biogen, are staking big money on the idea that they can develop drugs that toggle that switch to relieve pain without the risk of addiction. The gene in question is SCN9A, which is responsible for producing a pain-related protein called Nav1.7. In patients who feel nothing, SCN9A is pretty much broken. In those who feel searing random pain, the gene is cranking out far too much Nav1.7. That discovery raises an obvious question: Can blocking Nav1.7 provide relief for many types of pain—and someday, perhaps, replace dangerous opioid therapies? “That’s the dream,” said David Hackos, a senior scientist at Genentech, which has two Nav1.7 treatments in the first stage of clinical development. It’s too early make any sweeping predictions—and, indeed, a Pfizer pill targeting Nav1.7 has already stumbled—but the pharma industry clearly sees the potential for a blockbuster. © 2016 Scientific American
Keyword: Pain & Touch
Link ID: 22400 - Posted: 07.06.2016
By Jessica Hamzelou Imagine if each of the words in this article had their own taste, or the music you’re listening to played out as visual scene in your mind. For synaesthetes – a small proportion of people whose senses intertwine – this is the stuff of the every day. “Most people describe it as a gift,” says Jamie Ward, a neuroscientist at the University of Sussex in the UK. Now, he and his colleagues have found a new form of synaesthesia – one that moves beyond written language to sign language. It is the first time the phenomenon has been observed. “People with synaesthesia experience the ordinary world in extraordinary ways,” says Ward. In theory, any two senses can overlap. Some synaesthetes connect textures with words, while others can taste them. More commonly, written letters seem to have corresponding colours. An individual synaesthete may always associate the letter A with the colour pink, for instance. This type of synaesthesia has been found across many written languages, prompting Ward’s team to wonder if it can also apply to sign language. They recruited 50 volunteers with the type of synaesthesia that means they experience colours with letters, around half of whom were fluent in sign language too. All the participants watched a video of sign language and were asked if it triggered any colours. © Copyright Reed Business Information Ltd.
Link ID: 22390 - Posted: 07.02.2016
By Rachel Rabkin Peachman It began with a simple roller-skating accident three years ago. Taylor Aschenbrenner, then 8 years old, lost her balance amid a jumble of classmates, tumbled to the floor and felt someone else’s skate roll over her left foot. The searing pain hit her immediately. The diagnosis, however, would take much longer. An X-ray, M.R.I.s, a CT scan and blood tests over several months revealed no evidence of a break, sprain or other significant problem. Taylor’s primary symptom was pain — so severe that she could not put weight on the foot. “Our family doctor first told us to give it some time,” said Taylor’s mother, Jodi Aschenbrenner, of Hudson, Wis. But time didn’t heal the pain. After about a month, an orthopedist recommended physical therapy. That didn’t end the problem, either. “I couldn’t walk or play outside or do anything,” Taylor said. After she had spent a year and a half on crutches, her orthopedist suggested she see Dr. Stefan Friedrichsdorf, the medical director ofpain medicine, palliative care and integrative medicine at Children’s Hospitals and Clinics of Minnesota. He and his team promptly recognized Taylor’s condition as complex regional pain syndrome, a misfiring within the peripheral and central nervous systems that causes pain signals to go into overdrive and stay turned on even after an initial injury or trauma has healed. He came up with a treatment plan for Taylor that included cognitive behavioral therapy, physical therapy, mind-body techniques, stress-reduction strategies, topical pain-relief patches and a focus on returning to her normal life and sleep routine, among other things. © 2016 The New York Times Company
Emily Conover Sharks have a sixth sense that helps them locate prey in murky ocean waters. They rely on special pores on their heads and snouts, called ampullae of Lorenzini, that can sense electric fields generated when nearby prey move. The pores were first described in 1678, but scientists haven’t been sure how they work. Now, the answer is a bit closer. The pores, which connect to electrosensing cells, are filled with a mysterious clear jelly. This jelly is a highly efficient proton conductor, researchers report May 13 in Science Advances. In the jelly, positively charged particles move and transmit current. Marco Rolandi of the University of California, Santa Cruz and colleagues squeezed jelly from the pores of one kind of shark and two kinds of skate and tested how well protons could flow through the substance. Good proton conductors, including a protein found in squid skin, occur in nature. But the jelly is the best biological proton conductor discovered so far. In fact, even humankind’s best technology isn’t wildly better. The most efficient proton conductor devised by people — a polymer known as Nafion — is a mere 40 times better than the stuff sharks are born with. Citations E.E. Josberger et al. Proton conductivity in ampullae of Lorenzini jelly. Science Advances. Published online May 13, 2016. doi:10.1126/sciadv.1600112. Further Reading |© Society for Science & the Public 2000 - 2016.
Keyword: Pain & Touch
Link ID: 22366 - Posted: 06.28.2016
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