Chapter 11. Motor Control and Plasticity

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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 clinicaltrials.gov 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

By David Blum Many of us have personally experienced or witnessed the impact of Parkinson’s disease (PD), a movement disorder that affects nearly 10 million people worldwide. This chronic, progressive neurodegenerative disorder leads to disability from motor impairments, such as tremors, rigidity, absence or slowness of movement and impaired balance, as well as from non-motor symptoms including sleep disruption, gastrointestinal issues, sexual dysfunction or loss of sense of smell or taste, to name a few. The ideal outcome of PD clinical research would be to find a cure. But researchers are also looking at novel ways to administer proven Parkinson’s medicines in order to help people living with the disease better control their symptoms and maintain their regular, daily activities. The brain cells that die from PD are responsible for producing dopamine, a neurotransmitter involved in complex behaviors including motor coordination, addiction and motivation. As a result, treatment typically includes the use of levodopa—a medication that is converted into dopamine in the brain and relieves PD symptoms. For the first few years after diagnosis, many individuals’ symptoms are well controlled by levodopa. The average age of onset is 60, but some people are diagnosed at 40 or even younger, potentially requiring treatment for decades. Over time, a patient’s response to levodopa changes, and the therapeutic window, or period when levodopa is effective, narrows, often leading to the prescription of additional levodopa or more frequent dosing of levodopa to manage symptoms. © 2019 Scientific American

Keyword: Parkinsons
Link ID: 25883 - Posted: 01.19.2019

By Elie Dolgin The compound eyes of the common fruit fly are normally brick red. But in neurologist Tom Lloyd's lab at Johns Hopkins University School of Medicine in Baltimore, Maryland, many of the fly eyes are pocked with white and black specks, a sign that neurons in each of their 800-odd eye units are shriveling away and dying. Those flies have the genetic equivalent of amyotrophic lateral sclerosis (ALS), the debilitating neurodegenerative disorder also known as Lou Gehrig's disease, and their eyes offer a window into the soul of the disease process. By measuring the extent of damage to each insect's eyes, researchers can quickly gauge whether a drug, genetic modification, or some other therapeutic intervention helps stop neuronal loss. Those eyes have also offered an answer to the central mystery of ALS: just what kills neurons—and, ultimately, the patient. The flies carry a mutation found in about 40% of ALS patients who have a family history of the disease, and in about 10% of sporadic cases. The mutation, in a gene called C9orf72, consists of hundreds or thousands of extra copies of a short DNA sequence, just six bases long. They lead to unusually large strands of RNA that glom onto hundreds of proteins in the cell nucleus, putting them out of action. Some of those RNA-ensnared proteins, Lloyd and his Hopkins colleague Jeffrey Rothstein hypothesized, might hold the key to ALS. © 2018 American Association for the Advancement of Science

Keyword: ALS-Lou Gehrig's Disease
Link ID: 25874 - Posted: 01.17.2019

By Laura Spinney A disease mystery with no shortage of leads now has an intriguing new one. Since the 1960s, thousands of children in poor, war-torn regions of East Africa have developed epilepsy-like seizures in which their heads bob to their chest; over time, the seizures worsen, cognitive problems develop, and the victims ultimately die. Researchers have proposed causes for nodding syndrome that include malnutrition, parasites, and viruses, but have not proved a clear link to any of them. Now, the first published examination of the brains of children who died after developing the condition suggests it has a key similarity to certain brain diseases of old age, such as Alzheimer's and Parkinson's: It leaves victims' brains riddled with fibrous tangles containing a protein called tau. "Nodding syndrome is a tauopathy," concludes Michael Pollanen, a pathologist at the University of Toronto in Canada who is lead author of a report published last month in Acta Neuropathologica. Pollanen believes the finding "suggests a totally new line of investigation" into the syndrome. As significant as the discovery of the tangles may be what his group of Canadian and Ugandan researchers didn't find: any sign of the brain inflammation that might be triggered by a parasite or virus. "Our hypothesis is that nodding syndrome is a neurodegenerative disease, like Alzheimer's," Pollanen says. Some who study the condition are skeptical, but the possibility excites researchers working on other tauopathies including Alzheimer's. Childhood forms of those diseases are exceedingly rare, but the nodding syndrome finding "means [tau deposition] is not an age-dependent problem," says John Hardy, of the UK Dementia Research Institute at University College London. Something else must have triggered the tauopathy in these children. And because nodding syndrome struck a small region of East Africa, over a specific time period—in Uganda, the condition appears to be vanishing—its trigger might be relatively easy to identify, and could shed light on the causes of diseases like Alzheimer's, Hardy and others say. © 2018 American Association for the Advancement of Science.

Keyword: Alzheimers; Parkinsons
Link ID: 25805 - Posted: 12.20.2018

Laura Sanders An Alzheimer’s protein found in contaminated vials of human growth hormone can spread in the brains of mice. That finding, published online December 13 in Nature, adds heft to the idea that, in very rare cases, amyloid-beta can travel from one person’s brain to another’s. Decades ago, over a thousand young people in the United Kingdom received injections of growth hormone derived from cadavers’ brains as treatment for growth deficiencies. Four of these people died with unusually high levels of A-beta in their brains, a sign of Alzheimer’s disease (SN: 10/17/15, p. 12). The results hinted that A-beta may have been delivered along with the growth hormone. Now researchers have confirmed not only that A-beta was in some of those old vials, but also that it can spark A-beta accumulation in mice’s brains. Neurologist John Collinge of University College London and colleagues found that brain injections of the contaminated growth hormone led to clumps of A-beta in the brains of mice genetically engineered to produce the protein, while brain injections with synthetic growth hormone did not. The results suggest that A-beta can “seed” the protein in people’s brains, under the right circumstances. Still, that doesn’t mean that Alzheimer’s disease is transmissible in day-to-day life. |© Society for Science & the Public 2000 - 2018

Keyword: Alzheimers; Prions
Link ID: 25788 - Posted: 12.15.2018

Tom Goldman Tim Green first noticed the symptoms about five years ago. The former NFL player, whose strength was a job requirement, suddenly found his hands weren't strong enough to use a nail clipper. His words didn't come out as fast as he was thinking them. "I'm a strange guy," Tim says. "I get something in my head and I can just run with it. I was really afraid I had ALS. But there was enough doubt that I said, 'Alright, I don't. Let's not talk about it. Let's not do anything.' " Denying pain and injury had been a survival strategy in football. "I was well trained in that verse," he says. But a diagnosis in 2016 made denial impossible. Doctors confirmed that Tim, also a former NPR commentator, had ALS, known as Lou Gehrig's disease. The degenerative illness attacks the body's motor nerve cells, weakening muscles in the arms and legs as well as the muscles that control speech, swallowing and breathing. Tim tried to keep it private — he didn't want people feeling sorry for him. But he says, "I got to a point where I couldn't hide it anymore." So Tim went on 60 Minutes and revealed his illness. "What we said is, you either write your own history or someone's going to write it for you," says his 24-year-old son, Troy Green. When one isn't enough I was one of Tim Green's producers for his Morning Edition commentaries back in the 1990s. We went to dinner once when he was in Washington, D.C., for a game — his Atlanta Falcons were playing Washington. Tim had a huge plate of pasta. When we finished, the waiter came over and asked, "Anything else?" Tim pointed to his clean plate and said, "Yeah. Let's do it again." © 2018 npr

Keyword: ALS-Lou Gehrig's Disease
Link ID: 25785 - Posted: 12.13.2018

Laura Beil Martha Carlin married the love of her life in 1995. She and John Carlin had dated briefly in college in Kentucky, then lost touch until a chance meeting years later at a Dallas pub. They wed soon after and had two children. John worked as an entrepreneur and stay-at-home dad. In his free time, he ran marathons. Almost eight years into their marriage, the pinky finger on John’s right hand began to quiver. So did his tongue. Most disturbing for Martha was how he looked at her. For as long as she’d known him, he’d had a joy in his eyes. But then, she says, he had a stony stare, “like he was looking through me.” In November 2002, a doctor diagnosed John with Parkinson’s disease. He was 44 years old. Carlin made it her mission to understand how her seemingly fit husband had developed such a debilitating disease. “The minute we got home from the neurologist, I was on the internet looking for answers,” she recalls. She began consuming all of the medical literature she could find. With her training in accounting and corporate consulting, Carlin was used to thinking about how the many parts of large companies came together as a whole. That kind of wide-angle perspective made her skeptical that Parkinson’s, which affects half a million people in the United States, was just a malfunction in the brain. “I had an initial hunch that food and food quality was part of the issue,” she says. If something in the environment triggered Parkinson’s, as some theories suggest, it made sense to her that the disease would involve the digestive system. Every time we eat and drink, our insides encounter the outside world. |© Society for Science & the Public 2000 - 2018.

Keyword: Parkinsons; Neuroimmunology
Link ID: 25765 - Posted: 12.08.2018

Sara Reardon Infectious-disease researchers hunting for the cause of a mysterious illness that is paralysing children are combining machine learning with a new gene-sequencing technique to pin down the culprit. The disease, called acute flaccid myelitis (AFM), causes limb weakness and paralysis that resembles the symptoms of polio. The US Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia, has confirmed 134 cases of AFM in the United States so far this year. Many of those who develop the illness never recover. Most of the evidence suggests that an enterovirus called EV-D681 is causing the illness, but researchers haven’t been able to find the pathogen in the spinal fluid of sick children. Scientists are trying to identify the culprit by using a combination of host-response diagnostics — which look at how the immune system responds to pathogens — and machine-learning analysis. The approach could lead to better diagnostics and provide hints about new treatments. Host-response diagnostic tests haven’t been used in the clinic yet. But researchers are developing similar tests to help pinpoint other conditions that can be tricky to diagnose, including tuberculosis and bacterial meningitis. This year’s AFM outbreak started in October, and is the third in a series of outbreaks in the United States that began in 2014. They have occurred every other year since, though researchers have yet to find a definitive explanation for the pattern. It is also taking scientists an unusually long time to determine the cause of the illness, says William Weldon, a microbiologist at the CDC. © 2018 Springer Nature Publishing AG

Keyword: Movement Disorders; Neuroimmunology
Link ID: 25758 - Posted: 12.07.2018

Robin McKie Science Editor Lawyers are bringing a case against a London hospital trust that could trigger major changes to the rules governing patient confidentiality. The case involves a woman who is suing doctors because they failed to tell her about her father’s fatal hereditary disease before she had her own child. The woman discovered – after giving birth – that her father carried the gene for Huntington’s disease, a degenerative, incurable brain condition. Later she found out she had inherited the gene and that her own daughter, now eight, has a 50% chance of having it. The woman – who cannot be named for legal reasons – says she would have had an abortion had she known about her father’s condition, and is suing the doctors who failed to tell her about the risks she and her child faced. It is the first case in English law to deal with a relative’s claim over issues of genetic responsibility. “This could really change the way we do medicine, because it is about the duty that doctors have to share genetic test results with relatives and whether the duty exists in law,” said Anna Middleton, head of society and ethics research at the Wellcome Genome Campus in Cambridge. Experts say that as more is discovered about the genetic components of medical conditions, including cancer and dementia, doctors will come under increasing pressure to consider not only their patients’ needs but also those of relatives who may share affected genes. The case also raises questions over how much effort clinicians need to put into tracing relatives, and whether they will be sued if their attempts do not go far enough. © 2018 Guardian News and Media Limited

Keyword: Huntingtons
Link ID: 25720 - Posted: 11.26.2018

Ashley Yeager For an hour a day, five days a week, mice in Hiroshi Maejima’s physiology lab at Hokkaido University in Sapporo, Japan, hit the treadmill. The researcher’s goal in having the animals follow the exercise routine isn’t to measure their muscle mass or endurance. He wants to know how exercise affects their brains. Researchers have long recognized that exercise sharpens certain cognitive skills. Indeed, Maejima and his colleagues have found that regular physical activity improves mice’s ability to distinguish new objects from ones they’ve seen before. Over the past 20 years, researchers have begun to get at the root of these benefits, with studies pointing to increases in the volume of the hippocampus, development of new neurons, and infiltration of blood vessels into the brain. Now, Maejima and others are starting to home in on the epigenetic mechanisms that drive the neurological changes brought on by physical activity. In October, Maejima’s team reported that the brains of rodents that ran had greater than normal histone acetylation in the hippocampus, the brain region considered the seat of learning and memory.1 The epigenetic marks resulted in higher expression of Bdnf, the gene for brain-derived neurotrophic factor (BDNF). By supporting the growth and maturation of new nerve cells, BDNF is thought to promote brain health, and higher levels of it correlate with improved cognitive performance in mice and humans. With a wealth of data on the benefits of working out emerging from animal and human studies, clinicians have begun prescribing exercise to patients with neurodegenerative diseases such as Parkinson’s and Alzheimer’s, as well as to people with other brain disorders, from epilepsy to anxiety. Many clinical trials of exercise interventions for neurodegenerative diseases, depression, and even aging are underway. Promising results could bolster the use of exercise as a neurotherapy. © 1986 - 2018 The Scientist

Keyword: Learning & Memory; Muscles
Link ID: 25713 - Posted: 11.24.2018