Chapter 11. Motor Control and Plasticity

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National Institutes of Health scientists have used human skin cells to create what they believe is the first cerebral organoid system, or “mini-brain,” for studying sporadic Creutzfeldt-Jakob disease (CJD). CJD is a fatal neurodegenerative brain disease of humans believed to be caused by infectious prion protein. It affects about 1 in 1 million people. The researchers, from NIH’s National Institute of Allergy and Infectious Diseases (NIAID), hope the human organoid model will enable them to evaluate potential therapeutics for CJD and provide greater detail about human prion disease subtypes than the rodent and nonhuman primate models currently in use. Human cerebral organoids are small balls of human brain cells ranging in size from a poppy seed to a small pea. Their organization, structure, and electrical signaling are similar to brain tissue. Because these cerebral organoids can survive in a controlled environment for months, nervous system diseases can be studied over time. Cerebral organoids have been used as models to study Zika virus infection, Alzheimer’s disease, and Down syndrome. In a new study published in Acta Neuropathologica Communications, scientists at NIAID’s Rocky Mountain Laboratories discovered how to infect five-month-old cerebral organoids with prions using samples from two patients who died of two different CJD subtypes, MV1 and MV2. Infection took about one month to confirm, and the scientists monitored the organoids for changes in health indicators, such as metabolism, for more than six months. By the end of the study, the scientists observed that seeding activity, an indication of infectious prion propagation, was present in all organoids exposed to the CJD samples. However, seeding was greater in organoids infected with the MV2 sample than the MV1 sample. They also reported that the MV1-infected organoids showed more damage than the MV2-infected organoids.

Keyword: Prions; Development of the Brain
Link ID: 26331 - Posted: 06.15.2019

By: Karen Moxon, Ph.D., Ignacio Saez, Ph.D., and Jochen Ditterich, Ph.D. Technology that is sparking an entirely new field of neuroscience will soon let us simply think about something we want our computers to do and watch it instantaneously happen. In fact, some patients with severe neurological injury or disease are already reaping the benefits of initial advances by using their thoughts to signal and control robotic limbs. This brain-computer interface (BCI) idea is spawning a new area of neuroscience called cognitive neuroengineering that holds the promise of improving the quality of life for everyone on the planet in unimaginable ways. But the technology is not yet ready for prime time. There are three basic aspects of BCIs—recording, decoding, and operation, and progress will require refining all three. BCI works because brain activity generates a signal—typically an electrical field—that can be recorded through a dedicated device, which feeds it to a computer whose analysis software (i.e., a decoding algorithm) “translates” the signal to a simple command. This command signal operates a computer or other machine. The resulting operation can be as simple as moving a cursor on a screen, for which the command need contain just X and Y coordinates, or as complex as controlling a robotic arm, which requires information about position, orientation, speed, rotation, and more. Recent work from University of Pittsburgh has shown that subjects with amyotrophic lateral sclerosis (ALS) can control a complex robot arm—having it pick up a pitcher and pour water into a glass—just by thinking about it. The downside is that it is necessary to surgically implant recording microelectrodes intothe brain and that, most importantly, such electrodes are not reliable for more than a few years. © 2019 The Dana Foundation.

Keyword: Robotics; ALS-Lou Gehrig's Disease
Link ID: 26306 - Posted: 06.06.2019

Ashley Yeager The US Food and Drug Administration has approved a new treatment for a rare childhood disorder that costs $2.125 million for single dose—the most expensive medicine on the market. The medicine is designed to treat spinal muscular atrophy (SMA), a condition driven by defects in the SMN1 gene, which causes afflicted babies to lose muscle control. The illness affects about 400 babies in the US each year and kills those with the most common form of the disease in just a few years. The new treatment is a gene therapy that uses genetically modified viruses to deliver healthy copies of the SMN1 gene to patients’ cells so they can generate a protein that helps the babies develop normally. In tests of the treatment, babies who received it by 6 months of age didn’t have as severe muscle problems as those who didn’t get the drug. Infants getting the drug after six months also didn’t lose muscle control, but they suffered irreversible damage. Babies who got the treatment the earliest were the healthiest, according to the Associated Press. “We saw just remarkable results for these kids,” David Lennon tells NPR. Lennon is the president of AveXis, the company, owned by Novartis that developed the drug, called Zolgensma. It is only the second FDA-approved gene therapy designed to treat a genetic disorder. While the success of the treatment is being celebrated, the price tag is taking heat. “It's absolutely stunning,” Peter Bach, who studies health policy at Memorial Sloan Kettering Cancer Center in New York, tells NPR. The drug’s price tag, he says, drains resources from society, and it’s not alone. © 1986–2019 The Scientist

Keyword: Movement Disorders; Muscles
Link ID: 26274 - Posted: 05.29.2019

By Anna Groves | Bipolar patients are seven times more likely to develop Parkinson’s disease, according to a new study. Though the news may be disheartening to those suffering from the already-trying condition, the link might also lead to clues about the causes behind the two conditions. Parkinson’s is a complex disease associated with a gradual decline in dopamine levels produced by neurons, or brain cells. It eventually leads to impaired movements and other bodily functions. The causes are unknown, and there is no cure. Bipolar disorder, also known as manic-depressive illness, is characterized by episodic fluctuations in mood, concentration or energy levels. Its causes are also unknown, though some bipolar-associated genes have been identified. Researchers are still figuring out how brain structure and function changes under the disease. Previous research has linked Parkinson’s with depression. So when the authors of the new study, most of whom are practicing physicians, noticed some of their bipolar patients developing Parkinson’s, they wondered if there was a connection. The study, out today in Neurology, was led by Huang Mao-Hsuan, who practices in the department of psychiatry at Taipei Veterans General Hospital. The researchers compared data from two groups of adults in the Taiwan National Health Insurance Research Database. Members of one group — over 56,000 individuals — were diagnosed with bipolar disorder between 2001 and 2009. The other — 225,000 individuals — had never been diagnosed with the disorder. No one in either cohort had received a Parkinson’s diagnosis and all the patients were over 20. And researchers ensured the two groups had similar ages, socioeconomic status, and other traits that might influence health.

Keyword: Parkinsons; Schizophrenia
Link ID: 26264 - Posted: 05.23.2019

Sarah Boseley Health editor A drug that could prolong the lives of children with a rare muscle-wasting disease has been approved by the NHS in England after lengthy negotiations with the manufacturer over the high price. Spinraza could help between 600 and 1,200 children and adults in England and Wales who have the genetic condition spinal muscular atrophy (SMA). It affects the nerves in the spinal cord, making muscles weaker and causing problems with movement, breathing and swallowing. It can shorten the life expectancy of babies and toddlers. The drug can slow the progress of the disease but the company making the drug, Biogen, was asking for a high price, that effectively amounted to more than £400,000 for a year of good quality life, according to the National Institute for Health and Care Excellence (Nice), which assesses value for money. Nice said there was limited data on its long-term effectiveness and turned it down last August, to the distress of affected families. Simon Stevens, the NHS England chief executive, said agreement had been reached and children would shortly get Spinraza, the market name of the drug nusinursen. “This promising treatment has the potential to be life changing for children and their families,” said Stevens. “The NHS has now reached one of the most comprehensive deals in the world, which allows us to assess real-world evidence of its long-term benefits. © 2019 Guardian News & Media Limited

Keyword: Movement Disorders; Muscles
Link ID: 26235 - Posted: 05.15.2019

By Gretchen Reynolds A need and desire to be in motion may have been bred into our DNA before we even became humans and could have helped to guide the evolution of our species, according to a fascinating new study of the genetics of physical activity. The study uses big data and sophisticated genetic analyses to determine that some of the gene variants associated with how much and whether people move seem to have joined our ancestors’ genome hundreds of thousands of years ago, making them integral to human existence and well-being and raising interesting questions about what that means today, when most humans are sedentary. There has been evidence for some time that whether and how much people and other animals move depends to some extent on family history and genetics. Past twin studies and genome-wide association studies — which scan genomes looking for snippets of DNA shared by individuals who also share certain traits — suggest that about 50 percent of physical activity behavior in people may depend on genes. Our tendency to move or not is different from our innate aerobic fitness. Someone could be born with a large inherited endurance capacity and no interest at all in leaving the couch, or vice versa. Little has been known, though, about when any of the gene variants associated with moving became integrated into the human genome, and that question matters. Many of the most common chronic illnesses and conditions in people today, including Type 2 diabetes, obesity, heart disease, osteoarthritis and others, are associated with being inactive. But some other species, including chimps, which share much of our DNA, retain robust good health even when they move relatively little. © 2019 The New York Times Company

Keyword: Genes & Behavior
Link ID: 26234 - Posted: 05.15.2019

By Meredith Wadman The data behind the promising trial of a drug that blocks the production of a mutant protein that causes brain damage in people with Huntington disease—an inherited and ultimately fatal neurological disorder—were published today in The New England Journal of Medicine, giving an official imprimatur to news that first electrified the community of patients with the disease 17 months ago. The results, originally announced in December 2017, were published alongside an editorial that called the trial “pathbreaking.” The new paper reports that the drug, a short stretch of synthetic DNA called HTTRx that blocks the production of the mutant protein huntingtin, is safe in humans; no serious adverse events were reported by the 46 people who participated in the trial. (Last summer, Science wrote in depth about the first participant, Michelle Dardengo.) The results also provide details behind the source of excitement about the trial: that HTTRx reduced levels of huntingtin in the cerebrospinal fluid (CSF) that bathes the spinal cord—a proxy, it is hoped, for what is happening in the brain—by amounts that had reversed Huntington-like motor and cognitive symptoms in mice. And the reductions in the mutant protein in the CSF of patients were dose-dependent: Through a range of dosing levels, the bigger the dose, the more the reduction of the mutant protein. © 2019 American Association for the Advancement of Science

Keyword: Huntingtons; Prions
Link ID: 26217 - Posted: 05.07.2019

By Jocelyn Kaiser WASHINGTON, D.C.—A new gene therapy treatment has had striking results in nine boys born with myotubular myopathy (MTM), a rare disease that causes extreme muscle weakness often from birth. All of the boys have better neuromuscular function, most can sit on their own, and four are now breathing without ventilators. As videos of their improvements were shown here on 1 May at the annual meeting of the American Society of Gene & Cell Therapy (ASGCT), the audience broke out in applause. The results, the first of their kind for this rare disease, cap a year of early signs of success in using gene therapy for inherited muscle diseases. As far as muscle function is concerned, the boys “have gone from nothing to something,” says principal investigator Perry Shieh, a neurologist at the University of California, Los Angeles. “Time will tell how much that something will be.” The patients in the new study have X-linked MTM, caused by a defect in a gene called MTM1 that encodes an enzyme, myotubularin. Skeletal muscles need the enzyme to develop and function. Boys with the disease have low muscle tone and, in many cases, can barely breathe or move on their own; most require a ventilator and feeding tube. Half of patients die by 18 months, and few live past age 10. In the trial, sponsored by Audentes Therapeutics, a gene therapy company in San Francisco, California, nine boys between 8 months and 6 years old with X-linked MTM received an intravenous (IV) infusion of many trillions of particles of a harmless virus, called an adeno-associated virus. The viruses were designed to carry a good copy of the MTM1 gene into the boys’ muscle cells. The gene, a free-floating piece of DNA, could then trigger the cell’s proteinmaking machinery to produce myotubularin. Three patients had serious side effects that may have been related to the therapy, such as heart inflammation, but all were treatable. © 2019 American Association for the Advancement of Science

Keyword: Movement Disorders; Muscles
Link ID: 26204 - Posted: 05.03.2019

By Rahul Desikan What is it like to be locked into your body, to be alive but not living? I’m dying — fast. My lungs are at 20 percent of vital capacity and it’s a matter of time before the nerves supplying my breathing muscles degenerate. I have a rapid form of ALS — amyotrophic lateral sclerosis, or Lou Gehrig’s disease. Two years ago, I was running around with my kids, hiking with my wife. All that is over. My body no longer moves. I cannot talk — my only voice is the one in my head, telling me over and over that I am going to die. Soon. I can’t even breathe for myself anymore — I am tethered to a ventilator that breathes for me. I don’t want you to feel sorry for me. At all. It is just ironic, this new, condensed life of mine. I went into medicine to take care of patients with brain diseases. Now, I have one of the diseases that I study. Even with this lethal disease, I continue to find neurology fascinating and beautiful. I wish you knew the old me. ALS has completely destroyed my body and parts of my brain. The new version has stripped me of control over regulating my emotions. I laugh and cry inappropriately during movies, and even during conversations. The cognitive parts of my brain are still working perfectly fine so I’m able to get through the day. But because swallowing has become increasingly difficult, eating and drinking are a battle: continuous bouts of choking, vomiting, crying, sweating, drooling — until finally, it goes through. It is not a pretty picture. What is it like to be locked in? When I swallow, I imagine my childhood in India — driving with my parents and sister in our sky-blue Maruti minivan through the wide roads of New Delhi, relishing my grandmother’s sambar, a savory soup of lentils and vegetables. In my mind, I am always in Boston where I lived for 15 years during college and then medical school and for my doctorate in neurobiology. In my mind, which is all I have left, I am playing house music records at Satellite Records in the Back Bay or trying the Persian eggplant dish at Lala Rokh with my wife or going out with my friends to River Gods or the Enormous Room in Central Square. I am so good at imagining the old me that I see, taste, hear, touch everything. And relive every single detail. © 1996-2019 The Washington Post

Keyword: ALS-Lou Gehrig's Disease
Link ID: 26183 - Posted: 04.29.2019

By Pallab Ghosh Science correspondent, BBC News A treatment that has restored the movement of patients with chronic Parkinson's disease has been developed by Canadian researchers. Previously housebound patients are now able to walk more freely as a result of electrical stimulation to their spines. A quarter of patients have difficulty walking as the disease wears on, often freezing on the spot and falling. Parkinson's UK hailed its potential impact on an aspect of the disease where there is currently no treatment. Prof Mandar Jog, of Western University in London, Ontario, told BBC News the scale of benefit to patients of his new treatment was "beyond his wildest dreams". "Most of our patients have had the disease for 15 years and have not walked with any confidence for several years," he said. "For them to go from being home-bound, with the risk of falling, to being able to go on trips to the mall and have vacations is remarkable for me to see." Normal walking involves the brain sending instructions to the legs to move. It then receives signals back when the movement has been completed before sending instructions for the next step. Prof Jog believes Parkinson's disease reduces the signals coming back to the brain - breaking the loop and causing the patient to freeze. The implant his team has developed boosts that signal, enabling the patient to walk normally. However, Prof Jog was surprised that the treatment was long-lasting and worked even when the implant was turned off. He believes the electrical stimulus reawakens the feedback mechanism from legs to brain that is damaged by the disease. "This is a completely different rehabilitation therapy," he said. "We had thought that the movement problems occurred in Parkinson's patients because signals from the brain to the legs were not getting through. "But it seems that it's the signals getting back to the brain that are degraded." © 2019 BBC

Keyword: Parkinsons
Link ID: 26166 - Posted: 04.23.2019

By Gina Kolata Lucas was 5 before his parents, Bill and Marci Barton of Grand Haven, Mich., finally got an explanation for his difficulties standing up or climbing stairs. The diagnosis: muscular dystrophy. Mr. Barton turned to Google. “The first thing I read was, ‘no cure, in a wheelchair in their teens, pass in their 20s,” Mr. Barton said. “I stopped. I couldn’t read any more. I couldn’t handle it.” Then he found a reason to hope. For the first time ever, there are clinical trials — nearly two dozen — testing treatments that might actually stop the disease. The problem, as Mr. Barton soon discovered, is that the enrollment criteria are so restrictive that very few children qualify. As a result, families like the Bartons often are turned away. “There is so much hope, but it’s not for them,” said Kristin Stephenson, vice president of policy and advocacy at the Muscular Dystrophy Association in Chicago. Even for the parents whose lucky child qualifies, good news may be followed by agonizing, life-or-death choices. What treatments seem most promising? Should he be enrolled in a trial with a placebo arm? Should he be placed in a less risky study that aims to slow the progress of the disease but will not stop it? Should the parents take their chances with a trial now — or wait a year or two, as their child’s condition worsens, until something better comes along? Often there is no easy way to decide. “We talk to families every day,” said Debra Miller who founded the advocacy group, Cure Duchenne, after her son was diagnosed with the disease. “So many times they are looking at us and saying, ‘What do I do?’” © 2019 The New York Times Company

Keyword: Movement Disorders; Muscles
Link ID: 26076 - Posted: 03.25.2019

Katarina Zimmer It’s well established that exercise is good for the mammalian brain. As early as 1999, researchers discovered considerably more newborn neurons in the hippocampi of mice that had access to a running wheel than in animals that didn’t. But 20 years later, scientists are still trying to understand why. A team of Australian and German researchers has uncovered one mechanism that explains how exercise boosts neurogenesis in mice: the activity causes platelets circulating in the blood to release factors that boost the growth of neural precursor cells in the hippocampus, the researchers report today (March 21) in Stem Cell Reports. “We all know about the positive effect of exercise on the brain and other organ systems, but what the actual mechanism is to promote new neuron production is still a bit of a mystery,” remarks Vince Tropepe, who studies neurogenesis at the University of Toronto and who was not involved in the study. “This paper is quite interesting in that they’ve identified a player—these platelets and platelet-derived factors that are circulating in the blood after exercise—that might be a mediator of this effect.” The researchers came to this conclusion through a series of experiments comparing mice that had access to a running wheel for four days with control mice that didn’t. Lab mice voluntarily run up to 10 kilometers per night, “equivalent to us running more than a marathon a day,” explains coauthor Tara Walker, a senior research associate at the Queensland Brain Institute. © 1986 - 2019 The Scientist

Keyword: Neurogenesis; Development of the Brain
Link ID: 26066 - Posted: 03.23.2019

Ian Sample Science editor Scientists have developed a test for Parkinson’s disease based on its signature odour after teaming up with a woman who can smell the condition before tremors and other clinical symptoms appear. The test could help doctors diagnose patients sooner and identify those in the earliest stages of the disease, who could benefit from experimental drugs that aim to protect brain cells from being killed off. Perdita Barran, of the University of Manchester, said the test had the potential to decrease the time it took to distinguish people with normal brain ageing from those with the first signs of the disorder. “Being able to say categorically, and early on, that a person has Parkinson’s disease would be very useful,” she said. Get Society Weekly: our newsletter for public service professionals Read more Most people cannot detect the scent of Parkinson’s, but some who have a heightened sense of smell report a distinctive, musky odour on patients. One such “super smeller” is Joy Milne, a former nurse, who first noticed the smell on her husband, Les, 12 years before he was diagnosed. Milne only realised she could sniff out Parkinson’s when she attended a patient support group with her husband and found everyone in the room smelled the same. She thought little more about it until she mentioned the odour to Tilo Kunath, a neurobiologist who studies Parkinson’s at Edinburgh University. © 2019 Guardian News & Media Limited

Keyword: Parkinsons; Chemical Senses (Smell & Taste)
Link ID: 26056 - Posted: 03.20.2019

By: Kelly Howell, Ph.D., Rebecca Gibbs, and Lee L. Rubin, Ph.D. Editor’s Note: Spinal muscular atrophy is the number one genetic cause of infant death. Until recently, half the babies born with it would die before their second birthdays, their hearts and lungs becoming too weak to continue. Medical care improved the odds somewhat, but new discoveries and therapeutic developments have improved survival rates significantly—and more good news may be on the horizon. In 2016, Bloomberg published an article that described Lauren Gibbs, who was born with spinal muscular atrophy (SMA) and enrolled in a clinical trial for a drug called nusinersen. The story reported that Gibbs enjoyed wheelchair basketball but was known primarily for her defense because she didn’t have enough strength to heave the ball high enough to reach the rim. “After the second time I got the drug, I hit probably 50 baskets in a row,” said Gibbs, who later attended Baylor University. Later that year, nusinersen became the first SMA treatment to be approved by the Federal Drug Administration (FDA). It is one of many promising developments in the past decade in understanding and treating SMA, a genetic neuromuscular disorder first described in the 1890s by Austrian physicians Guido Werdnig and Johann Hoffman. The pair observed infants with flaccid limb and trunk muscles, accompanied by the degeneration of motor neurons in the spinal cord.1 They learned that the loss of these neurons—specialized nerve cells responsible for stimulating skeletal muscle contraction—results in muscle atrophy and weakness, the hallmarks of SMA. Over the next century, further studies revealed highly variable disease severity and age of onset, making it unclear if SMA was one disease with a broad array of symptoms in different patients, or a number of distinct diseases. © 2019 The Dana Foundation.

Keyword: Movement Disorders
Link ID: 26049 - Posted: 03.19.2019

John D. Loike, Martin Grumet On February 18, 2019, The Asahi Shimbun reported, “Ministry [of Health, Labor and Welfare in Japan] OKs 1st iPS [induced pluripotent stem] cell therapy for spinal cord injuries.” This announcement disseminated at a press conference has been viewed as an exciting clinical trial on the use of stem cells to treat spinal cord injury. However, caution is warranted here, for at least three reasons: the uncertainty of the stem cell type to be used in their clinical trial, the safety of transplanting stem cells into humans, and the responsibility of scientists and the press to communicate clearly the benefits and risks of the stem cell treatments, especially to desperate patients who would seek such unproven treatments. First, reports of the announcement by the lead scientist Hideyuki Okano of Keio University School of Medicine provide no indication where this trial is described or registered. It is of concern that it is not listed at or Japanese registries including UMIN Clinical Trials Registry (UMIN-CTR) and the Japan Medical Association Center for Clinical Trials (JMACCT). Second, Okano’s group reported in a study on mice that transplanted human iPSC-derived neural stem/progenitor cells (NSPC) retain unwanted proliferative characteristics, which they attributed to karyotype abnormalities. To protect against these abnormalities, Okano and colleagues have developed a “Fail-Safe System against Potential Tumorigenicity after Transplantation of iPSC Derivatives,” to quote the title of their report. Based on their results, they stated in the study that their technique “may serve as an important countermeasure against post-transplantation adverse events in stem cell transplant therapies.” However, they also caution that “a number of problems . . . need to be resolved, and at present [the Fail-Safe System] is still not suitable for clinical application.” © 1986 - 2019 The Scientist

Keyword: Stem Cells; Regeneration
Link ID: 26021 - Posted: 03.09.2019

Robin McKie Matt Ellison was seven when his father was diagnosed with Huntington’s disease. The condition – which is progressive, incurable and invariably fatal – took 15 years to kill John Ellison. The impact on Matt’s life was profound. His father, who had inherited the disease from his mother, found he could no longer concentrate enough to hold down his job as an engineer at Jaguar. Later he began to lose the power of movement and, eventually, lost his ability to speak. At his local school Matt was mocked because of his father’s odd, uncoordinated gait. The taunting got so bad that Matt stopped attending. “I stayed at home and helped Mum look after Dad,” he recalls. Then in 2007, when Matt reached 18, he decided to find out whether he faced a similar fate. He was tested and told: yes, he had the Huntington’s gene. A few years later his father died, aged 55. “I had had time to prepare myself, but it still hits you hard when you are told you are positive,” says Matt. “I had wanted to be negative as much for my mum, who had gone through enough pain.” For Matt, and thousands of others who have been told they have inherited this affliction, the future would appear bleak, a prospect of inexor able physical and mental decline. The Huntington’s gene is remorseless in its impact. But recently this dark outlook has brightened. Scientists believe they are closing in on a treatment to control Huntington’s worst effects. © 2019 Guardian News & Media Limited

Keyword: Huntingtons
Link ID: 26008 - Posted: 03.05.2019

By Alex Therrien Health reporter, BBC News A radical Parkinson's treatment that delivers a drug directly to the brain has been tested in people. Patients in the trial were either given the drug, which is administered via a "port" in the side of the head, or a dummy treatment (placebo). Both groups showed improved symptoms, meaning it was not clear if the drug was responsible for the benefits. However, scans did find visual evidence of improvements to affected areas of the brain in those given the drug. The study's authors say it hints at the possibility of "reawakening" brain cells damaged by the condition. Other experts, though, say it is too early to know whether this finding might result in improvements in Parkinson's symptoms. Researchers believe the port implant could also be used to administer chemotherapy to those with brain tumours or to test new drugs for Alzheimer's and stroke patients. Parkinson's causes parts of the brain to become progressively damaged, resulting in a range of symptoms, such as involuntary shaking and stiff, inflexible muscles. About 145,000 people a year in the UK are diagnosed with the degenerative condition, which cannot be slowed down or reversed. For this new study, scientists gave patients an experimental treatment called glial cell line-derived neurotrophic factor (GDNF), in the hope it could regenerate dying brain cells and even reverse the condition. © 2019 BBC.

Keyword: Parkinsons; Trophic Factors
Link ID: 25989 - Posted: 02.27.2019

Catherine Offord The Japanese government’s health ministry has given the go-ahead for a trial of human induced pluripotent stem cells to treat spinal cord injury, Reuters reports today (February 18). Researchers at Keio University plan to recruit four adults who have sustained recent nerve damage in sports or traffic accidents. “It’s been 20 years since I started researching cell treatment. Finally we can start a clinical trial,” Hideyuki Okano of Keio University School of Medicine told a press conference earlier today, The Japan Times reports. “We want to do our best to establish safety and provide the treatment to patients.” The team’s intervention involves removing differentiated cells from patients and reprogramming them via human induced pluripotent stem cells (iPSCs) into neural cells. Clinicians will then inject about 2 million of these cells into each patient’s site of injury. The approach has been successfully tested in a monkey, which recovered the ability to walk after paralysis, according to the Times. It’s not the first time Japan has approved the use of iPSCs in clinical trials. Last year, researchers at Kyoto University launched a trial using the cells to treat Parkinson’s disease. And in 2014, a team at the RIKEN Center for Developmental Biology led the first transplant of retina cells grown from iPSCs to treat a patient’s eye disease. © 1986 - 2019 The Scientist

Keyword: Regeneration; Stem Cells
Link ID: 25976 - Posted: 02.21.2019

By Gretchen Reynolds Exercise and eating have a fraught, unsettled relationship with each other. Workouts can blunt or boost appetites. People who start an exercise program often overeat and gain weight — and yet studies and lived experience demonstrate that regular exercise is needed to avoid regaining the weight lost during a successful diet. Intrigued by these contradictory outcomes, researchers at the University of Texas Southwestern Medical Center, along with colleagues from other institutions, ran an experiment on the melanocortin circuit, a brain network in the hypothalamus known to be involved in metabolism. The resulting study, published in December in Molecular Metabolism, suggests that intense exercise might change the workings of certain neurons in ways that could have beneficial effects on appetite and metabolism. The melanocortin circuit consists mainly of two types of neurons. The neuropeptide Y (NPY) cells relay signals encouraging the body to seek food, while the pro-opiomelanocortin (POMC) neurons countermand those orders, reducing interest in food. Animals, including humans, that lack healthy POMC neurons usually become morbidly obese. The researchers focused on what exercise would do to these cells in mice, whose melanocortin circuits resemble ours. Healthy adult male mice either ran on small treadmills or, in a control group, were placed on unmoving treadmills. The exercise routine consisted of 60 minutes of fast, intense running, broken into three 20-minute blocks. Afterward, the mice were free to eat or not, as they chose. The researchers then checked neuronal activity in some of their brains by microscopically probing individual cells in living tissue to measure their electrical and biochemical signals. The tests were repeated throughout the study, which ran for as many as 10 days for some mice. © 2019 The New York Times Company

Keyword: Obesity
Link ID: 25911 - Posted: 01.29.2019

David Cyranoski Japan has approved a stem-cell treatment for spinal-cord injuries. The event marks the first such therapy for this kind of injury to receive government approval for sale to patients. “This is an unprecedented revolution of science and medicine, which will open a new era of healthcare,” says oncologist Masanori Fukushima, head of the Translational Research Informatics Center, a Japanese government organization in Kobe that has been giving advice and support to the project for more than a decade. But independent researchers warn that the approval is premature. Ten specialists in stem-cell science or spinal-cord injuries, who were approached for comment by Nature and were not involved in the work or its commercialization, say that evidence that the treatment works is insufficient. Many of them say that the approval for the therapy, which is injected intravenously, was based on a small, poorly designed clinical trial. They say that the trial’s flaws — including that it was not double-blinded — make it difficult to assess the treatment’s long-term efficacy, because it is hard to rule out whether patients might have recovered naturally. And, although the cells used — known as mesenchymal stem cells (MSCs) — are thought to be safe, the infusion of stem cells into the blood has been connected with dangerous blood clots in the lungs. And all medical procedures carry risks, which makes them hard to justify unless they are proven to offer a benefit. © 2019 Springer Nature Publishing AG

Keyword: Regeneration; Stem Cells
Link ID: 25896 - Posted: 01.24.2019