Chapter 5. The Sensorimotor System

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 21 - 40 of 2729

By LISA SANDERS, M.D. “Mom?” the middle-aged man asked. He recognized the voice, but the words were muffled and strange. I’ll be right over, he said into the phone. The 15-minute drive from his small Connecticut town to his mother’s seemed to last forever. Had she had a stroke? She was 94, and though she’d always been healthy, at her age, anything could happen. He burst into her tidy brick home to find her sitting in the living room, waiting. Her eyes were bright but scared, and her voice was just a whisper. He helped her to his car, then raced to the community hospital a couple of towns over. The doctors in the emergency room were also worried about a stroke. Her left eyelid hung lower across her eye than her right. She was seeing double, she told them. And the left side of her mouth and tongue felt strangely heavy, making it hard to speak. Initial blood tests came back normal; so did the CT scan of her brain. It wasn’t clear what was wrong with the patient, so she was transferred to nearby Yale New Haven Hospital. Dr. Paul Sanmartin, a resident in the second year of his neurology training, met the patient early the next morning. He’d already heard about her from the overnight resident: a 94-year-old woman with the sudden onset of a droopy eyelid, double vision and difficulty speaking, probably due to a stroke. As he entered the room, he realized he wasn’t sure what 94 was supposed to look like, but this woman looked much younger. She did have a droopy left lid, but her eyes moved in what looked to him to be perfect alignment, and her speech, though quiet, was clear. The patient’s story was also different from what he expected. She had macular degeneration and had been getting shots in her left eye for more than a decade. Her last injection was nearly two weeks earlier, and she’d had double vision and the droopy eyelid on and off ever since. © 2017 The New York Times Company

Keyword: Movement Disorders
Link ID: 24111 - Posted: 09.26.2017

By JANE E. BRODY If you’ve never had a migraine, I have two things to say to you: 1) You’re damn lucky. 2) You can’t begin to imagine how awful they are. I had migraines – three times a month, each lasting three days — starting from age 11 and finally ending at menopause. Although my migraines were not nearly as bad as those that afflict many other people, they took a toll on my work, family life and recreation. Atypically, they were not accompanied by nausea or neck pain, nor did I always have to retreat to a dark, soundless room and lie motionless until they abated. But they were not just “bad headaches” — the pain was life-disrupting, forcing me to remain as still as possible. Despite being the seventh leading cause of time spent disabled worldwide, migraine “has received relatively little attention as a major public health issue,” Dr. Andrew Charles, a California neurologist, wrote recently in The New England Journal of Medicine. It can begin in childhood, becoming more common in adolescence and peaking in prevalence at ages 35 to 39. It afflicts two to three times more women than men, and one woman in 25 has chronic migraines on more than 15 days a month. But while the focus has long been on head pain, migraines are not just pains in the head. They are a body-wide disorder that recent research has shown results from “an abnormal state of the nervous system involving multiple parts of the brain,” said Dr. Charles, of the U.C.L.A. Goldberg Migraine Program at the David Geffen School of Medicine in Los Angeles. He told me he hoped the journal article would educate practicing physicians, who learn little about migraines in medical school. Before it was possible to study brain function through a functional M.R.I. or PET scan, migraines were thought to be caused by swollen, throbbing blood vessels in the scalp, usually – though not always — affecting one side of the head. This classic migraine symptom prompted the use of medications that narrow blood vessels, drugs that help only some patients and are not safe for people with underlying heart disease. © 2017 The New York Times Company

Keyword: Pain & Touch
Link ID: 24072 - Posted: 09.18.2017

Mariah Quintanilla Kenneth Catania knows just how much it hurts to be zapped by an electric eel. For the first time, the biologist at Vanderbilt University in Nashville has measured the strength of a defensive electrical attack on a real-life potential predator — himself. Catania placed his arm in a tank with a 40-centimeter-long electric eel (relatively small as eels go) and determined, in amperes, the electrical current that flowed into him when the eel struck. At its peak, the current reached 40 to 50 milliamperes in his arm, he reports online September 14 in Current Biology. This zap was painful enough to cause him to jerk his hand from the tank during each trial. “If you’ve ever been on a farm and touched an electric fence, it’s pretty similar to that,” he says. This is Catania’s latest study in a body of research analyzing the intricacies of an electric eel’s behavior. The way electric eels have been described by biologists in the past has been fairly primitive, says Jason Gallant, a biologist who heads the Michigan State University Electric Fish Lab in East Lansing who was not involved in the study. Catania’s work reveals that “what the electric eel is doing is taking the electric ability that it has and using that to its absolute advantage in a very sophisticated, deliberate way,” he says. Electric eels use electric current to navigate, communicate and hunt for small prey. But when faced with a large land-based predator, eels will launch themselves from the water and electrify the animal with a touch of the head. |© Society for Science & the Public 2000 - 2017.

Keyword: Aggression
Link ID: 24068 - Posted: 09.15.2017

By Nathaniel P. Morris A growing trend in medicine has doctors prescribing visits to parks for their patients. A pediatrician named Robert Zarr at Unity Health Care in Washington, D.C., has worked with the National Park Service and other institutions to create DC Park Rx, an initiative that helps health care providers prescribe activity in outdoor spaces to patients. And National Geographic recently highlighted the rise of this practice in Vermont, where doctors are now prescribing thousands of visits to state parks. In the last several years park prescription programs have spread nationwide, from Maine to California, South Dakota to New Mexico. Proponents of these programs promote outdoor activity as a means of tackling chronic medical conditions like obesity, high blood pressure and type 2 diabetes. But park prescriptions also hold considerable promise for patients suffering from mental health issues. A large body of evidence suggests that exposure to nature may promote mental well-being. A 2010 meta-analysis of 10 studies including over 1,200 participants found people who exercised in green environments demonstrated significant improvements in mood and self-esteem. A 2011 systematic review looked at 11 trials that compared indoor and outdoor activity, finding that exercise in natural settings was “associated with greater feelings of revitalization and positive engagement, decreases in tension, confusion, anger and depression, and increased energy.” Another recent review of studies found activity in natural environments correlated with reductions in negative emotions like sadness, anger and fatigue. © 2017 Scientific American,

Keyword: Depression
Link ID: 24065 - Posted: 09.15.2017

By Helen Thomson DON’T mind the gap. A woman has reached the age of 24 without anyone realising she was missing a large part of her brain. The case highlights just how adaptable the organ is. The discovery was made when the woman was admitted to the Chinese PLA General Hospital of Jinan Military Area Command in Shandong Province complaining of dizziness and nausea. She told doctors she’d had problems walking steadily for most of her life, and her mother reported that she hadn’t walked until she was 7 and that her speech only became intelligible at the age of 6. Doctors did a CAT scan and immediately identified the source of the problem – her entire cerebellum was missing (see scan, above). The space where it should be was empty of tissue. Instead it was filled with cerebrospinal fluid, which cushions the brain and provides defence against disease. The cerebellum – sometimes known as the “little brain” – is located underneath the two hemispheres. It looks different from the rest of the brain because it consists of much smaller and more compact folds of tissue. It represents about 10 per cent of the brain’s total volume but contains 50 per cent of its neurons. Although it is not unheard of to have part of your brain missing, either congenitally or from surgery, the woman joins an elite club of just nine people who are known to have lived without their entire cerebellum. A detailed description of how the disorder affects a living adult is almost non-existent, say doctors from the Chinese hospital, because most people with the condition die at a young age and the problem is only discovered on autopsy (Brain, doi.org/vh7). © Copyright New Scientist Ltd.

Keyword: Development of the Brain
Link ID: 24056 - Posted: 09.12.2017

By JANE E. BRODY Many years ago I was plagued with debilitating headaches associated with a number of seemingly unrelated activities that included cooking for company and sewing drapes for the house. I thought I might be allergic to natural gas or certain fabrics until one day I realized that I tensed my facial muscles when I concentrated intently on a project. The cure was surprisingly simple: I became aware of how my body was reacting and changed it through self-induced behavior modification. I consciously relaxed my muscles whenever I focused on a task that could precipitate a tension-induced headache. Fast-forward about five decades: Now it was my back that ached when I hurriedly cooked even a simple meal. And once again, after months of pain, I realized that I was transferring stress to the muscles of my back and had to learn to relax them, and to allow more time to complete a project to mitigate the stress. Happy to report, I recently prepared dinner for eight with nary a pain. I don’t mean to suggest that every ache and pain can be cured by self-awareness and changing one’s behavior. But recent research has demonstrated that the mind – along with other nonpharmacological remedies — can be powerful medicine to relieve many kinds of chronic or recurrent pains, especially low back pain. As Dr. James Campbell, a neurosurgeon and pain specialist, put it, “The best treatment for pain is right under our noses.” He suggests not “catastrophizing” – not assuming that the pain represents something disastrous that keeps you from leading the life you’ve chosen. Acute pain is nature’s warning signal that something is wrong that should be attended to. Chronic pain, however, is no longer a useful warning signal, yet it can lead to perpetual suffering if people remain afraid of it, the doctor said. © 2017 The New York Times Company

Keyword: Pain & Touch
Link ID: 24053 - Posted: 09.11.2017

Laura Sanders The brain chemical missing in Parkinson’s disease may have a hand in its own death. Dopamine, the neurotransmitter that helps keep body movements fluid, can kick off a toxic chain reaction that ultimately kills the nerve cells that make it, a new study suggests. By studying lab dishes of human nerve cells, or neurons, derived from Parkinson’s patients, researchers found that a harmful form of dopamine can inflict damage on cells in multiple ways. The result, published online September 7 in Science, “brings multiple pieces of the puzzle together,” says neuroscientist Teresa Hastings of the University of Pittsburgh School of Medicine. The finding also hints at a potential treatment for the estimated 10 million people worldwide with Parkinson’s: Less cellular damage occurred when some of the neurons were treated early on with antioxidants, molecules that can scoop up harmful chemicals inside cells. Study coauthor Dimitri Krainc, a neurologist and neuroscientist at Northwestern University Feinberg School of Medicine in Chicago, and colleagues took skin biopsies from healthy people and people with one of two types of Parkinson’s disease, inherited or spontaneously arising. The researchers then coaxed these skin cells into becoming dopamine-producing neurons. These cells were similar to those found in the substantia nigra, the movement-related region of the brain that degenerates in Parkinson’s. |© Society for Science & the Public 2000 - 2017.

Keyword: Parkinsons
Link ID: 24049 - Posted: 09.08.2017

A test that involves drawing a spiral on a sheet of paper could be used to diagnose early Parkinson's disease. Australian researchers have trialled software that measures writing speed and pen pressure on the page. Both are useful for detecting the disease, which causes shaking and muscle rigidity. The Melbourne team said the test could be used by GPs to screen their patients after middle age and to monitor the effect of treatments. The study, published in Frontiers of Neurology, involved 55 people - 27 had Parkinson's and 28 did not. Speed of writing and pen pressure while sketching are lower among Parkinson's patients, particularly those with a severe form of the disease. Image copyright RMIT University Image caption Treatment options are effective only when the disease is diagnosed early In the trial, a tablet computer with special software took measurements during the drawing test and was able to distinguish those with the disease, and how severe it was. Poonam Zham, study researcher from RMIT University, said: "Our aim was to develop an affordable and automated electronic system for early-stage diagnosis of Parkinson's disease, which could be easily used by a community doctor or nursing staff." The system combines pen speed and pressure into one measurement, which can be used to tell how severe the disease is. David Dexter, deputy research director at Parkinson's UK, said current tests for the disease were not able to accurately measure how advanced someone's condition was. "This can impact on the ability to select the right people for clinical research, which is essential to develop new and better treatments for Parkinson's. "This new test could provide a more accurate assessment by measuring a wider range of features that may be affected by Parkinson's, such as co-ordination, pressure, speed and cognitive function." He added that the test could be a "stepping stone" to better clinical trials for Parkinson's. © 2017 BBC.

Keyword: Parkinsons
Link ID: 24042 - Posted: 09.07.2017

By Matt Reynolds Putting on a brave face won’t fool this algorithm. A new system that rates how much pain someone is in just by looking at their face could help doctors decide how to treat patients. By examining tiny facial expressions and calibrating the system to each person, it provides a level of objectivity in an area where that’s normally hard to come by. “These metrics might be useful in determining real pain from faked pain,” says Jeffrey Cohn at the University of Pittsburgh in the US. The system could make the difference between prescribing potentially addictive painkillers and catching out a faker. Objectively measuring pain levels is a tricky task, says Dianbo Liu, who created the system with his colleagues at the Massachusetts Institute of Technology. People experience and express pain differently, so a doctor’s estimate of a patient’s pain can often differ from a self-reported pain score. In an attempt to introduce some objectivity, Liu and his team trained an algorithm on videos of people wincing and grimacing in pain. Each video consisted of a person with shoulder pain, who had been asked to perform a different movement and then rate their pain levels. The result was an algorithm that can use subtle differences in facial expressions to inform a guess about how a given person is feeling. Certain parts of the face are particularly revealing, says Liu. Large amounts of movement around the nose and mouth tended to suggest higher self-reported pain scores. © Copyright New Scientist Ltd.

Keyword: Pain & Touch; Emotions
Link ID: 24026 - Posted: 09.02.2017

By Mitch Leslie When people with asthma have trouble breathing, they may reach for an inhaler containing salbutamol, a drug that expands the airways. Salbutamol may have another beneficial effect—protecting against Parkinson’s disease. Individuals who inhaled the highest doses of salbutamol were about half as likely to develop the devastating neurological condition as those who didn’t take the drug, a study reveals. “I’m sure it’s going to be a landmark paper,” says neurologist Joseph Jankovic of Baylor College of Medicine in Houston, Texas, who wasn’t involved in the research. In Parkinson’s disease, gobs of the protein α-synuclein accumulate in certain brain cells and may kill them. Scientists have tried to craft drugs that speed the elimination of the protein or prevent it from clumping. Neurologist and genomicist Clemens Scherzer of Harvard Medical School in Boston and colleagues decided to try a different strategy. “We wanted to find a drug that could turn down the production of α-synuclein,” he says. To identify promising compounds, the team grew human nerve cells in the lab and tested whether more than 1100 medications, vitamins, dietary supplements, and other molecules altered their output of α-synuclein. Three of the drugs that cut the protein’s production, including salbutamol, work by stimulating the b2-adrenoreceptor—a molecule on some body cells that triggers a variety of effects, including relaxing the airways. The researchers found that these drugs appear to alter how tightly the DNA containing the α-synuclein gene coils, and thus whether the gene is active. © 2017 American Association for the Advancement of Science

Keyword: Parkinsons
Link ID: 24023 - Posted: 09.01.2017

Ewen Callaway Japanese researchers report promising results from an experimental therapy for Parkinson’s disease that involves implanting neurons made from ‘reprogrammed’ stem cells into the brain. A trial conducted in monkeys with a version of the disease showed that the treatment improved their symptoms and seemed to be safe, according to a report published on 30 August in Nature1. The study’s key finding — that the implanted cells survived in the brain for at least two years without causing any dangerous effects in the body — provides a major boost to researchers’ hopes of testing stem-cell treatments for Parkinson’s in humans, say scientists. Jun Takahashi, a stem-cell scientist at Kyoto University in Japan who led the study, says that his team plans to begin transplanting neurons made from induced pluripotent stem (iPS) cells into people with Parkinson’s in clinical trials soon. The research is also likely to inform several other groups worldwide that are testing different approaches to treating Parkinson’s using stem cells, with trials also slated to begin soon. Parkinson’s is a neurodegenerative condition caused by the death of cells called dopaminergic neurons, which make a neurotransmitter called dopamine in certain areas of the brain. Because dopamine-producing brain cells are involved in movement, people with the condition experience characteristic tremors and stiff muscles. Current treatments address symptoms of the disease but not the underlying cause. © 2017 Macmillan Publishers Limited,

Keyword: Parkinsons; Stem Cells
Link ID: 24019 - Posted: 08.31.2017

By Mo Costandi Voluntary movements are one of the brain’s main “outputs,” yet science still knows very little about how networks of neurons plan, initiate and execute them. Now, researchers from Columbia University and the Champalimaud Center for the Unknown in Lisbon, Portugal, say they have discovered an “activity map” that the brain uses to guide animals’ movements. The findings, published Wednesday in Neuron, could advance our understanding of how the brain learns new movements—and of what goes wrong in related disorders such as Parkinson's disease. Movements are controlled and coordinated by multiple brain structures including the primary motor cortex. Located at the back of the frontal lobe, it contains cells whose long fibers extend down through the spinal cord, where they contact “secondary” motor neurons that signal the body muscles. A set of deep brain structures called the basal ganglia are also critical for movement, as evidenced by their degeneration in conditions such as Parkinson’s. One component of the basal ganglia, called the striatum, receives information about possible actions from the motor cortex and is thought to be involved in selecting, preparing and executing the appropriate commands before they are sent to the body. Earlier research had shown that signals leave the striatum along one of two distinct pathways: one that facilitates movement, and another that suppresses it. A number of more recent studies show that both pathways are active during motion, however, suggesting that they do not act by simply sending “stop” and “go” signals. And although it has long been suspected that different groups of neurons in the striatum represent distinct actions, exactly how they might do so has remained unclear. © 2017 Scientific American

Keyword: Parkinsons; Brain imaging
Link ID: 24016 - Posted: 08.31.2017

Andrea Hsu Dan Fabbio was 25 and working on a master's degree in music education when he stopped being able to hear music in stereo. Music no longer felt the same to him. When he was diagnosed with a brain tumor, he immediately worried about cancer. Fortunately, his tumor was benign. Unfortunately, it was located in a part of the brain known to be active when people listen to and make music. Fabbio told his surgeon that music was the most important thing is his life. It was his passion as well as his profession. His surgeon understood. He's someone whose passion has been mapping the brain so he can help patients retain as much function as possible. Dr. Web Pilcher, chair of the Department of Neurosurgery at the University of Rochester Medical Center, and his colleague Brad Mahon, a cognitive neuroscientist, had developed a brain mapping program. Since 2011, they've used the program to treat all kinds of patients with brain tumors: mathematicians, lawyers, a bus driver, a furniture maker. Fabbio was their first musician. The idea behind the program is to learn as much as possible about the patient's life and the patient's brain before surgery to minimize damage to it during the procedure. "Removing a tumor from the brain can have significant consequences depending upon its location," Pilcher says. "Both the tumor itself and the operation to remove it can damage tissue and disrupt communication between different parts of the brain." © 2017 npr

Keyword: Hearing; Pain & Touch
Link ID: 24002 - Posted: 08.26.2017

Laurel Hamers Scientists have traced the sensation of itch to a place you can’t scratch. The discomfort of a mosquito bite or an allergic reaction activates itch-sensitive nerve cells in the spinal cord. Those neurons talk to a structure near the base of the brain called the parabrachial nucleus, researchers report in the Aug. 18 Science. It’s a region that’s known to receive information about other sensations, such as pain and taste. The discovery gets researchers one step closer to finding out where itch signals ultimately end up. “The parabrachial nucleus is just the first relay center for [itch signals] going into the brain,” says study coauthor Yan-Gang Sun, a neuroscientist at the Chinese Academy of Sciences in Shanghai. Understanding the way these signals are processed by the brain could someday provide relief for people with chronic itch, Sun says. While the temporary itchiness of a bug bite is annoying, longer term, “uncontrollable scratching behavior can cause serious skin damage.” Previous studies have looked at the way an itch registers on the skin or how neurons convey those sensations to the spinal cord. But how those signals travel to the brain has been a trickier question, and this research is a “major step” toward answering it, says Zhou-Feng Chen, director of the Center for the Study of Itch at Washington University School of Medicine in St. Louis. |© Society for Science & the Public 2000 - 2017.

Keyword: Pain & Touch
Link ID: 23972 - Posted: 08.18.2017

Researchers from the National Institutes of Health have identified a class of sensory neurons (nerve cells that electrically send and receive messages between the body and brain) that can be activated by stimuli as precise as the pulling of a single hair. Understanding basic mechanisms underlying these different types of responses will be an important step toward the rational design of new approaches to pain therapy. The findings were published in the journal Neuron. “Scientists know that distinct types of neurons detect different types of sensations, such as touch, heat, cold, pain, pressure, and vibration,” noted Alexander Chesler, Ph.D., lead author of the study and principal investigator with the National Center for Complementary and Integrative Health’s (NCCIH) Division of Intramural Research (DIR). “But they know more about neurons involved with temperature and touch than those underlying mechanical pain, like anatomical pain related to specific postures or activities.” In this study, Chesler and his colleagues used a novel strategy that combined functional imaging (which measures neuronal activity), recordings of electrical activity in the brain, and genetics to see how neurons respond to various stimuli. The scientists focused on a class of sensory neurons that express a gene called Calca, as these neurons have a long history in pain research. The scientists applied various stimuli to the hairy skin of mice cheeks, including gentle mechanical stimuli (air puff, stroking, and brushing), “high-threshold” mechanical stimuli (hair pulling and skin pinching), and temperature stimulation. They found that the target neurons belong to two broad categories, both of which were insensitive to gentle stimulation. The first was a well-known type of pain fiber—a polymodal nociceptor—that responds to a host of high intensity stimuli such as heat and pinching. The second was a unique and previously unknown type of neuron that responded robustly to hair pulling. They called this previously undescribed class of high-threshold mechanoreceptors (HTMRs) “circ-HTMRs,” due to the unusual nerve terminals these neurons made in skin. They observed that the endings of the fibers made lasso-like structures around the base of each hair follicle.

Keyword: Pain & Touch
Link ID: 23970 - Posted: 08.17.2017

By Kerry Grens The rare, severe effects of Zika infection in adults may go beyond Guillain-Barre syndrome. Doctors in Brazil report today in JAMA Neurology that among a group of hospitalized patients, those with the virus sometimes presented with other neurological problems—namely, an inflamed nervous system. The physicians tracked 40 patients who came to a hospital in Rio de Janeiro between December 2015 and May 2016 for acute neuroinflammation. Among them, 35 turned out to have been infected with Zika, and within this group, 27 had Guillain-Barre syndrome, which causes debilitating paralysis. Five patients had encephalitis, or inflammation of the brain, two had inflamed spinal cords, and one had nerve inflammation. Such symptoms are thought to indicate “post-infectious syndromes, where you have a viral infection, you clear the infection by mounting an antibody response, and the antibodies actually attack parts of the central and peripheral nervous system, causing these neurological symptoms,” Richard Temes, director of the Center for Neurocritical Care at North Shore University Hospital in Manhasset, New York, tells HealthDay. He was not involved in this study. Zika infection in adults is typically not dangerous, and many people won’t develop symptoms at all. Doctors have noticed an uptick in Guillain-Barre syndrome among those who have caught the virus. The authors note in their study that admissions to their hospital for both Guillain-Barre syndrome and encephalitis rose after May 2014, when the Zika outbreak hit Brazil.

Keyword: Movement Disorders
Link ID: 23960 - Posted: 08.15.2017

By GRETCHEN REYNOLDS Some types of exercise may be better than others at blunting appetite and potentially aiding in weight management, according to an interesting new study of workouts and hunger. It finds that pushing yourself during exercise affects appetite, sometimes in surprising ways. As anyone who has begun an exercise program knows, the relationships between exercise, appetite, weight control and hunger are complex and often counterintuitive. The arithmetic involved seems straightforward. You burn calories during exercise and, over time, should drop pounds. But the reality is more vexing. In both scientific studies and the world inhabited by the rest of us, most people who start exercising lose fewer pounds than would be expected, given the number of calories they are burning during workouts. Many people even gain weight. The problem with exercise as a weight-loss strategy seems to be in large part that it can make you hungry, and many of us wind up consuming more calories after a workout than we torched during it, a biological response that has led some experts and frustrated exercisers to conclude that exercise by itself — without strict calorie reduction — is useless for shedding pounds. But much of the past research into exercise and appetite has concentrated on walking or other types of relatively short or light activities. Some scientists have begun to wonder whether exercise that was physically taxing, either because it was prolonged or intense, might affect appetite differently than more easeful exercise. So for the new study, which was published recently in the Journal of Endocrinology, scientists from Loughborough University in Britain and other institutions who have been studying exercise and appetite for years recruited 16 healthy, fit young men. (They did not include women because this was a small, pilot study, the authors say, and controlling for the effects of women’s menstrual cycles would have been difficult.) © 2017 The New York Times Company

Keyword: Obesity
Link ID: 23934 - Posted: 08.09.2017

Nicola Davis A drug commonly used to treat diabetes could help those living with Parkinson’s disease, research has revealed. By 2020 it is predicted that 162,000 individuals in the UK will be living with the condition. While existing drugs help to control its symptoms, there are currently none available which slow or halt its progression. But now scientists say they have found that a drug commonly used to treat type 2 diabetes appears to improve movement-related issues. The benefit persisted even when the drug had not been taken for 12 weeks, suggesting it might be helping to slow the progression of the disease. “It is not ready for us to say ‘well, everyone needs to start this drug’,” said Thomas Foltynie, professor of neurology at University College London and co-author of the study. “[But] if we can replicate these findings in a multicentre trial, especially with longer follow-up, then this can change the face of our approach to treating Parkinson’s.” Writing in the Lancet, Foltynie and colleagues in the UK and US describe how they tested the impact of the drug, known as exenatide. With recent studies suggesting problems with insulin signalling in the brain could be linked to neurodegenerative disorders, hopes have been raised that diabetes drugs could also be used to tackle Parkinson’s, with previous research – including in cell cultures and animals, as well as a recent pilot study on humans by Foltynie and colleagues – backing up the notion.. But the latest study is the first robust clinical trial of the drug, randomly allocating 60 people with Parkinson’s to one of two treatments – either receiving injections of exenatide or a placebo once a week. © 2017 Guardian News and Media Limited

Keyword: Parkinsons
Link ID: 23918 - Posted: 08.05.2017

By Mitch Leslie Prions are insidious proteins that spread like infectious agents and trigger fatal conditions such as mad cow disease. A protein implicated in diabetes, a new study suggests, shares some similarities with these villains. Researchers transmitted diabetes from one mouse to another just by injecting the animals with this protein. The results don’t indicate that diabetes is contagious like a cold, but blood transfusions, or even food, may spread the disease. The work is “very exciting” and “well-documented” for showing that the protein has some prionlike behavior, says prion biologist Witold Surewicz of Case Western Reserve University in Cleveland, Ohio, who wasn’t connected to the research. However, he cautions against jumping to the conclusion that diabetes spreads from person to person. The study raises that possibility, he says, but “it remains to be determined.” Prions are misfolded proteins that can cause normally folded versions of the same protein to misfold themselves. When this conversion occurs in the brain, the distorted proteins bunch up inside cells and kill them. Although prion diseases are rare in people, they share some similarities with more common illnesses. In Alzheimer’s disease, for instance, globs of a misshapen protein known as β amyloid build up in the brain. Parkinson’s disease and Huntington disease, two other brain maladies, also feature aggregates, or lumps of misfolded proteins. © 2017 American Association for the Advancement of Science.

Keyword: Obesity; Prions
Link ID: 23910 - Posted: 08.02.2017

By DAVID C. ROBERTS Five years ago, I still lived a double life. I was 35, looking out over the Gulf of Thailand and a few weathered beach tenders. Inside, where dark suits filled the conference room, I could feel the eyes of my fellow diplomats. No doubt they were wondering why I was sitting on my briefcase. I joked to no one in particular “My nuclear codes,” trying to deflect awkwardness. The case actually concealed an orthotic sitting cushion that muffled the pain in my lower back; without it, silent shrieking was all I heard. Or maybe they had noticed I was the only one sweating. The air-conditioning tempered the tropical heat, but it was no match for the corset heat wrap that lay discreetly under my tailored suit. Over the previous decade I had become adept at hiding the unexplained pain that racked my back and joints. To all appearances, I was a fit 6-foot-3 man with an easy gait. No one in that conference room knew my suit pants disguised a lace-up ankle brace and a strap velcroed around my left knee. Nor did they know that during breaks I would sneak back to my hotel room where my wife, an artist who moonlighted as my one-person pit crew, waited to press my quadratus lumborum muscle back into submission. I lasted through that meeting as I had through countless others. But in the months that followed, sitting and walking became increasingly difficult. I started to stand during meetings, avoid plane travel, and take motorcycle taxis to go just a couple of buildings’ distance. Eventually, I let the doctors at the embassy in on my secret. They deemed me unfit for work and medevac’ed me from Bangkok back to the United States for treatment. I left quickly, without awkward explanations or goodbyes. © 2017 The New York Times Company

Keyword: Pain & Touch
Link ID: 23908 - Posted: 08.02.2017