Chapter 11. Motor Control and Plasticity

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By Meredith Wadman The hallmark brain damage in Parkinson’s disease is thought to be the work of a misfolded, rogue protein that spreads from brain cell to brain cell like an infection. Now, researchers have found that the normal form of the protein—α-synuclein (αS)—may actually defend the intestines against invaders by marshaling key immune cells. But chronic intestinal infections could ultimately cause Parkinson’s, the scientists suggest, if αS migrates from overloaded nerves in the gut wall to the brain. “The gut-brain immune axis seems to be on a cusp of an explosion of new insights, and this work offers an exceptionally exciting new hypothesis,” says Charles Bevins, an expert in intestinal immunity at the University of California, Davis, who was not involved with the study. The normal function of αS has long been a mystery. Though the protein is known to accumulate in toxic clumps in the brain and the nerves of the gut wall in patients with Parkinson’s disease, no one was sure what it did in healthy people. Noting that a region of the αS molecule behaves similarly to small, microbe-targeting proteins that are part of the body’s immune defenses, Michael Zasloff, an immunologist at Georgetown University Medical Center in Washington, D.C., set out to find whether αS, too, might help fend off microbial invaders. © 2017 American Association for the Advancement of Science

Keyword: Parkinsons
Link ID: 23784 - Posted: 06.28.2017

By Michael Price Contrary to popular lore that portrays chimpanzees as having “super strength,” studies have only found modest differences with humans. But our closest relatives are slightly stronger by several measures, and now a study comparing the muscle fibers of different primates reveals a potential explanation: Humans may have traded strength for endurance, allowing us to travel farther for food. To determine why chimpanzees are stronger than humans—at least on a pound-for-pound basis—Matthew O’Neill, an anatomy and evolution researcher at the University of Arizona College of Medicine in Phoenix, and colleagues biopsied the thigh and calf muscles of three chimps housed at the State University of New York at Stony Brook. They dissected the samples into individual fibers and stimulated them to figure out how much force they could generate. Comparing their measurements to known data from humans, the team found that, at the individual fiber level, muscle output was about the same. Given that different fibers throughout the muscle might make a difference, the researchers conducted a more thorough analysis of tissue samples from pelvic and hind limb muscles of three chimpanzee cadavers from various zoos and research institutes around the United States. Previous studies in mammals have found that muscle composition between trunk, forelimb, and hind limb muscles is largely the same, O’Neill says, so he’s confident the samples are representative across most of the chimp’s musculature. The team used a technique called gel electrophoresis to break down the muscles into individual muscle fibers, and compared this breakdown to human muscle fiber data. © 2017 American Association for the Advancement of Science.

Keyword: Muscles; Evolution
Link ID: 23782 - Posted: 06.27.2017

Carl Zimmer Mark D. Zabel wants to set some fires. Dr. Zabel and his colleagues are developing plans to burn plots of National Park Service land in Arkansas and Colorado. If the experiments turn out as the researchers hope, they will spare some elk and deer a gruesome death. Across a growing swath of North America, these animals are dying from a mysterious disorder called chronic wasting disease. It’s caused not by a virus or bacterium, but a deformed protein called a prion. When ingested, prions force normal proteins in the animal’s body to become deformed as well. Over the course of months, prions can gradually wreck the animal’s nervous system, ultimately killing it. This year is the 50th anniversary of the discovery of chronic wasting disease. In the September issue of Microbiology and Molecular Biology Reviews, Dr. Zabel, an immunologist at Colorado State University, and his former graduate student Aimee Ortega survey what scientists have learned about the slow-spreading plague. It makes for ominous reading. “There’s a lot that we still don’t know and don’t understand about the disease,” Dr. Zabel said in an interview. Once chronic wasting disease gets a foothold, it can spread relentlessly. It’s now documented in 24 states, and continues to expand into new ranges. In some herds, as many as half of the animals carry prions. It’s only been in recent years that scientists have gained crucial clues to how the disease spreads. Direct contact, it turns out, isn’t the only way that the prions get from one animal to another. © 2017 The New York Times Company

Keyword: Prions
Link ID: 23781 - Posted: 06.27.2017

By Sam Wong People who have had amputations can control a virtual avatar using their imagination alone, thanks to a system that uses a brain scanner. Brain-computer interfaces, which translate neuron activity into computer signals, have been advancing rapidly, raising hopes that such technology can help people overcome disabilities such as paralysis or lost limbs. But it has been unclear how well this might work for people who have had limbs removed some time ago, as the brain areas that previously controlled these may become less active or repurposed for other uses over time. Ori Cohen at IDC Herzliya, in Israel, and colleagues have developed a system that uses an fMRI brain scanner to read the brain signals associated with imagining a movement. To see if it can work a while after someone has had a limb removed, they recruited three volunteers who had had an arm removed between 18 months and two years earlier, and four people who have not had an amputation. While lying in the fMRI scanner, the volunteers were shown an avatar on a screen with a path ahead of it, and instructed to move the avatar along this path by imagining moving their feet to move forward, or their hands to turn left or right. The people who had had arm amputations were able to do this just as well with their missing hand as they were with their intact hand. Their overall performance on the task was almost as good as of those people who had not had an amputation. © Copyright New Scientist Ltd.

Keyword: Robotics
Link ID: 23770 - Posted: 06.24.2017

By KATIE THOMAS Nolan and Jack Willis, twins from upstate New York, and just 10 other boys took part in a clinical trial that led to the approval last fall of the very first drug to treat their rare, deadly muscle disease. Now the Willis boys are again test cases as a different type of medical question comes to the fore: whether insurers will cover the controversial drug, Exondys 51, which can cost more than $1 million a year even though it’s still unclear if it works. The boys’ insurer, Excellus BlueCross BlueShield, refused to cover the cost of the drug because the twins, who are 15, can no longer walk. Their disease, Duchenne muscular dystrophy, overwhelmingly affects boys and causes muscles to deteriorate, killing many of them by the end of their 20s. “I’m cycling between rage and just sadness,” their mother, Alison Willis Hoke, said recently, on the day she learned that an appeal for coverage had been denied. For now, the company that sells the drug, Sarepta Therapeutics, is covering the treatment’s costs, but Mrs. Hoke does not know how long that will last. The desperation in Mrs. Hoke’s voice reflects a sobering reality for families of boys with the disease since their elation last fall over the drug’s approval. Because the Food and Drug Administration overruled its own experts — who weren’t convinced the Exondys 51 had shown sufficiently good results — and gave the drug conditional approval, many insurers are now declining to cover it or are imposing severe restrictions that render patients ineligible. The story of Exondys 51 raises complex and emotionally charged questions about what happens when the F.D.A. approves an expensive drug based on a lower bar of proof. In practice, health insurers have taken over as gatekeeper in determining who will get the drug. © 2017 The New York Times Company

Keyword: Muscles; Movement Disorders
Link ID: 23768 - Posted: 06.23.2017

By Alice Klein EVIDENCE that Parkinson’s disease may be an autoimmune disorder could lead to new ways to treat the illness. Parkinson’s begins with abnormal clumping of a protein called synuclein in the brain. Neighbouring dopamine-producing neurons then die, causing tremors and difficulty moving. The prevailing wisdom has been that these neurons die from a toxic reaction to synuclein deposits. However, Parkinson’s has been linked to some gene variants that affect how the immune system works, leading to an alternative theory that synuclein causes Parkinson’s by triggering the immune system to attack the brain. An argument against this theory has been that brain cells are safe from immune system attack, because most neurons don’t have antigens – the markers immune cells use to recognise a target. But by studying postmortem brain tissue samples, David Sulzer at Columbia University and his team have discovered that dopamine-producing neurons do display antigens. The team has now conducted blood tests to reveal that people with Parkinson’s show an immune response to these antigens, while people who don’t have the condition do not (Nature, DOI: 10.1038/nature22815). These findings suggest Parkinson’s may be an autoimmune disorder, in which the immune system mistakenly attacks part of the body. There have been hints before that the immune system is involved in Parkinson’s, but this is the first evidence that it plays a major pathological role, says Roger Barker at the University of Cambridge. “It would be an attractive target for therapeutic intervention,” he says. However, it isn’t clear yet if the immune response directly causes neuron death, or if it is merely a side effect of the disease. Sulzer’s team plans to try blocking the autoimmune response in Parkinson’s, to see if this can stop the disease progressing. © Copyright New Scientist Ltd.

Keyword: Parkinsons; Neuroimmunology
Link ID: 23760 - Posted: 06.22.2017

Parkinson’s disease is commonly thought of as a movement disorder, but after years of living with the disease, approximately 25 percent of patients also experience deficits in cognition that impair function. A newly developed research tool may help predict a patient’s risk for developing dementia and could enable clinical trials aimed at finding treatments to prevent the cognitive effects of the disease. The research was published in Lancet Neurology and was partially funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “This study includes both genetic and clinical assessments from multiple groups of patients, and it represents a significant step forward in our ability to effectively model one of the most troublesome non-motor aspects of Parkinson’s disease,” said Margaret Sutherland, Ph.D., program director at the NINDS. For the study, a team of researchers led by Clemens Scherzer, M.D., combined data from 3,200 people with Parkinson’s disease, representing more than 25,000 individual clinical assessments and evaluated seven known clinical and genetic risk factors associated with developing dementia. From this information, they built a computer-based risk calculator that may predict the chance that an individual with Parkinson’s will develop cognitive deficits. Dr. Scherzer is head of the Neurogenomics Lab and Parkinson Personalized Medicine Program at Harvard Medical School and a member of the Ann Romney Center for Neurologic Diseases at Brigham and Women’s Hospital, Boston.

Keyword: Parkinsons
Link ID: 23759 - Posted: 06.22.2017

By Neuroskeptic A high-profile paper in Cell reports on a new brain stimulation method that’s got many neuroscientists excited. The new technique, called temporal interference (TI) stimulation, is said to be able to reach structures deep inside the brain, using nothing more than scalp electrodes. Currently, the only way to stimulate deep brain structures is by implanting electrodes (wires) into the brain – which is an expensive and potentially dangerous surgical procedure. TI promises to make deep brain stimulation an everyday, non-invasive tool. But will it really work? The paper comes from Nir Grossman et al. from the lab of Edward S. Boyden at MIT. Their technique is based around applying two electrical fields to the subject’s head. Each field is applied using two scalp electrodes. It is the interaction between the two fields that creates brain stimulation. Both fields oscillate at slightly different frequencies, for instance 2 kHz and 2.01 kHz. Where these fields overlap, a pattern of interference is created which oscillates with an ‘envelope’ at a much lower frequency, say 10 Hz. The frequency of the two fields is too high to have any effect on neural activity, but the interference pattern does have an effect. Crucially, while the electric fields are strongest close to the electrodes, the interference pattern is most intense at a remote point – which could be deep in the brain.

Keyword: Brain imaging; Parkinsons
Link ID: 23740 - Posted: 06.14.2017

Jon Hamilton Researchers are working to revive a radical treatment for Parkinson's disease. The treatment involves transplanting healthy brain cells to replace cells killed off by the disease. It's an approach that was tried decades ago and then set aside after disappointing results. Now, groups in Europe, the U.S. and Asia are preparing to try again, using cells they believe are safer and more effective. "There have been massive advances," says Claire Henchcliffe, a neurologist at Weill Cornell Medicine in New York. "I'm optimistic." "We are very optimistic about ability of [the new] cells to improve patients' symptoms," says Viviane Tabar, a neurosurgeon and stem cell biologist at Memorial Sloan Kettering Cancer Center in New York. Henchcliffe and Tabar joined several other prominent scientists to describe plans to revive brain cell transplants during a session Tuesday at the International Society for Stem Cell Research meeting in Boston. Their upbeat message marks a dramatic turnaround for the approach. During the 1980s and 1990s, researchers used cells taken directly from the brains of aborted fetuses to treat hundreds of Parkinson's patients. The goal was to halt the disease. © 2017 npr

Keyword: Parkinsons; Stem Cells
Link ID: 23738 - Posted: 06.14.2017

By Edd Gent There’s been a lot of hype coming out of Silicon Valley about technology that can meld the human brain with machines. But how will this help society, and which companies are leading the charge? Elon Musk, chief executive of Tesla and SpaceX, made waves in March when he announced his latest venture, Neuralink, which would design what are called brain-computer interfaces. Initially, BCIs would be used for medical research, but the ultimate goal would be to prevent humans from becoming obsolete by enabling people to merge with artificial intelligence. Musk is not the only one who’s trying to bring humans closer to machines. Here are five organizations working hard on hacking the brain. According to Musk, the main barrier to human-machine co­operation is communication bandwidth. Because using a touch screen or a keyboard is a slow way to communicate with a computer, Musk’s new venture aims to create a “high-bandwidth” link between the brain and machines. What that system would look like is not entirely clear. Words such as “neural lace” and “neural dust” have been bandied about, but all that has really been revealed is a business model. Neuralink has been registered as a medical research company, and Musk said the firm will produce a product to help people with severe brain injuries within four years. This will lay the groundwork for developing BCIs for healthy people, enabling them to communicate by “consensual telepathy,” possibly within five years, Musk said. Some scientists, particularly those in neuroscience, are skeptical of Musk’s ambitious plans. © 1996-2017 The Washington Post

Keyword: Robotics
Link ID: 23733 - Posted: 06.12.2017

By Clare Wilson Would you have pig cells implanted in your brain? Some people with Parkinson’s disease have, in the hope it will stop their disease progressing. The approach is still in the early stages of testing, but initial results from four people look promising, with all showing some improvement 18 months after surgery. People with Parkinson’s disease, which causes tremors and difficulty moving, usually get worse over time. The disease is caused by the gradual loss of brain cells that make dopamine, a compound that helps control our movements. Current medicines replace the missing dopamine, but their effectiveness wears off over the years. So Living Cell Technologies, based in Auckland, New Zealand, has been developing a treatment that uses cells from the choroid plexus in pigs. This brain structure makes a cocktail of growth factors and signalling molecules known to help keep nerve cells healthy. Last month, surgery was completed on a further 18 people in a placebo-controlled trial, using the choroid plexus cell implants. The hope is that compounds made by these cells will nourish the remaining dopamine-producing cells in the patients’ brains, slowing further loss. © Copyright New Scientist Ltd.

Keyword: Parkinsons; Stem Cells
Link ID: 23731 - Posted: 06.12.2017

By Nicholette Zeliadt, For 6-year-old Macey, lunchtime at school is not so much a break from reading and math as it is an hour rife with frustration. Here’s how Macey’s mother, Victoria, describes Macey’s typical lunch break: In her special-education classroom an hour north of San Francisco, Macey’s classmates gather at a big square table, chattering away and snatching one another’s food. Macey, meanwhile, is sequestered away at a small white table in a corner, facing a bookshelf. She grabs the handle of a spoon using the palm of her right hand, awkwardly scoops up rice and spills it onto her lap. She wants to be at the big table with her peers, but she sits with an aide away from the other children to minimize distractions while she eats. (Victoria requested that we use her and Macey’s first names only, to protect their privacy.) After lunch, the children spill out onto the playground. Macey, wearing a helmet, trails behind, holding her aide’s hand. She can walk, but she often trips on uneven surfaces and falls over. She tends to misjudge heights, and once pulled a muscle while climbing on playground equipment. When she was 3, she tripped and fell headfirst out of a sandbox, scraping her face, chipping one tooth and dislodging another. Macey has little trouble moving around the house because it has few stairs and her mother never changes the layout of the rooms. Victoria’s biggest concern is that Macey’s movement troubles interfere with her social life. © 2017 Scientific American,

Keyword: Autism; Movement Disorders
Link ID: 23713 - Posted: 06.06.2017

Mo Costandi Since 1997, more than 100,000 Parkinson’s Disease patients have been treated with deep brain stimulation (DBS), a surgical technique that involves the implantation of ultra-thin wire electrodes. The implanted device, sometimes referred to as a ‘brain pacemaker’, delivers electrical pulses to a structure called the subthalamic nucleus, located near the centre of the brain, and effectively alleviates many of the physical symptoms of the disease, such as tremor, muscle rigidity, and slowed movements. DBS is generally safe but, like any surgical procedure, comes with some risks. First and foremost, it is highly invasive, requiring small holes to be drilled in the patient’s skull, through which the electrodes are inserted. Potential complications of this include infection, stroke, and bleeding on the brain. The electrodes, which are implanted for long periods of time, sometimes move out of place; they can also cause swelling at the implantation site; and the wire connecting them to the battery, typically placed under the skin of the chest, can erode, all of which require additional surgical procedures. Now, researchers at the Massachusetts Institute of Technology have a developed a new method that can stimulate cells deep inside the brain non-invasively, using multiple electric fields applied from outside the organ. In a study published today in the journal Neuron, they show that the method can selectively stimulate deep brain structures in live mice, without affecting the activity of cells in the overlying regions, and also that it can be easily adjusted to evoke movements by stimulation of the motor cortex. © 2017 Guardian News and Media Limited o

Keyword: Parkinsons
Link ID: 23700 - Posted: 06.02.2017

By Bob Grant Prosthetic limbs are rejected by amputees’ bodies at a rate of about 20 percent. Researchers at MIT are seeking to reduce that number, using an amputation procedure that encourages increased feedback between muscles, tendons, and the nervous system so that an artificial limb might stimulate them in a more natural way—giving patients a better sense of proprioception, or where their limb is in space. The key to the surgical technique, demonstrated in rats so far, is to emulate the normal agonist-antagonist pairing of muscles (think biceps and triceps) at the amputation site so that the muscles and nerves surrounding a prosthetic can sense and transmit proprioceptive information about the artificial limb and how much force is being applied to it. The researchers published their work today (May 31) in Science Robotics. “We’re talking about a dramatic improvement in patient care,” Hugh Herr, an MIT professor of media arts and sciences and a coauthor of the study, said in a statement. “Right now there’s no robust neural method for a person with limb amputation to feel proprioceptive positions and forces applied to the prosthesis. Imagine how that would completely hinder one’s ability to move, to successfully balance, or to manipulate objects.” Herr, himself a double-amputee, and his team operated on seven rats, cutting through muscles and nerves in their hind legs. The researchers then grafted on paired muscles, wiring them up to severed nerves. After healing for four months, the rats’ new muscles were contracting and relaxing in tandem, as in naturally paired muscles, and sending electrical signals that reflected the amplitude of the artificial stimulation Herr and his colleagues applied. © 1986-2017 The Scientist

Keyword: Movement Disorders
Link ID: 23693 - Posted: 06.02.2017

By JANE E. BRODY A neighbor of mine was recently told he has a devastating neurological disorder that is usually fatal within a few years of diagnosis. Though a new drug was recently approved for the illness, treatments may only slow progression of the disease for a time or extend life for maybe two or three months. He is a man of about 60 I’ve long considered the quintessential Mr. Fix-it, able to repair everything from bicycles to bathtubs. Now he is facing amyotrophic lateral sclerosis, or Lou Gehrig’s disease — a disease that no one yet knows how to fix. I can only imagine what he is going through because he does not want to talk about it. However, many others similarly afflicted have openly addressed the challenges they faced, though it is usually up to friends and family to express them and advocate for more and better research and public understanding. A.L.S. attacks the nerve cells in the brain and spinal cord that control voluntary muscle movements, like chewing, walking, breathing, swallowing and talking. It is invariably progressive. Lacking nervous system stimulation, the muscles soon begin to weaken, twitch and waste away until individuals can no longer speak, eat, move or even breathe on their own. Last year, the Centers for Disease Control and Prevention estimated that between 14,000 and 15,000 Americans have A.L.S., which makes it sound like a rare disease, but only because life expectancy is so short. A.L.S. occurs throughout the world, and it is probably far more common than generally thought. Over the course of a lifetime, one person in about 400 is likely to develop it, a risk not unlike that of multiple sclerosis. But with the rare exception of an outlier like the brilliant physicist Stephen Hawking, who has had A.L.S. for more than 50 years, it usually kills so quickly that many people do not know anyone living with this disease. Only one person in 10 with A.L.S. is likely to live for a decade or longer. © 2017 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 23675 - Posted: 05.29.2017

Susan Milius A question flamingo researchers get asked all the time — why the birds stand on one leg — may need rethinking. The bigger puzzle may be why flamingos bother standing on two. Balance aids built into the birds’ basic anatomy allow for a one-legged stance that demands little muscular effort, tests find. This stance is so exquisitely stable that a bird sways less to keep itself upright when it appears to be dozing than when it’s alert with eyes open, two Atlanta neuromechanists report May 24 in Biology Letters. “Most of us aren’t aware that we’re moving around all the time,” says Lena Ting of Emory University, who measures what’s called postural sway in standing people as well as in animals. Just keeping the human body vertical demands constant sensing and muscular correction for wavering. Even standing robots “are expending quite a bit of energy,” she says. That could have been the case for flamingos, she points out, since effort isn’t always visible. Translate that improbably long flamingo leg into human terms, and the visible part of the leg would be just the shin down. A flamingo’s hip and knee lie inside the bird’s body. Ting and Young-Hui Chang of the Georgia Institute of Technology tested balance in fluffy young Chilean flamingos coaxed onto a platform attached to an instrument that measures how much they sway. Keepers at Zoo Atlanta hand-rearing the test subjects let researchers visit after feeding time in hopes of catching youngsters inclined toward a nap — on one leg on a machine. “Patience,” Ting says, was the key to any success in this experiment. |© Society for Science & the Public 2000 - 2017

Keyword: Sleep
Link ID: 23656 - Posted: 05.24.2017

By LISA SANDERS, M.D. The woman woke to the sound of her 57-year-old husband sobbing. They’d been married for 30 years, and she had never heard him cry before. “I hurt so much,” he wailed. “I have to go back to the hospital.” The symptoms started two weeks earlier. One afternoon, coming home from his job as a carpenter, he felt hot and tired. He shook with shivers even though the day was warm. He drank a cup of tea and went to bed. The next day he felt fine, until the end of the day, when he felt overwhelmed by the heat and chills again. The day after that was the same. When he woke one morning and saw that his body was covered with pale pink dots — his arms, his face, his chest and thighs — he started to worry. His wife took him to the Griffin Hospital emergency room in Derby, Conn. The first doctor who saw him thought he probably had Lyme disease. Summer had just started, and he’d already seen a lot of cases. He sent the patient home with an antibiotic and steroid pills for the rash. The man took the medications but didn’t get any better. Soon everything started to hurt. His muscles, his joints and his back felt as if he’d been beaten. He dragged himself back to the E.R. He was given pain pills. A few days later, he went to the E.R. a third time and was given more pain meds. After waking up crying, he went yet again, and this time, the doctors admitted him. By then the patient had had several blood tests, which showed no sign of Lyme or other tick-borne diseases. A CT scan was equally uninformative. The next day, the man was walking to the bathroom when his legs gave out and he fell down. The doctor in charge of his care came and examined him once again. The man looked fit and healthy, despite the now-bright-red rash, but his legs were extremely weak. If the doctor applied even light pressure to the raised leg, it sagged back down to the bed. And his feet felt numb. He had a sensation of tingling in his hands, as if they had gone to sleep. That was how the weakness and numbness in his legs started, he told the doctor. And the next day, his hands were so weak he had to use both just to drink a cup of water. © 2017 The New York Times Company

Keyword: Movement Disorders; Neuroimmunology
Link ID: 23644 - Posted: 05.22.2017

By: Ted Dinan, M.D., Ph.D, and John F. Cryan, Ph.D. O ver the past few years, the gut microbiota has been implicated in developmental disorders such as schizophrenia and autism, neurodegenerative disorders such as Alzheimer’s disease and Parkinson’s disease, mood disorders such as depression, and even addiction disorders. It now seems strange that for so many decades we viewed the gut microbiota as bacteria that did us no harm but were of little benefit. This erroneous view has been radically transformed into the belief that the gut microbiota is, in effect, a virtual organ of immense importance. What we’ve learned is that what is commonly referred to as “the brain-gut-microbiota axis” is a bidirectional system that enables gut microbes to communicate with the brain and the brain to communicate back to the gut. It may be hard to believe that the microbes in the gut collectively weigh around three pounds—the approximate weight of the adult human brain—and contain ten times the number of cells in our bodies and over 100 times as many genes as our genome. 1 If the essential microbial genes were to be incorporated into our genomes, it is likely that our cells would not be large enough for the extra DNA. Many of those genes in our microbiota are important for brain development and function; they enable gut bacteria to synthesize numerous neurotransmitters and neuromodulators such as γ-aminobutyric acid (GABA), serotonin, dopamine, and short-chain fatty acids. While some of these compounds act locally in the gut, many products of the microbiota are transported widely and are necessary for the proper functioning of diverse organs. This is a two-way interaction: gut microbes are dependent on us for their nourishment. Any pathological process that reduces or increases food intake has implications for our microbes. © 2017 The Dana Foundation. All Rights Reserved.

Keyword: Parkinsons
Link ID: 23636 - Posted: 05.19.2017

By DENISE GRADY A new drug for amyotrophic lateral sclerosis, or Lou Gehrig’s disease, was approved on Friday by the Food and Drug Administration. The drug, called Radicava or edaravone, slowed the progression of the degenerative disease in a six-month study in Japan. It must be given by intravenous infusion and will cost $145,524 a year, according to its manufacturer, MT Pharma America, a subsidiary of the Japanese company Mitsubishi Tanabe Pharma Corporation. Radicava is only the second drug ever approved to treat A.L.S. The first, riluzole, was approved by the F.D.A. more than 20 years ago. Riluzole can increase survival by two or three months. There is no information yet about whether Radicava has any effect on survival. In the study in Japan, 137 patients were picked at random to receive either Radicava or a placebo. At the end of six months, the condition of those taking the drug declined less than those receiving placebos. Dr. Neil A. Shneider, director of the Eleanor and Lou Gehrig ALS Center at Columbia University Medical Center, said, “The effect is modest but significant.” He added, “I’m very happy, frankly, that there is a second drug approved for A.L.S.” The disease kills nerve cells that control voluntary muscles, so patients gradually weaken and become paralyzed. Most die within three to five years, usually from respiratory failure. About 12,000 to 15,000 people in the United States have A.L.S., according to the Centers for Disease Control and Prevention. Dr. Shneider predicted that patients would be eager to try the new drug. He said several of his patients were already receiving it because they had obtained it themselves from Japan. If more want it, he will prescribe it, he said. “It’s very safe,” he said. But he was uncertain about whether he would actually recommend it, because the method of administration is difficult. Patients have to have an intravenous line inserted and left in place indefinitely, which poses an infection risk. The first round of treatment requires a one-hour infusion every day for 14 days, followed by 14 days off. After that, the infusions are given daily for 10 out of 14 days, with 14 days off. © 2017 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease ; Trophic Factors
Link ID: 23585 - Posted: 05.06.2017

By Andy Coghlan Using a virus to reprogram cells in the brain could be a radical way to treat Parkinson’s disease. People with Parkinson’s have difficulty controlling their movements due to the death of neurons that make dopamine, a brain signalling chemical. Transplants of fetal cells have shown promise for replacing these dead neurons in people with the disease, and a trial is currently under way. But the transplant tissue comes from aborted pregnancies, meaning it is in short supply, and some people may find this ethically difficult. Recipients of these cells have to take immunosuppressant drugs too. Ernest Arenas, at the Karolinska Institute in Stockholm, Sweden, and his team have found a new way to replace lost dopamine-making neurons. They injected a virus into the brains of mice whose dopamine neurons had been destroyed. This virus had been engineered to carry four genes for reprogramming astrocytes – the brain’s support cells – into dopamine neurons. Five weeks later, the team saw improvements in how the mice moved. “They walked better and their gait showed less asymmetry than controls,” says Arenas. This is the first study to show that reprogramming cells in the living brain can lead to such improvements, he says. © Copyright Reed Business Information Ltd.

Keyword: Parkinsons
Link ID: 23488 - Posted: 04.14.2017