Chapter 5. The Sensorimotor System
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By Bob Grant More and more Americans are using cannabis both for medicinal and recreational purposes, but scientists still know little about the drug’s effects on human physiology, according to a National Academies report released this month (January 12). Part of this knowledge gap owes to the fact that cannabis is classified as a Schedule I drug under the US Controlled Substances Act. In the eyes of the federal government, marijuana is a dangerous substance—on par with heroin—that “has no currently accepted medical use in treatment in the United States.” But researchers in Canada are not far ahead of their US counterparts, even though cannabis has since 2001 been functionally legal for medicinal use at the federal level there. See “National Academies Detail the State of Weed Science” “I wish I could say that [legalizing medical marijuana] had led to more research” in Canada, said Mark Ware, a McGill University pain management physician who has researched the safety and efficacy of cannabinoids for the past 18 years. “I think there’s certainly a willingness to be able to document real world use of cannabis under a legal framework.” Ware, who served as a reviewer on the National Academies report, added that while there are several public registries that track the legal use of cannabis among Canadians, experimental evidence on the effects of that use are lacking. “The clinical trials, I think for most people that’s an expensive undertaking,” he said. “There are still questions around who owns the intellectual property, who’s going to sponsor the trials. . . . Those remain barriers even in a legal framework as to the cost of that kind of research and the drug development piece of it.” © 1986-2017 The Scientist
By JANE E. BRODY Susan Sills, a Brooklyn artist who until recently made life-size cutouts on plywood using a power saw, long suspected she might be at risk for developing Parkinson’s disease. Both her mother and grandfather had this neurological movement disorder, and she knew that it sometimes runs in families. So she was not surprised when at age 72 she first noticed hand tremors and a neurologist confirmed that she had the disease. But to watch her in action three years later, it would be hard for a layperson to tell. She stands straight, walks briskly, speaks in clarion tones and maintains a schedule that could tire someone half her age. Having wisely put the power saw aside, Ms. Sills now makes intricately designed art jewelry. She is also a docent at the Brooklyn Museum, participates in a cooperative art gallery and assists her husband’s business by entertaining customers. Ms. Sills attributes her energy and well-being partly to the medication she takes but primarily to the hours she spends working out with a physical therapist and personal trainer, who have helped her develop an exercise regimen that, while not a cure, can alleviate Parkinson’s symptoms and slow progression of the disease. “The exercises opened me up,” said Ms. Sills, allowing such symptoms as small steps, slow movements and tiny, cramped handwriting to subside. “The earlier people begin exercising after a Parkinson’s diagnosis, and the higher the intensity of exercise they achieve, the better they are,” Marilyn Moffat, a physical therapist on the faculty of New York University, said. “Many different activities have been shown to be beneficial, including cycling, boxing, dancing and walking forward and backward on a treadmill. If someone doesn’t like one activity, there are others that can have equally good results.” © 2017 The New York Times Company
Link ID: 23132 - Posted: 01.23.2017
By Catherine Offord In the early 20th century, Danish biologist Johannes Schmidt solved a puzzle that had confounded European fisherman for generations. Freshwater eels—popular for centuries on menus across northern Europe—were abundant in rivers and creeks, but only as adults, never as babies. So where were they coming from? In 1922, after nearly two decades of research, Schmidt published the answer: the Sargasso Sea, the center of a massive, swirling gyre in the North Atlantic Ocean. Now regarded as some of the world’s most impressive animal migrators, European eels (Anguilla anguilla) journey westward across the Atlantic to spawning sites in the Sargasso; their eggs hatch into larvae that are carried back across the ocean by the Gulf Stream, arriving two or three years later to repopulate European waterways. For decades, researchers have assumed that adults made the journey in one short and rapid migration, leaving European coastlines in autumn and arriving in the Sargasso Sea, ready to spawn, the following spring. But this assumption rests on surprisingly little evidence, says behavioral ecologist David Righton of the UK Centre for Environment, Fisheries, and Aquaculture Science. “Since Johannes Schmidt identified this spawning area in the Sargasso Sea, people have been wondering about that great journey and trying to figure out how to follow the eels,” says Righton, whose work on epic marine migrations includes appropriately titled projects such as CODYSSEY and EELIAD. “But the technology hasn’t been available. . . . They just slip away into the darkness, really, in autumn, and no one knows what happens to them.” © 1986-2017 The Scientist
Keyword: Animal Migration
Link ID: 23116 - Posted: 01.18.2017
Charles Q. Choi Prions, the infectious agents best known for causing degenerative brain disorders such as ‘mad cow’ disease, may have been spotted in bacteria. A section of a protein in Clostridium botulinum, the microbe that causes botulism, can behave like a prion when it is inserted into yeast and Escherichia coli bacteria, researchers report in the 13 January issue of Science1. Prions are formed by proteins that can fold in a number of structurally distinct ways. A prion version of a protein can perpetuate itself in an infectious manner by converting normal forms of that protein into the prion version. Scientists first discovered prions in the 1980s as the agents behind fatal brain disorders known as transmissible spongiform encephalopathies. Since then, researchers have found the misfolded proteins in mammals, insects, worms, plants and fungi2, and learned that not all prions harm their hosts. But until now, prions were only seen in the cells of eukaryotic organisms, a group that includes animals, plants and fungi. In the latest study, researchers analysed roughly 60,000 bacterial genomes using software trained to recognize prion-forming proteins in yeast. They focused on a section of the bacterial protein Rho. In many bacteria, such as C. botulinum and E. coli, Rho is a global regulator of gene expression, meaning that it can control the activity of many genes. © 2017 Macmillan Publishers Limited,
Link ID: 23104 - Posted: 01.14.2017
Bruce Bower Marijuana’s medical promise deserves closer, better-funded scientific scrutiny, a new state-of-the-science report concludes. The report, released January 12 by the National Academies of Sciences, Engineering and Medicine in Washington, D.C., calls for expanding research on potential medical applications of cannabis and its products, including marijuana and chemical components called cannabinoids. Big gaps in knowledge remain about health effects of cannabis use, for good or ill. Efforts to study these effects are hampered by federal classification of cannabis as a Schedule 1 drug, meaning it has no accepted medical use and a high potential for abuse. Schedule 1 status makes it difficult for researchers to access cannabis. The new report recommends reclassifying the substance to make it easier to study. Recommendations from the 16-member committee that authored the report come at a time of heightened acceptance of marijuana and related substances. Cannabis is a legal medical treatment in 28 states and the District of Columbia. Recreational pot use is legal in eight of those states and the District. “The legalization and commercialization of cannabis has allowed marketing to get ahead of science,” says Raul Gonzalez, a psychologist at Florida International University in Miami who reviewed the report before publication. While the report highlights possible medical benefits, Gonzalez notes that it also underscores negative consequences of regular cannabis use. These include certain respiratory and psychological problems. |© Society for Science & the Public 2000 - 2017.
Parkinson’s disease, a chronic, progressive movement disorder characterized by tremors and stiffness, is not considered a fatal disease in and of itself, though it may reduce life expectancy by a modest amount. It is often said that people die “with” Parkinson’s rather than “of” the disease. “People who are healthy when diagnosed will generally live about as long as other people in their age cohort,” said James Beck, the vice president for scientific affairs at the Parkinson’s Disease Foundation, which is involved in research, education and advocacy. “It is not a death sentence.” Since Parkinson’s generally affects people later in life — patients are typically given a diagnosis in their 60s — patients often die of unrelated age-related diseases like cancer, heart disease or stroke. But the most common cause of death in those with Parkinson’s is pneumonia, because the disease impairs patients’ ability to swallow, putting them at risk for inhaling or aspirating food or liquids into their lungs, leading to aspiration pneumonia. Since Parkinson’s also impairs mobility and balance, those with the disease are also at high risk for falls and accidents, which can trigger a cascade of medical problems, including being bedridden and developing pneumonia, Dr. Beck said. In its advanced stages, the disease can make walking and talking difficult and cause other problems not related to movement, including cognitive impairment. Patients often cannot care for themselves and need assistance carrying out simple activities of daily living. One long-term study followed a group of 142 Parkinson’s patients after they were given their diagnosis; their mean age at diagnosis was around 70. The researchers found that 23 percent were generally doing well 10 years later, meaning they could maintain their balance and did not have dementia. But over half of the patients in the original group had died, with the most common cause related to Parkinson’s being pneumonia. © 2017 The New York Times Company
Link ID: 23094 - Posted: 01.13.2017
Rachel Ehrenberg A protein that sounds the alarm when the body encounters something painful also helps put out the fire. Called Nav1.7, the protein sits on pain-sensing nerves and has long been known for sending a red alert to the brain when the body has a brush with pain. Now, experiments in rodent cells reveal another role for Nav1.7: Its activity triggers the production of pain-relieving molecules. The study, published online January 10 in Science Signaling, suggests a new approach to pain management that takes advantage of this protein’s dual role. “This is very interesting research,” says neuroscientist Munmun Chattopadhyay of Texas Tech University Health Sciences Center El Paso. The findings suggest that when opiates are given for certain kinds of pain relief, also targeting Nav1.7 might lessen the need for those pain relievers, Chattopadhyay says. That could reduce opiate use and their associated side effects. The new research also solves a puzzle that has frustrated researchers and pharmaceutical companies alike. People with rare mutations in the gene for making Nav1.7 feel no pain at all. That discovery, made more than a decade ago, suggested that Nav1.7 was an ideal target for controlling pain. If a drug could block Nav1.7 activity, some kinds of pain might be eradicated (SN: 6/30/12, p 22). Yet drugs designed to do just that didn’t wipe out people’s pain. “It seemed so obvious and simple,” says study leader Tim Hucho, a neuroscientist at the University Hospital Cologne in Germany. “But it was not so simple.” |© Society for Science & the Public 2000 - 2017
Keyword: Pain & Touch
Link ID: 23090 - Posted: 01.12.2017
Valerie Piro The alarm goes off at 4:30 a.m. Groggy, I turn on the lamp on my night stand and try to sit up. I put my right hand on the wall next to my bed to steady myself, and push my left into the bed. Right away, my abs and back seize up and my legs spasm and kick out straight, forcing me back down onto the bed. Clearly my body thinks it is too early to get up, but I don’t have time to argue with it. I have to get physical therapy out of the way so I can be on time for my medieval history class. After I sit up, I place my hands under my right knee and clasp them together as I bring my knee up and closer to my chest. I reach out to my right foot and cross its heel over my left thigh so that I can plant my heel on the bed. I hug my right leg against my torso and chest and feel a stretch in my lower back and butt. I repeat this on my other side and then proceed to stretch each ankle. Paralysis requires maintenance. I then hop toward the foot of my bed, where my commode chair sits. I set both feet on the footrests as best I can, grab the armrest on the far side of the chair with my left hand, and, using my right hand to drive down into my bed, lift myself onto the commode wheelchair, and wheel to the bathroom. I emerge at 5:35 a.m. I transfer now into a wheelchair whose dimensions are friendly toward my Functional Electrical Stimulation (F.E.S.) cycle — something like a gym exercise bike, without the seat. I pull some milk out of the mini-fridge and pour it over a bowl of cereal. I eat while checking and answering email. At 6:30 it’s time to start cycling. I put two small rectangular electrodes on my left shin muscles, and then two on my right, connect them to the cycle, then strap in my legs and feet. Then two more electrodes then two more, and so on, until most of my lower body is tapped and wired. After I turn on the tablet that’s attached to the cycle, I choose from one of several preset programs to start my workout. Within a couple of minutes, electrical shocks are pulsing into my legs, causing them to contract into pedaling. Imagine pedaling a bicycle uphill for an hour; this is my workout. © 2017 The New York Times Company
Keyword: Movement Disorders
Link ID: 23081 - Posted: 01.11.2017
By Anna Azvolinsky Hummingbirds are efficient hoverers, suspending their bodies midair using rapid forward and backward strokes. Aside from their unique ability to hover, the tiny avians are also the only known birds that can fly in any direction, including sideways. Hummingbird brains appear to be adapted for this flying ability, researchers have now shown. According to a study published today (January 5) in Current Biology, a highly conserved area of the brain—the lentiformis mesencephali (LM), which receives panoramic visual motion information directly from the retina—processes the movement of objects from all directions. In contrast, the LMs of other bird species and all other four-limbed vertebrates studied to date predominantly sense back-to-front motion. While the authors had predicted the neurons of this hummingbird brain region would be tuned to slow motion, they in fact found the opposite: LM neurons were sensitive to quick visual motion, most likely because hummingbirds must process and respond to their environments quickly to avoid collisions, both during hovering and in other modes of flight. “This ancient part of the brain the authors studied has one job: to detect the motion of the image in front of the eyes,” explained Michael Ibbotson, a neuroscientist at the University of Melbourne who penned an accompanying editorial but was not involved in the research. The results of this study suggest that “hummingbirds evolved this area of the brain to have fine motor control to be able to hover and push in every direction possible,” Ibbotson said. © 1986-2017 The Scientist
Link ID: 23064 - Posted: 01.07.2017
By Jessica Hamzelou One woman’s unique experiences are helping us understand the nature of synaesthesia. We don’t know yet what causes synaesthesia, which links senses and can enable people to taste words or smell sounds, for example. It may be at least partly genetic, as it tends to run in families. Some researchers think a brain chemical called serotonin might play a role, because hallucinogenic drugs that alter serotonin levels in the brain can create unusual perceptions. There’s also some evidence that synaesthesia can change or disappear, and a detailed assessment of one woman’s experiences is helping Kevin Mitchell at Trinity College Dublin in Ireland and his team investigate. The woman, referred to as “AB”, sees colours when she hears music, linked to pitch, volume or instrument – higher notes have more pastel shades. She also associates colours with people, largely based on personality. Green is linked to loyalty, for instance. But several experiences in her life have caused her synaesthesia to change. “To say she had a series of unfortunate events would be an understatement,” says Mitchell. As a teenager and young adult, AB sustained several concussions, had migraines, contracted viral meningitis and was struck by lightning. © Copyright Reed Business Information Ltd.
Link ID: 23054 - Posted: 01.04.2017
By KATIE THOMAS The Food and Drug Administration has approved the first drug to treat patients with spinal muscular atrophy, a savage disease that, in its most severe form, kills infants before they turn 2. “This is a miracle — seriously,” Dr. Mary K. Schroth, a lung specialist in Madison, Wis., who treats children who have the disease, said of the approval, which was made last week. “This is a life-changing event, and this will change the course of this disease.” Dr. Schroth has previously worked as a paid consultant to Biogen, which is selling the drug. The drug, called Spinraza, will not come cheap — and, by some estimates, will be among the most expensive drugs in the world. Biogen, which is licensing Spinraza from Ionis Pharmaceuticals, said this week that one dose will have a list price of $125,000. That means the drug will cost $625,000 to $750,000 to cover the five or six doses needed in the first year, and about $375,000 annually after that, to cover the necessary three doses a year. Patients will presumably take Spinraza for the rest of their lives. The pricing could put the drug in the cross hairs of lawmakers and other critics of high drug prices, and perhaps discourage insurers from covering it. High drug prices have attracted intense scrutiny in the last year, and President-elect Donald J. Trump has singled them out as an important issue. “We believe the Spinraza pricing decision is likely to invite a storm of criticism, up to and including presidential tweets,” Geoffrey C. Porges, an analyst for Leerink Partners, said in a note to investors on Thursday. Mr. Porges said the price could lead some insurers to balk or to limit the drug to patients who are the most severely affected, such as infants, even though the F.D.A. has approved Spinraza for all patients with the condition. © 2016 The New York Times Company
Ian Sample Science editor The first subtle hints of cognitive decline may reveal themselves in an artist’s brush strokes many years before dementia is diagnosed, researchers believe. The controversial claim is made by psychologists who studied renowned artists, from the founder of French impressionism, Claude Monet, to the abstract expressionist Willem de Kooning. While Monet aged without obvious mental decline, de Kooning was diagnosed with Alzheimer’s disease more than a decade before his death in 1997. Strobe lighting provides a flicker of hope in the fight against Alzheimer’s Alex Forsythe at the University of Liverpool analysed more than 2,000 paintings from seven famous artists and found what she believes are progressive changes in the works of those who went on to develop Alzheimer’s. The changes became noticeable when the artists were in their 40s. Though intriguing, the small number of artists involved in the study means the findings are highly tentative. While Forsythe said the work does not point to an early test for dementia, she hopes it may open up fresh avenues for investigating the disease. The research provoked mixed reactions from other scientists. Richard Taylor, a physicist at the University of Oregon, described the work as a “magnificent demonstration of art and science coming together”. But Kate Brown, a physicist at Hamilton College in New York, was less enthusiastic and dismissed the research as “complete and utter nonsense”. © 2016 Guardian News and Media Limited
Link ID: 23033 - Posted: 12.29.2016
By KEVIN DEUTSCH An anesthetic commonly used for surgery has surpassed heroin to become the deadliest drug on Long Island, killing at least 220 people there in 2016, according to medical examiners’ records. The drug, fentanyl, is a synthetic opioid, which can be 100 times more potent than morphine. The numbers from Long Island are part of a national pattern, as fentanyl fatalities have already surpassed those from heroin in other parts of the country, including New England, as its use has skyrocketed. Part of the reason for the increase is economic — because fentanyl can be manufactured in the lab, it is much cheaper and easier than cultivating heroin. In New York City, more than 1,000 people are expected to die from drug overdoses this year — the first recorded four-digit death total in city history, according to statistics compiled by the Department of Health and Mental Hygiene. Nearly half of all unintentional drug overdose deaths in the city since July have involved fentanyl, the health department said. The medical examiners of Long Island’s two counties, Nassau and Suffolk, compiled the new numbers. “Fentanyl has surpassed heroin as the most commonly detected drug in fatal opioid overdoses,” Dr. Michael J. Caplan, the Suffolk County medical examiner, said in a written statement about the statistics, which were obtained by The New York Times ahead of their release. “The influx of illicitly manufactured fentanyl from overseas is a nationwide issue that requires a multidisciplinary intervention from all levels of government.” Nationwide, recorded deaths from opioids surpassed 30,000 in 2015, according to data compiled by the Centers for Disease Control and Prevention. And overdoses caused by synthetic opioids like fentanyl increased by 72.2 percent in 2015 over 2014 — one of the deadliest year-over-year surges for any drug in United States history, the same data shows. © 2016 The New York Times Company
By Ben Andrew Henry Traveling from the forests and fields of Europe to the grasslands south of the Sahara desert is a monumental trip for anyone, and especially for a diminutive insect. Yet every year, populations of the painted lady (Vanessa cardui) butterfly make that journey over the course of several generations. The logistics of this migratory feat had been speculated for some time, but never fully understood, in part because of the difficulty of tracking the tiny insects across long distances. In a study published October 4 in Biology Letters, researchers reported having measured the isotopic composition of butterfly wings in Europe and south of the Sahara. Since the fraction of heavy hydrogen isotopes in the environment varies geographically, the team used its analysis to identify the origins of butterflies captured, confirming that groups of butterflies in the Sahara did originate in Europe. The butterflies do not linger in Africa long. They most likely make their trip, the authors suggested, to take advantage of the burst of productivity in the tropical savannah that follows the rainy season—and to breed the generation that will start the trip back. Europe’s freshwater eels (Anguilla anguilla) live out their days in rivers and streams, but they never spawn there. Massive catches of larval eels in the Sargasso Sea tipped researchers off a century ago that eels must spawn in the swirling mid-Atlantic gyre of free-floating seaweed and then migrate to Europe. Eels leave their homes in the late fall, but other than that, the details of their journey have been a mystery. © 1986-2016 The Scientist
Keyword: Animal Migration
Link ID: 23029 - Posted: 12.28.2016
by Bethany Brookshire An opioid epidemic is upon us. Prescription painkillers such as fentanyl and morphine can ease terrible pain, but they can also cause addiction and death. The Centers for Disease Control and Prevention estimates that nearly 2 million Americans are abusing or addicted to prescription opiates. Politicians are attempting to stem the tide at state and national levels, with bills to change and monitor how physicians prescribe painkillers and to increase access to addiction treatment programs. Those efforts may make access to painkillers more difficult for some. But pain comes to everyone eventually, and opioids are one of the best ways to make it go away. Morphine is the king of pain treatment. “For hundreds of years people have used morphine,” says Lakshmi Devi, a pharmacologist at the Ichan School of Medicine Mount Sinai in New York City. “It works, it’s a good drug, that’s why we want it. The problem is the bad stuff.” The “bad stuff” includes tolerance — patients have to take higher and higher doses to relieve their pain. Drugs such as morphine depress breathing, an effect that can prove deadly. They also cause constipation, drowsiness and vomiting. But “for certain types of pain, there are no medications that are as effective,” says Bryan Roth, a pharmacologist and physician at the University of North Carolina at Chapel Hill. The trick is constructing a drug with all the benefits of an opioid painkiller, and few to none of the side effects. Here are three ways that scientists are searching for the next big pain buster, and three of the chemicals they’ve turned up. |© Society for Science & the Public 2000 - 2016
By DANNY HAKIM LONDON — Syngenta, the Swiss pesticide giant, claims on its website that data from an influential 2011 study shows that farmers who use the weed killer paraquat are less likely to develop Parkinson’s disease than the general population. However, Syngenta’s claim is at odds with the actual findings of the study, according to two of its authors. The 2011 study, carried out by the National Institutes of Health and researchers from other institutions around the world, found that people who used paraquat or another pesticide, called rotenone, were roughly two and a half times more likely to develop Parkinson’s. The work is known as the Farming and Movement Evaluation, or FAME, study. It drew on a sweeping United States government project called the Agricultural Heath Study, which tracked more than 80,000 farmers and their spouses, as well as other people who applied pesticides, in Iowa and North Carolina. The FAME researchers identified 115 people from the Agricultural Health Study who developed Parkinson’s, and studied 110 of them who provided information on the pesticides they used. The study was influential even among some people who had been skeptics of a connection between the chemicals and the disease. Gary W. Miller, a professor of environmental health at Emory University, referred to a link between Parkinson’s and paraquat as a “red herring” in a 2007 publication. But while Dr. Miller said in a recent email exchange that he had concerns about some previous research making the connection, “the FAME data are strong and should be considered.” He said the study “appears to show a connection between paraquat exposure and Parkinson’s disease.” Because of the prominence of the FAME study, Syngenta addresses it on one of its websites, paraquat.com. Syngenta claims that the study shows that only 115 people had Parkinson’s out of the more than 80,000 people in the broader Agricultural Health Study. Therefore, “the incidence of Parkinson’s disease” in the study “appears to be lower than in the general U.S. population,” Syngenta says. © 2016 The New York Times Company
By Kelly Servick The “mad cow disease” epidemic that killed more than 200 people in Europe peaked more than a decade ago, but the threat it poses is still real. Eating meat contaminated with bovine spongiform encephalopathy and its hallmark misshapen proteins, called prions, can cause a fatal and untreatable brain disorder, variant Creutzfeldt-Jakob disease (vCJD). Thousands of Europeans are thought to be asymptomatic carriers, and they can spread prions through blood donations. So for years, researchers have sought a test to safeguard blood supplies. This week, two teams bring that goal closer. They describe methods for detecting prions in blood that proved highly accurate in small numbers of samples from infected people and controls. “There is new technology to go forward, and it looks promising,” says Jonathan Wadsworth, a biochemist who studies prion disease at University College London. “These are definitely very welcome papers.” Analyses of discarded appendix and tonsil samples suggest that as many as one in 2000 people in the United Kingdom carries abnormal prions—misfolded variations of a naturally abundant protein, which prompt surrounding healthy proteins to fold and clump abnormally. No one knows how many of these carriers will ever develop vCJD; incubation periods as long as 50 years have been reported. Once symptoms occur—first depression and hallucinations, and eventually dementia and loss of motor control—patients survive about a year. Four people are known to have contracted vCJD through a blood transfusion from an infected donor. © 2016 American Association for the Advancement of Science.
Link ID: 23007 - Posted: 12.22.2016
Rachel Ehrenberg Scientists investigating what keeps lungs from overinflating can quit holding their breath. Experiments in mice have identified a protein that senses when the lungs are full of air. This protein helps regulate breathing in adult mice and gets breathing going in newborn mice, researchers report online December 21 in Nature. If the protein plays a similar role in people — and a few studies suggest that it does — exploring its activity could help explain disorders such as sleep apnea or chronic obstructive pulmonary disease. “These are extremely well done, very elegant studies,” says neonatologist Shabih Hasan of the University of Calgary in Canada, a specialist in breathing disorders in newborns. Researchers knew that feedback between the lungs and brain maintains normal breathing. But “this research give us an understanding at the cellular level,” says Hasan. “It’s a major advance.” Called Piezo2, the protein forms channels in the membranes of nerve cells in the lungs. When the lungs stretch, the Piezo2 channels detect the distortion caused by the mechanical force of breathing and spring open, triggering the nerves to send a signal. Led by neuroscientist Ardem Patapoutian, researchers discovered that the channels send signals along three different pathways. Mice bred to lack Piezo2 in a cluster of nerve cells that send messages to the spinal cord had trouble breathing and died within 24 hours. Similarly, newborn mice missing Piezo2 channels in nerves that communicate with the brain stem via a structure called the jugular ganglion also died. |© Society for Science & the Public 2000 - 2016.
Keyword: Pain & Touch
Link ID: 23006 - Posted: 12.22.2016
By Meredith Wadman There have been few happy endings when it comes to spinal muscular atrophy (SMA), the most common genetic cause of death in childhood. The disease inexorably destroys the motor neurons of the spinal cord and brainstem that control movement, including swallowing and breathing. In its most severe form, SMA kills those afflicted at about age 2, most commonly by suffocating them. There are no Food and Drug Administration (FDA)–approved drugs for the disease. That is almost certainly about to change. An innovative drug that helps cells bypass the genetic flaw responsible for SMA may be approved as soon as this month, on the heels of strongly positive results from late-stage clinical trials. On 7 November, a trial of the drug, nusinersen, in wheelchair-bound children aged 2 to 12, was stopped on the grounds that it was unethical to deny the drug to children in the control arm, given the positive results in the treated children. In August, a similar trial in infants was stopped for the same reason, allowing the untreated infants in a control arm to begin receiving the drug. And today, a paper appearing in The Lancet provides compelling biological evidence that nusinersen is having its desired effect in the cells of the brain and spinal cord. “These [infant-onset] SMA kids are going to die. And not only are they now not dying, you are essentially on the path to a true cure of a degenerative [neurological] disease, which is unheard of,” says Jeffrey Rothstein, a neurologist at the Johns Hopkins School of Medicine in Baltimore, Maryland, who was not affiliated with the trials of the drug and is not connected with either of the two companies involved in its development: Ionis of Carlsbad, California, and Biogen of Cambridge, Massachusetts. © 2016 American Association for the Advancement of Science
Sometimes the biggest gifts arrive in the most surprising ways. A couple in Singapore, Tianqiao Chen and Chrissy Luo, were watching the news and saw a Caltech scientist help a quadriplegic use his thoughts to control a robotic arm so that — for the first time in more than 10 years — he could sip a drink unaided. Inspired, Chen and Luo flew to Pasadena to meet the scientist, Richard Andersen, in person. Now they’ve given Caltech $115 million to shake up the way scientists study the brain in a new research complex. Construction of the Tianqiao and Chrissy Chen Institute for Neuroscience at Caltech will begin as early as 2018 and bring together biology, engineering, chemistry, physics, computer science and the social sciences to tackle brain function in an integrated, comprehensive way, university officials announced Tuesday. The goal of connecting these traditionally separate departments is to make “transformational advances” that will lead to new scientific tools and medical treatments, the university said. Research in shared labs will include looking more deeply into fundamentals of the brain and exploring the complexities of sensation, perception, cognition and human behavior. Neuroscience research has advanced greatly in recent years, Caltech President Thomas Rosenbaum said. The field now has the tools to look at individual neurons, for example, as well as the computer power to analyze massive data sets and an entire system of neurons. Collaborating across traditional academic boundaries takes it to the next level, he said. “The tools are at a time and place where we think that the field is ready for that sort of combination.”
Link ID: 22960 - Posted: 12.07.2016