Chapter 11. Motor Control and Plasticity

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Meredith Wadman Progress in treating Parkinson’s disease—a progressive neurological illness that causes tremors, muscle rigidity, and dementia—has been painfully slow, in large part because scientists still don’t fully understand the molecular events that kill select brain cells. What they do know is Parkinson’s leaves behind a telltale mark: clumps of the misfolded alpha synuclein (αS) protein in the brains and guts of patients at autopsy. In its normal form, the protein is widely thought to help brain cells communicate, but researchers have now uncovered another role—αS plays an essential part in immune and inflammatory responses in the gut. The new work is “extremely well done and very exciting,” says physician-scientist Michael Schlossmacher, who studies Parkinson’s disease at the Ottawa Hospital Research Institute but was not involved with the study. He adds that the protein’s “pivotal role” in immunity may help explain why chronic infection or inflammation can lead to a higher risk of Parkinson’s. Others in the field, however, question the work’s relevance to the brain disorder. The dominant view among researchers is that misfolded αS aggregates and takes on new toxic properties, and some say the natural role of the protein, although interesting, may be irrelevant to pursuing needed treatments. Parkinson’s disease, the second most common neurodegenerative ailment after Alzheimer’s, affects one in 331, or about 1 million, people in the United States and at least 7 million people globally. Many patients are diagnosed in their 60s, as brain cells that make the neurotransmitter dopamine die and lead to symptoms. But the disease can also strike the young—including those who produce too much αS, or fail to break it down—because of rare genetic mutations. Other risk factors include sex—prevalence is 40% to 50% higher in men than in women—and some chronic inflammatory diseases, such as inflammatory bowel disease and chronic hepatitis C. Oral dopamine can mitigate symptoms, but the 60-year-old treatment isn’t a cure and ultimately fails to prevent worsening symptoms and death. © 2022 American Association for the Advancement of Science.

Keyword: Parkinsons
Link ID: 28155 - Posted: 01.15.2022

Leyland Cecco A whistleblower in the Canadian province of New Brunswick has warned that a progressive neurological illness that has baffled experts for more than two years appears to be affecting a growing number of young people and causing swift cognitive decline among some of the afflicted. Speaking to the Guardian, an employee with Vitalité Health Network, one of the province’s two health authorities, said that suspected cases are growing in number and that young adults with no prior health triggers are developing a catalog of troubling symptoms, including rapid weight loss, insomnia, hallucinations, difficulty thinking and limited mobility. The official number of cases under investigation, 48, remains unchanged since it was first announced in early spring 2021. But multiple sources say the cluster could now be as many as 150 people, with a backlog of cases involving young people still requiring further assessment. “I’m truly concerned about these cases because they seem to evolve so fast,” said the source. “I’m worried for them and we owe them some kind of explanation.” At the same time, at least nine cases have been recorded in which two people in close contact – but without genetic links – have developed symptoms, suggesting that environmental factors may be involved. One suspected case involved a man who was developing symptoms of dementia and ataxia. His wife, who was his caregiver, suddenly began losing sleep and experiencing muscle wasting, dementia and hallucinations. Now her condition is worse than his. A woman in her 30s was described as non-verbal, is feeding with a tube and drools excessively. Her caregiver, a nursing student in her 20s, also recently started showing symptoms of neurological decline. © 2021 Guardian News & Media Limited

Keyword: Movement Disorders; Alzheimers
Link ID: 28140 - Posted: 01.05.2022

By Nicholas Bakalar Need more incentive to get a flu shot, or to keep taking extra precautions this flu season? A new study suggests there may be a link between influenza infection and an increased risk for Parkinson’s disease. For decades, neurologists have suspected there may be a link between the flu and Parkinson’s disease, a chronic and progressive disorder of the nervous system marked by problems with movement, cognitive changes and a range of other symptoms. Several earlier studies, for example, reported a sharp increase in Parkinson’s cases following the 1918 influenza pandemic. Some cases of Parkinson’s have been linked to environmental exposures to pesticides and other toxic chemicals, and genetics may also play a role, but most cases of Parkinson’s have no known cause. Treatments for Parkinson’s can help delay its progression, but there is no known cure. The new study, using Danish health care databases, included 10,231 men and women who had been diagnosed with Parkinson’s between 2000 and 2016. Researchers compared them with 51,196 controls who were matched for age and sex. The researchers tracked influenza infections beginning in 1977 using hospital and outpatient discharge records. The report appeared in JAMA Neurology. Parkinson’s takes years, if not decades, to develop, and initially may produce only subtle symptoms like a hand tremor. It may take years for doctors to diagnose the condition, so any connection between a flu infection and the disease would be evident only many years later. The researchers found that compared with people who had not had a flu infection, those who had the flu had a 70 percent higher risk of Parkinson’s 10 years later, and a 90 percent higher risk 15 years after. © 2021 The New York Times Company

Keyword: Parkinsons
Link ID: 28127 - Posted: 12.29.2021

By Gretchen Reynolds People who work out regularly and are aerobically fit tend to guzzle a surprising amount of alcohol, according to a new study, well timed for the holidays, of the interplay between fitness, exercise and imbibing. The study, which involved more than 40,000 American adults, finds that active, physically fit men and women are more than twice as likely to be moderate or heavy drinkers as people who are out of shape. The results add to mounting evidence from previous studies — and many of our bar tabs — that exercise and alcohol frequently go hand in hand, with implications for the health effects of each. Many people, and some researchers, might be surprised to learn how much physically active people tend to drink. In general, people who take up one healthy habit, such as working out, tend to practice other salubrious habits, a phenomenon known as habit clustering. Fit, active people seldom smoke, for instance, and tend to eat healthful diets. So, it might seem logical that people who often exercise would drink alcohol sparingly. But multiple studies in recent years have found close ties between working out and tippling. In one of the earliest, from 2001, researchers used survey answers from American men and women to conclude that moderate drinkers, defined in that study as people who finished off about a drink a day, were twice as likely as those who didn’t drink at all to exercise regularly. Later studies found similar patterns among college athletes, who drank substantially more than other collegians, a population not famous for its temperance. © 2021 The New York Times Company

Keyword: Drug Abuse; Obesity
Link ID: 28121 - Posted: 12.22.2021

By Gretchen Reynolds Staying physically active as we age substantially drops our risk of developing dementia during our lifetimes, and it doesn’t require prolonged exercise. Walking or moving about, rather than sitting, may be all it takes to help bolster the brain, and a new study of octogenarians from Chicago may help to explain why. The study, which tracked how often older people moved or sat and then looked deep inside their brains after they passed away, found that certain vital immune cells worked differently in the brains of older people who were active compared to their more sedentary peers. Physical activity seemed to influence their brain’s health, their thinking abilities and whether they experienced the memory loss of Alzheimer’s disease. The findings add to growing evidence that when we move our bodies, we change our minds, no matter how advanced our age. Already, plenty of scientific evidence indicates that physical activity bulks up our brains. Older, sedentary people who begin walking for about an hour most days, for instance, typically add volume to their hippocampus, the brain’s memory center, reducing or reversing the shrinkage that otherwise commonly occurs there over the years. Active people who are middle-aged or older also tend to perform better on tests of memory and thinking skills than people of the same age who rarely exercise, and are nearly half as likely eventually to be diagnosed with Alzheimer’s disease. Almost as heartening, active people who do develop dementia usually show their first symptoms years later than inactive people do. But precisely how movement remodels our brains is still mostly mysterious, although scientists have hints from animal experiments. When adult lab mice and rats run on wheels, for example, they goose production of hormones and neurochemicals that prompt the creation of new neurons, as well as synapses, blood vessels and other tissues that connect and nurture those young brain cells. © 2021 The New York Times Company

Keyword: Alzheimers
Link ID: 28094 - Posted: 12.01.2021

Riluzole, a drug approved to treat amyotrophic lateral sclerosis (ALS), a disease affecting nerve cells controlling movement, could slow the gradual loss of a particular brain cell that occurs in Niemann-Pick disease type C1 (NPC1), a rare genetic disorder affecting children and adolescents, suggests a study in mice by scientists at the National Institutes of Health. The study was conducted by Forbes D. Porter, M.D., Ph.D., of NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), and colleagues in the National Human Genome Research Institute and National Institute of Arthritis and Musculoskeletal and Skin Disease. It appears in Molecular Genetics and Metabolism. The study was supported in part by a grant from the Ara Parseghian Medical Research Foundation. NPC1 results from an impaired ability to move cholesterol through cells, leading to difficulty controlling movements, liver and lung disease, impaired swallowing, intellectual decline and death. Much of the movement difficulties in NPC1 result from gradual loss of brain cells known as Purkinje neurons. The researchers found that mice with a form of NPC1 have a diminished ability to lower levels of glutamate — a brain chemical that stimulates neurons — after it has bound to a neuron’s surface. High levels of glutamate can be toxic to cells. The researchers believe the buildup of glutamate contributes to the brain cell loss seen in the disease. Riluzole blocks the release of glutamate and hence delays the progression of ALS in people.

Keyword: Movement Disorders
Link ID: 28083 - Posted: 11.20.2021

By Gina Kolata CAMBRIDGE, Mass. — When Sharif Tabebordbar was born in 1986, his father, Jafar, was 32 and already had symptoms of a muscle wasting disease. The mysterious illness would come to define Sharif’s life. Jafar Tabebordbar could walk when he was in his 30s but stumbled and often lost his balance. Then he lost his ability to drive. When he was 50, he could use his hands. Now he has to support one hand with another. No one could answer the question plaguing Sharif and his younger brother, Shayan: What was this disease? And would they develop it the way their father had? As he grew up and watched his father gradually decline, Sharif vowed to solve the mystery and find a cure. His quest led him to a doctorate in developmental and regenerative biology, the most competitive ranks of academic medical research, and a discovery, published in September in the journal Cell, that could transform gene therapy — medicine that corrects genetic defects — for nearly all muscle wasting diseases. That includes muscular dystrophies that affect about 100,000 people in the United States, according to the Muscular Dystrophy Association. Scientists often use a disabled virus called an adeno-associated virus, or AAV, to deliver gene therapy to cells. But damaged muscle cells like the ones that afflict Dr. Tabebordbar’s father are difficult to treat. Forty percent of the body is made of muscle. To get the virus to those muscle cells, researchers must deliver enormous doses of medication. Most of the viruses end up in the liver, damaging it and sometimes killing patients. Trials have been halted, researchers stymied. Dr. Tabebordbar managed to develop viruses that go directly to muscles — very few end up in the liver. His discovery could allow treatment with a fraction of the dosage, and without the disabling side effects. Dr. Jeffrey Chamberlain, who studies therapies for muscular diseases at the University of Washington and is not involved in Dr. Tabebordbar’s research, said the new method, “could take it to the next level,” adding that the same method also could allow researchers to accurately target almost any tissue, including brain cells, which are only beginning to be considered as gene therapy targets. © 2021 The New York Times Company

Keyword: Movement Disorders; Genes & Behavior
Link ID: 28066 - Posted: 11.06.2021

Abby Olena Delivering anything therapeutic to the brain has long been a challenge, largely due to the blood-brain barrier, a layer of cells that separates the vessels that supply the brain with blood from the brain itself. Now, in a study published August 12 in Nature Biotechnology, researchers have found that double-stranded RNA-DNA duplexes with attached cholesterol can enter the brains of both mice and rats and change the levels of targeted proteins. The results suggest a possible route to developing drugs that could target the genes implicated in disorders such as muscular dystrophy and amyotrophic lateral sclerosis (ALS). “It’s really exciting to have a study that’s focused on delivery to the central nervous system” with antisense oligonucleotides given systemically, says Michelle Hastings, who investigates genetic disease at the Rosalind Franklin University of Medicine and Science in Chicago and was not involved in the study. The authors “showed that it works for multiple targets, some clinically relevant.” In 2015, Takanori Yokota of Tokyo Medical and Dental University and colleagues published a study showing that a so-called heteroduplex oligonucleotide (HDO)—consisting of a short chain of both DNA and an oligonucleotide with modified bases paired with complementary RNA bound to a lipid on one end—was successful at decreasing target mRNA expression in the liver. Yokota’s team later joined forces with researchers at Ionis Pharmaceuticals to determine whether HDOs could cross the blood-brain barrier and target mRNA in the central nervous system. © 1986–2021 The Scientist.

Keyword: Genes & Behavior; ALS-Lou Gehrig's Disease
Link ID: 27998 - Posted: 09.18.2021

By Barbara Casassus PARIS—Five public research institutions in France have imposed a 3-month moratorium on the study of prions—a class of misfolding, infectious proteins that cause fatal brain diseases—after a retired lab worker who handled prions in the past was diagnosed with Creutzfeldt-Jakob disease (CJD), the most common prion disease in humans. An investigation is underway to find out whether the patient, who worked at a lab run by the National Research Institute for Agriculture, Food and Environment (INRAE), contracted the disease on the job. If so, it would be the second such case in France in the past few years. In June 2019, an INRAE lab worker named Émilie Jaumain died at age 33, 10 years after pricking her thumb during an experiment with prion-infected mice. Her family is now suing INRAE for manslaughter and endangering life; her illness had already led to tightened safety measures at French prion labs. The aim of the moratorium, which affects nine labs, is to “study the possibility of a link with the [new patient’s] former professional activity and if necessary to adapt the preventative measures in force in research laboratories,” according to a joint press release issued by the five institutions yesterday. “This is the right way to go in the circumstances,” says Ronald Melki, a structural biologist at a prion lab jointly operated by the French national research agency CNRS and the French Alternative Energies and Atomic Energy Commission (CEA). “It is always wise to ask questions about the whole working process when something goes wrong.” "The occurrence of these harsh diseases in two of our scientific colleagues clearly affects the whole prion community, which is a small 'familial' community of less than 1000 people worldwide," Emmanuel Comoy, deputy director of CEA's Unit of Prion Disorders and Related Infectious Agents, writes in an email to Science. Although prion research already has strict safety protocols, "it necessarily reinforces the awareness of the risk linked to these infectious agents," he says. © 2021 American Association for the Advancement of Science.

Keyword: Prions
Link ID: 27925 - Posted: 07.28.2021

By Pam Belluck He has not been able to speak since 2003, when he was paralyzed at age 20 by a severe stroke after a terrible car crash. Now, in a scientific milestone, researchers have tapped into the speech areas of his brain — allowing him to produce comprehensible words and sentences simply by trying to say them. When the man, known by his nickname, Pancho, tries to speak, electrodes implanted in his brain transmit signals to a computer that displays his intended words on the screen. His first recognizable sentence, researchers said, was, “My family is outside.” The achievement, published on Wednesday in the New England Journal of Medicine, could eventually help many patients with conditions that steal their ability to talk. “This is farther than we’ve ever imagined we could go,” said Melanie Fried-Oken, a professor of neurology and pediatrics at Oregon Health & Science University, who was not involved in the project. Three years ago, when Pancho, now 38, agreed to work with neuroscience researchers, they were unsure if his brain had even retained the mechanisms for speech. “That part of his brain might have been dormant, and we just didn’t know if it would ever really wake up in order for him to speak again,” said Dr. Edward Chang, chairman of neurological surgery at University of California, San Francisco, who led the research. The team implanted a rectangular sheet of 128 electrodes, designed to detect signals from speech-related sensory and motor processes linked to the mouth, lips, jaw, tongue and larynx. In 50 sessions over 81 weeks, they connected the implant to a computer by a cable attached to a port in Pancho’s head, and asked him to try to say words from a list of 50 common ones he helped suggest, including “hungry,” “music” and “computer.” As he did, electrodes transmitted signals through a form of artificial intelligence that tried to recognize the intended words. © 2021 The New York Times Company

Keyword: Brain imaging; Language
Link ID: 27913 - Posted: 07.17.2021

By Emily Anthes Johnson & Johnson’s beleaguered Covid-19 vaccine may be associated with a small increased risk of Guillain–Barré syndrome, a rare but potentially serious neurological condition, federal officials said on Monday. The Food and Drug Administration has added a warning about the potential side effect to its fact sheets about the vaccine. The risk appears to be very small. So far, there have been 100 reports of the syndrome in people who had received the Johnson & Johnson vaccine. Nearly 13 million doses of the vaccine have been administered in the United States. Here are answers to some common questions about the syndrome and its connection to vaccination. What is Guillain-Barré syndrome? Guillain-Barré is a rare condition in which the body’s immune system attacks nerve cells. It can cause muscle weakness and paralysis. Although the symptoms often pass within weeks, in some cases, the condition can cause permanent nerve damage. In the United States, there are typically 3,000 to 6,000 cases of the syndrome per year, according to the Centers for Disease Control and Prevention. It is most common in adults over 50. The precise cause of the syndrome is unknown, but in many cases the condition follows another illness or infection, such as the flu. It has also been reported in people with Covid-19. This is not the first vaccine that has been linked to Guillain-Barré, although the risk appears to be tiny. A large swine flu vaccination campaign in 1976 led to a small uptick in the incidence of syndrome; the vaccine caused roughly one extra case of Guillain-Barré for every 100,000 people vaccinated. The seasonal flu shot is associated with roughly one to two additional cases for every million vaccines administered. © 2021 The New York Times Company

Keyword: Movement Disorders; Neuroimmunology
Link ID: 27909 - Posted: 07.14.2021

By Lisa Sanders, M.D. The 22-year-old man struggled to get out of bed. The E.M.T.s were just outside his door, if he could only get there. The previous day he felt that he was coming down with something. Normally he never took naps, but that afternoon, he returned from class feeling completely wiped out and slept long and hard. Yet when he awoke, he felt even worse. Every muscle was sore. He felt feverish. This must be the flu, he told himself. He had the flu shot before starting school that year, but of course no vaccine is 100 percent effective. He spent the rest of that afternoon in bed, too tired and in too much pain to even get up to join his partner for dinner. When he awoke in the middle of the night to go to the bathroom, he was so weak and sore he could hardly sit up. He maneuvered to the edge of the bed and, using the headboard, pulled himself to his feet, but his partner had to help him get to the bathroom. Once he was there, the urine he produced was startlingly dark — the color of Coca-Cola. The next day he felt no better. His partner wanted to stay home with him, but he hurried her off to work. It’s just the flu, he assured her. But as the morning wore on, he started to worry. He called his parents, who were both nurses. They were worried too; influenza can be bad. When he got the same message from a doctor back home in New York, he started wondering if he should go to the hospital. He’d never been this sick before. © 2021 The New York Times Company

Keyword: Muscles; Genes & Behavior
Link ID: 27904 - Posted: 07.14.2021

By Marlene Cimons J. William Langston, who has been studying and treating Parkinson’s disease for nearly 40 years, always has found it striking that so many more men than women show up in his clinic. His observation is not anecdotal. It is grounded in science and shared by many physicians: Men are roughly 1.5 times more likely than women to develop Parkinson’s, a progressive disorder of the nervous system that impairs movement and can erode mental acuity. “It’s a big difference that is quite real,” says Langston, clinical professor of neurology, neuroscience and of pathology at the Stanford University School of Medicine and associate director of the Stanford Udall Center. “It’s pretty dramatic. I think anyone who sees a lot of Parkinson’s will tell you that.” While the disproportionate impact is clear, the reasons for it are not. “It’s a great mystery,” Langston says. Researchers still don’t know what it is that makes men more susceptible to Parkinson’s, or what it is about women that may protect them — or both. But they are trying to find out. “We in the research community have been working for decades to sort this out, but the answers are still elusive,” says Caroline Tanner, a neurology professor in the Weill Institute for Neurosciences at the University of California at San Francisco. “Nevertheless, it’s important to keep at it. We need to understand the mechanisms that underlie the specific differences between men and women so we can apply them to trying to prevent Parkinson’s.” Parkinson’s results from the death of key neurons in the substantia nigra region of the brain that produce the chemical messenger dopamine. Over time, the loss of these nerve cells disrupts movement, diminishes cognition, and can cause other symptoms, such as slurred speech and depression. © 1996-2021 The Washington Post

Keyword: Parkinsons; Sexual Behavior
Link ID: 27892 - Posted: 07.06.2021

Christopher McDermott, MBChB, FRCP, PhD Early in my clinical practice, my team and I subscribed to the traditional view of ALS: the disease was either familial or sporadic. People with “familial” ALS had some family history of ALS (and therefore a possible genetic component), while people with “sporadic” disease did not have a family history.1 But that view began to change with the discovery that mutations (or changes) in a gene called C9orf72 could play a role in both the sporadic and familial types of ALS. Over time, we learned that this one mutation accounted for approximately 40% of familial ALS cases. Even more surprising: it accounted for close to 10% of cases in people with no family history of ALS—people previously believed to have the sporadic form of the disease. As this story unfolded, we began to question our old assumptions about familial and sporadic ALS, and we realized that just asking our patients about their family history wasn’t enough. C9orf72 has been associated with other neurologic diseases as well, so now, I and other ALS specialists understood that someone with a family history of related conditions might also have a genetic cause for their ALS. At the same time, other genetic mutations were being found in people with no family history of the disease and whose ALS had seemingly appeared out of nowhere.1 It was becoming clear that some people with what we often referred to as sporadic ALS could actually have a genetic component to their disease.1 My own research supported this belief. The Sheffield Institute for Translational Neuroscience, where we help develop and study new therapies for neuromuscular diseases, had an extensive biobank of samples from people with ALS. As new genetic mutations were discovered, our researchers tested these samples and found that many people who we thought had sporadic ALS in fact had one or more genetic mutations. © 2013-2021 All rights reserved.

Keyword: ALS-Lou Gehrig's Disease ; Genes & Behavior
Link ID: 27885 - Posted: 07.03.2021

by Rachel Zamzow Most mornings, Huda Zoghbi, 67, climbs a glass-encased, curling staircase to reach her lab on the top and 13th floor of the Jan and Dan Duncan Neurological Research Institute in Houston, Texas. The twisting glass tower, which she designed with a team of architects, echoes the double helix of DNA — a structure that has been central to her career-long quest to uncover genes underlying neurological conditions. As the institute’s director — and as a scientist— she is known for going beyond the standard job description. Genetics researchers often cast a wide net and sequence thousands of genes at a time. But in her prolific career, Zoghbi has focused on a handful of genes, methodically building up an understanding of their function one careful step at a time. Thanks to that approach, Zoghbi has made a number of landmark discoveries, including identifying the genetic roots of Rett syndrome, an autism-related condition that primarily affects girls, as well as the genetic mutations that spur spinocerebellar ataxia, a degenerative motor condition. She has authored more than 350 journal articles. Her accomplishments have earned her almost every major biology and neuroscience research award, including the prestigious Breakthrough Prize in 2017 and the Brain Prize in 2020. “She’s clearly the international leader in the field,” said the late Stephen Warren, professor of human genetics at Emory University in Atlanta, Georgia. Zoghbi never set out to lead a large research center, she says — her heart is in the lab. That said, she has excelled at it: Since the institute’s inception in 2010, it has grown to host more than 200 scientists and fostered more than 70 new disease gene discoveries. © 2021 Simons Foundation

Keyword: Movement Disorders; Development of the Brain
Link ID: 27874 - Posted: 06.26.2021

By Nancy Clanton, Studies have shown COVID-19 can cause brain complications in some patients’ brains, from memory problems to strokes. A new study has found the brains of people who died from COVID-19 were remarkably similar to the brains of people who die from Alzheimer’s and Parkinson’s, showing inflammation and disrupted circuitry, researchers reported. “The brains of patients who died from severe COVID-19 showed profound molecular markers of inflammation, even though those patients didn’t have any reported clinical signs of neurological impairment,” study co-senior author Tony Wyss-Coray, a professor of neurology and neurological sciences at Stanford University, said in a press release. According to Wyss-Coray, about a third of hospitalized COVID-19 patients report neurological symptoms, such as fuzzy thinking, forgetfulness, difficulty concentrating and depression, and these problems continue for long haul patients even when they’ve recovered from COVID. For their study, his team analyzed brain tissue from eight people who died of COVID-19 and 14 who died of other causes. The researchers found significant inflammation in the brains of the deceased COVID-19 patients. However, their brain tissue showed no signs of SARS-CoV-2, the virus that causes COVID-19. Wyss-Coray added that scientists disagree about whether the virus is present in COVID-19 patients’ brains. © 2021 The Atlanta Journal-Constitution.

Keyword: Parkinsons; Alzheimers
Link ID: 27871 - Posted: 06.23.2021

Adrienne Matei Asked about the future of Parkinson’s disease in the US, Dr Ray Dorsey says, “We’re on the tip of a very, very large iceberg.” Dorsey, a neurologist at the University of Rochester Medical Center and author of Ending Parkinson’s Disease, believes a Parkinson’s epidemic is on the horizon. Parkinson’s is already the fastest-growing neurological disorder in the world; in the US, the number of people with Parkinson’s has increased 35% the last 10 years, says Dorsey, and “We think over the next 25 years it will double again.” Most cases of Parkinson’s disease are considered idiopathic – they lack a clear cause. Yet researchers increasingly believe that one factor is environmental exposure to trichloroethylene (TCE), a chemical compound used in industrial degreasing, dry-cleaning and household products such as some shoe polishes and carpet cleaners. Advertisement Employers think the pandemic was a time for earnest self-improvement. Screw that | Jessa Crispin To date, the clearest evidence around the risk of TCE to human health is derived from workers who are exposed to the chemical in the work-place. A 2008 peer-reviewed study in the Annals of Neurology, for example, found that TCE is “a risk factor for parkinsonism.” And a 2011 study echoed those results, finding “a six-fold increase in the risk of developing Parkinson’s in individuals exposed in the workplace to trichloroethylene (TCE).” Dr Samuel Goldman of The Parkinson’s Institute in Sunnyvale, California, who co-led the study, which appeared in the Annals of Neurology journal, wrote: “Our study confirms that common environmental contaminants may increase the risk of developing Parkinson’s, which has considerable public health implications.” It was off the back of studies like these that the US Department of Labor issued a guidance on TCE, saying: “The Board recommends [...] exposures to carbon disulfide (CS2) and trichloroethylene (TCE) be presumed to cause, contribute, or aggravate Parkinsonism.” © 2021 Guardian News & Media Limited

Keyword: Parkinsons
Link ID: 27856 - Posted: 06.16.2021

Ian Sample Science editor Regular strenuous exercise raises the risk of developing motor neurone disease (MND) in people who are genetically predisposed to the condition, researchers say. Scientists at the University of Sheffield found a causal relationship between high intensity physical activity and the disorder among those already susceptible to the disease. They believe the work marks a major step towards understanding the link between intense exercise, which may contribute to motor neurone injury in certain people, and the neurodegenerative disease, which affects about 5,000 individuals in the UK. “We have suspected for some time that exercise was a risk factor for MND, but until now this link was considered controversial,” said Dr Johnathan Cooper-Knoc, a neurologist at Sheffield. “This study confirms that in some people, frequent strenuous exercise leads to an increase in the risk of MND.” The life-time risk of developing MND is about 1 in 400, but previous studies have suggested it is six times greater in professional football players compared with the general population. A number of high-profile British sportsmen have shared their experience with MND in recent years, including rugby league’s Rob Burrow, rugby union’s Doddie Weir and the the footballer Stephen Darby. The Sheffield researchers emphasise that the vast majority of people who undertake vigorous exercise do not develop MND, and that their next step is to develop tests that identify people most at risk. © 2021 Guardian News & Media Limited

Keyword: ALS-Lou Gehrig's Disease
Link ID: 27848 - Posted: 06.11.2021

By Nayef Al-Rodhan o In Chile, the National Commission for Scientific and Technological Research has begun to debate a “neurorights” bill to be written into the country’s constitution. The world, and most importantly the OECD, UNESCO and the United Nations, should be watching closely. The Chilean bill sets out to protect the right to personal identity, free will, mental privacy, equitable access to technologies that augment human capacities, and the right to protection against bias and discrimination. The landmark bill would be the first of its kind to pioneer a regulatory framework which protects human rights from the manipulation of brain activity. The relatively nascent concept of neurorights follows a number of recent medical innovations, most notably brain-computer interface technology (BCI), which has the potential to revolutionize the field of neuroscience. BCI-based therapy may be useful for poststroke motor rehabilitation and may be a potential method for the accurate detection and treatment of neurological diseases such as Alzheimer’s. Advocates claim there is therefore a moral imperative to use the technology, given the benefits it could bring; others worry about its ethical, moral and societal consequences. Many (mistakenly) see this process as being potentially undermined by premature governance restrictions, or accuse any mention of brake mechanisms as an exaggerated reaction to an unlikely science-fiction scenario. © 2021 Scientific American

Keyword: Robotics; Consciousness
Link ID: 27841 - Posted: 06.02.2021

By Richard Sima An elephant’s trunk is a marvel of biology. Devoid of any joints or bone, the trunk is an appendage made of pure muscle that is capable of both uprooting trees and gingerly plucking individual leaves and also boasts a sense of smell more powerful than a bomb-sniffing dog’s. Elephants use their trunks in a variety of ways. They use it to drink, store and spray water, and they also blow air through it to communicate — their 110-decibel bellows can be heard for miles. “It’s like a muscular multitool,” said Andrew Schulz, a mechanical engineering doctoral student at the Georgia Institute of Technology. In a study published Wednesday in The Journal of the Royal Society Interface, Mr. Schulz and his colleagues reported on how elephants can use their trunks for yet another function: applying suction to grab food, a behavior previously thought to be exclusive to fishes. Despite the ubiquity of elephants in children’s books and nature documentaries, there are numerous gaps in scientific knowledge about the biomechanics of their trunks that the new study helps fill. For example, the most recent detailed account of elephant trunk anatomy is a hand-drawn monograph that was published in 1908, Mr. Schulz said. Contrary to popular belief, the trunk does not act like a straw. “What they do is actually drink water into their trunk and they store it,” Mr. Schulz said. “So the elephant trunk is actually like a trunk.” Mr. Schulz completed his research in the lab of David Hu, which studies how animals move and function with an eye toward applying the discoveries toward human engineering problems. He said one reason elephants’ anatomy is poorly understood is because they are difficult to work with. © 2021 The New York Times Company

Keyword: Evolution; Learning & Memory
Link ID: 27840 - Posted: 06.02.2021