Chapter 11. Motor Control and Plasticity

Follow us on Facebook or subscribe to our mailing list, to receive news updates. Learn more.


Links 1 - 20 of 1874

By Ferris Jabr To hear more audio stories from publications like The New York Times, download Audm for iPhone or Android. On the evening of Oct. 10, 2006, Dennis DeGray’s mind was nearly severed from his body. After a day of fishing, he returned to his home in Pacific Grove, Calif., and realized he had not yet taken out the trash or recycling. It was raining fairly hard, so he decided to sprint from his doorstep to the garbage cans outside with a bag in each hand. As he was running, he slipped on a patch of black mold beneath some oak trees, landed hard on his chin, and snapped his neck between his second and third vertebrae. While recovering, DeGray, who was 53 at the time, learned from his doctors that he was permanently paralyzed from the collarbones down. With the exception of vestigial twitches, he cannot move his torso or limbs. “I’m about as hurt as you can get and not be on a ventilator,” he told me. For several years after his accident, he “simply laid there, watching the History Channel” as he struggled to accept the reality of his injury. Some time later, while at a fund-raising event for stem-cell research, he met Jaimie Henderson, a professor of neurosurgery at Stanford University. The pair got to talking about robots, a subject that had long interested DeGray, who grew up around his family’s machine shop. As DeGray remembers it, Henderson captivated him with a single question: Do you want to fly a drone? Henderson explained that he and his colleagues had been developing a brain-computer interface: an experimental connection between someone’s brain and an external device, like a computer, robotic limb or drone, which the person could control simply by thinking. DeGray was eager to participate, eventually moving to Menlo Park to be closer to Stanford as he waited for an opening in the study and the necessary permissions. In the summer of 2016, Henderson opened DeGray’s skull and exposed his cortex — the thin, wrinkled, outermost layer of the brain — into which he implanted two 4-millimeter-by-4-millimeter electrode arrays resembling miniature beds of nails. Each array had 100 tiny metal spikes that, collectively, recorded electric impulses surging along a couple of hundred neurons or so in the motor cortex, a brain region involved in voluntary movement. © 2022 The New York Times Company

Keyword: Robotics
Link ID: 28326 - Posted: 05.14.2022

By Laura Sanders Deep in the human brain, a very specific kind of cell dies during Parkinson’s disease. For the first time, researchers have sorted large numbers of human brain cells in the substantia nigra into 10 distinct types. Just one is especially vulnerable in Parkinson’s disease, the team reports May 5 in Nature Neuroscience. The result could lead to a clearer view of how Parkinson’s takes hold, and perhaps even ways to stop it. The new research “goes right to the core of the matter,” says neuroscientist Raj Awatramani of Northwestern University Feinberg School of Medicine in Chicago. Pinpointing the brain cells that seem to be especially susceptible to the devastating disease is “the strength of this paper,” says Awatramani, who was not involved in the study. Parkinson’s disease steals people’s ability to move smoothly, leaving balance problems, tremors and rigidity. In the United States, nearly 1 million people are estimated to have Parkinson’s. Scientists have known for decades that these symptoms come with the death of nerve cells in the substantia nigra. Neurons there churn out dopamine, a chemical signal involved in movement, among other jobs (SN: 9/7/17). But those dopamine-making neurons are not all equally vulnerable in Parkinson’s, it turns out. “This seemed like an opportunity to … really clarify which kinds of cells are actually dying in Parkinson’s disease,” says Evan Macosko, a psychiatrist and neuroscientist at Massachusetts General Hospital in Boston and the Broad Institute of MIT and Harvard. © Society for Science & the Public 2000–2022.

Keyword: Parkinsons
Link ID: 28320 - Posted: 05.07.2022

Liam Drew James Johnson hopes to drive a car again one day. If he does, he will do it using only his thoughts. In March 2017, Johnson broke his neck in a go-carting accident, leaving him almost completely paralysed below the shoulders. He understood his new reality better than most. For decades, he had been a carer for people with paralysis. “There was a deep depression,” he says. “I thought that when this happened to me there was nothing — nothing that I could do or give.” But then Johnson’s rehabilitation team introduced him to researchers from the nearby California Institute of Technology (Caltech) in Pasadena, who invited him to join a clinical trial of a brain–computer interface (BCI). This would first entail neurosurgery to implant two grids of electrodes into his cortex. These electrodes would record neurons in his brain as they fire, and the researchers would use algorithms to decode his thoughts and intentions. The system would then use Johnson’s brain activity to operate computer applications or to move a prosthetic device. All told, it would take years and require hundreds of intensive training sessions. “I really didn’t hesitate,” says Johnson. The first time he used his BCI, implanted in November 2018, Johnson moved a cursor around a computer screen. “It felt like The Matrix,” he says. “We hooked up to the computer, and lo and behold I was able to move the cursor just by thinking.” Johnson has since used the BCI to control a robotic arm, use Photoshop software, play ‘shoot-’em-up’ video games, and now to drive a simulated car through a virtual environment, changing speed, steering and reacting to hazards. “I am always stunned at what we are able to do,” he says, “and it’s frigging awesome.” © 2022 Springer Nature Limited

Keyword: Brain imaging; Robotics
Link ID: 28292 - Posted: 04.20.2022

Allison Whitten Every time you reach for your coffee mug, a neuroscientific mystery takes shape. Moments before you voluntarily extend your arm, thousands of neurons in the motor regions of your brain erupt in a pattern of electrical activity that travels to the spinal cord and then to the muscles that power the reach. But just prior to this massively synchronized activity, the motor regions in your brain are relatively quiet. For self-driven movements like reaching for your coffee, the “go” signal that tells the neurons precisely when to act — instead of the moment just before or after — has yet to be found. In a recent paper in eLife, a group of neuroscientists led by John Assad at Harvard Medical School finally reveals a key piece of the signal. It comes in the form of the brain chemical known as dopamine, whose slow ramping up in a region lodged deep below the cortex closely predicted the moment that mice would begin a movement — seconds into the future. Dopamine is commonly known as one of the brain’s neurotransmitters, the fast-acting chemical messengers that are shuttled between neurons. But in the new work, dopamine is acting as a neuromodulator. It’s a term for chemical messengers that slightly alter neurons to cause longer-lasting effects, including making a neuron more or less likely to electrically communicate with other neurons. This neuromodulatory tuning mechanism is perfect for helping to coordinate the activity of large populations of neurons, as dopamine is likely doing to help the motor system decide precisely when to make a movement. The new paper is one of the latest results to expand our knowledge of the crucial and varied roles that neuromodulators play in the brain. With recent advances in technology, neuroscientists can now view neuromodulators at work in networks that traverse the entire brain. The new findings are overturning some long-held views about these modulators adrift in the brain, and they’re revealing exactly how these molecules allow the brain to flexibly change its internal state amid ever-changing environments. All Rights Reserved © 2022

Keyword: Movement Disorders; Drug Abuse
Link ID: 28251 - Posted: 03.23.2022

Linda Geddes A completely locked-in patient is able to type out words and short sentences to his family, including what he would like to eat, after being implanted with a device that enables him to control a keyboard with his mind. The findings, published in Nature Communications, overturn previous assumptions about the communicative abilities of people who have lost all voluntary muscle control, including movement of the eyes or mouth, as well as giving a unique insight into what it’s like to be in a “locked in” state. Locked-in syndrome – also known as pseudocoma - is a rare condition, where people are conscious and can see, hear, and smell, but are unable to move or speak due to complete paralysis of their voluntary muscles, eg as a result of the progressive neurodegenerative disease amyotrophic lateral sclerosis (ALS). Advertisement Some can communicate by blinking or moving their eyes, but those with completely locked-in syndrome (CLIS) cannot even control their eye muscles. In 2017, doctors at the University of Tübingen in Germany enabled three patients with CLIS to answer “yes” or “no” to questions by detecting telltale patterns in their brain activity, using a technology called functional near-infrared spectroscopy (fNIRS). The advance generated widespread media coverage, and prompted the parents of the current patient, who was diagnosed with ALS in 2015, to write to the medical team, saying he was losing the ability to communicate with his eye movements, and could they help. The problem with using fNIRS to help CLIS patients to communicate is that it is relatively slow, and only gives the correct answer 70% of the time, meaning questions have to be repeated to get a reliable answer. “It was always our goal to enable a patient in a completely locked down state to spell out words, but with a classification accuracy of 70%, it is almost impossible to enable free spelling,” said Dr Ujwal Chaudhary, a biomedical engineer and managing director of ALS Voice gGmbH in Mössingen, Germany, who co-led the research. © 2022 Guardian News & Media Limited

Keyword: ALS-Lou Gehrig's Disease ; Movement Disorders
Link ID: 28250 - Posted: 03.23.2022

By Linda Searing The more fit you are, the less likely you may be to develop Alzheimer’s disease — with those who are the most fit having a 33 percent lower risk for this dementia than the least fit, according to a report to be presented to the American Academy of Neurology at its annual meeting next month. FAQ: What to know about the omicron variant of the coronavirus D.C.-based researchers, from the Washington VA Medical Center and George Washington University, tested and tracked 649,605 veterans (average age 61) for nearly a decade. Based on their cardiorespiratory fitness, participants were divided into five categories, from lowest to highest fitness level. 10-minute exercising may slow progression to dementia for those with mild cognitive impairment The researchers found that, as fitness improved, people’s chances of developing the ailment decreased. Compared with the least-fit group, those slightly more fit had a 13 percent lower risk for Alzheimer’s; the middle group was 20 percent less likely to develop the disease; the next higher group was 26 percent less likely; with the odds reaching a 33 percent lower risk for those in the most-fit group. Alzheimer’s is the most common type of dementia. It is a progressive brain disorder that, over time, destroys memory and thinking skills and interferes with the ability to carry out daily tasks. About 6 million Americans 65 and older have Alzheimer’s. There are no proven ways to cure the disease. © 1996-2022 The Washington Post

Keyword: Alzheimers
Link ID: 28239 - Posted: 03.16.2022

By Gina Kolata Dr. John Q. Trojanowski, a neuropathologist whose work was at the forefront of research on Alzheimer’s and other neurodegenerative diseases, died on Feb. 8 in a hospital in Philadelphia. He was 75. His wife and longtime collaborator, Virginia M.-Y. Lee, said the cause was complications of chronic spinal cord injuries. Dr. Trojanowski “was a giant in the field,” said Leslie Shaw, a professor with Dr. Trojanowski in the department of pathology and laboratory medicine at the University of Pennsylvania — adding that he meant that in two ways. At 6 feet 4 inches, Dr. Trojanowski towered over his colleagues. And, Dr. Shaw said, he was also a towering figure in his field, whose scientific contributions were “phenomenal” because they combined pathology and biochemistry to figure out what goes wrong, and why, when people get diseases as disparate as Alzheimer’s, Parkinson’s and A.L.S. The results can lead to improved diagnosis and potential treatments. Key to the work Dr. Trojanowski did with Dr. Lee was their establishment of a brain bank: stored brains from patients with diseases like Alzheimer’s and Parkinson’s, as well as from people without degenerative brain diseases. It allowed them to compare the brains of people with and without the conditions and ask what proteins were involved in the diseases and what brain regions were affected. Among their first quests was an attempt to solve the mystery of strange areas in the brains of people with Alzheimer’s. Known as tangles and first described by Alois Alzheimer himself at the turn of the 20th century, they look like twisted strands of spaghetti in dying nerve cells. In 1991, Dr. Trojanowski and Dr. Lee determined that the regions are made up of a malformed protein called tau, which causes the structure of nerve cells to collapse. At a time when most Alzheimer’s researchers and drug companies were focused on a different protein, amyloid, Dr. Trojanowski and Dr. Lee insisted that tau was equally important. They then discovered that it also played a central role in a rare group of degenerative dementias known as frontotemporal lobar degeneration. © 2022 The New York Times Company

Keyword: Alzheimers; ALS-Lou Gehrig's Disease
Link ID: 28225 - Posted: 03.02.2022

By Amanda Coletta Health officials in New Brunswick released a long-awaited report Thursday into a mysterious and debilitating neurological disorder that has struck dozens of people with bizarre symptoms — including a belief that family members have been replaced by impostors — stumped doctors and stoked fears across the province. The conclusion? There is no new disorder. “The oversight committee has unanimously agreed that these 48 people should never have been identified as having a neurological syndrome of unknown cause, and that based on the evidence reviewed, no such syndrome exists,” said Jennifer Russell, chief medical officer of health for the Canadian province. “Public Health concurs with these findings. But I stress again, this does not mean that these people aren’t seriously ill. It means they are ill with a known neurological condition.” The report’s authors say the 48 cases in what was thought to be a cluster were randomly allocated to pairs of neurologists who reviewed them and presented their findings to an oversight committee of six New Brunswick neurologists and other officials. The committee said none of the cases met the full criteria of the case definition. But that finding, coming at the end of an investigation marred by accusations of opacity from the start and allegations that Canada’s top scientists and experts from around the world had been abruptly shut out of the process, appeared unlikely to assuage alarm in the province and more likely to deepen mistrust. Patients and their family members questioned the committee’s findings Thursday, saying the province has not carried out the relevant testing and opted to “abandon scientific rigor in exchange for political expediency.” © 1996-2022 The Washington Post

Keyword: Stress; Prions
Link ID: 28222 - Posted: 02.26.2022

by Laura Dattaro Some genomic areas that help determine cerebellar size are associated with autism, schizophrenia and bipolar disorder, according to a new study. But heritable genetic variants across the genome that also influence cerebellar size are not. The cerebellum sits at the base of the skull, below and behind the much larger cerebrum. It coordinates movement and may also play roles in social cognition and autism, according to previous research. The new work analyzed genetic information and structural brain scans from more than 33,000 people in the UK Biobank, a biomedical and genetic database of adults aged 40 to 69 living in the United Kingdom. A total of 33 genetic sequence variants, known as single nucleotide polymorphisms (SNPs), were associated with differences in cerebellar volume. Only one SNP overlapped with those linked to autism, but the association should be explored further in other cohorts, says lead investigator Richard Anney, senior lecturer in bioinformatics at Cardiff University in Wales. “There’s lots of caveats to say why it might be worth following up on,” Anney says. “But from this data alone, it’s not telling us there’s a major link between [autism] and cerebellar volume.” So far, cognitive neuroscientists have largely ignored the cerebellum, says Jesse Gomez, assistant professor of neuroscience at Princeton University, who was not involved in the work. The new study represents a first step in better understanding genetic influences on the brain region and its role in neurodevelopmental conditions, he says. “It’s a fun paper,” Gomez says. “It’s the beginning of what’s an exciting revolution in the field.” Of the 33 inherited variants Anney’s team found, 5 had not previously been significantly associated with cerebellar volume. They estimated that the 33 variants account for about 50 percent of the differences in cerebellar volume seen across participants. © 2022 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 28215 - Posted: 02.23.2022

Linda Geddes A simple test could end years of uncertainty for people with relatively common neurological conditions, new research has found. Historically, obtaining a definitive diagnosis for conditions including Huntingdon’s disease and some forms of amyotrophic lateral sclerosis has been difficult, because, although the cause of the symptoms is genetic, knowing which test to carry out has resulted in delays of many years. Now, a new study suggests that whole genome sequencing (WGS) can quickly and accurately detect the most common inherited neurological disorders, and could be implemented in routine clinical practice with immediate effect. “It is very exciting because it opens up the vista of a test that could end the diagnostic odyssey for many patients,” said Prof Sir Mark Caulfield from Queen Mary University of London and former chief scientist at Genomics England. “This work paves the way for this to be implemented immediately within the NHS.” WGS is already offered to people in England with rare disorders or childhood cancers through the NHS Genomic Medicine Service. However, the technique wasn’t thought to work on people with ‘repeat expansion disorders’ caused by the insertion of short repetitive chunks of DNA into the genetic code – in some cases, stretching across long distances – because they can be difficult to quantify. Such disorders are relatively common, affecting around one in 3,000 people, and include neurodegenerative and movement disorders such as Fragile X syndrome, Huntington’s disease, Friedreich’s ataxia, and some forms of amyotrophic lateral sclerosis or frontal lobe dementia. © 2022 Guardian News & Media Limited

Keyword: Huntingtons; Genes & Behavior
Link ID: 28210 - Posted: 02.19.2022

By Lisa Sanders, M.D. “OK, I give up,” said the 74-year-old man. “I’ll go to the hospital.” His wife of 46 years gave an inner sigh of relief. Her husband was stubborn, a seventh-​generation Mainer, not given to complaining. But a few weeks earlier, she noticed that he was parking his tractor next to the back porch so he could get on it without pulling himself up. Then he needed help getting out of his big chair. Now he could barely walk. It happened so suddenly it scared her. She eased the car right next to the porch. He needed both hands on the railing to get down, grunting with each step. His legs moved awkwardly, as if they had somehow forgotten what to do. At the LincolnHealth-Miles Campus Hospital in nearby Damariscotta, it was clear to the E.R. doctors that the patient wasn’t weak but ataxic, lacking not strength but coordination. Virtually every movement the body makes requires several muscles working together — a collaboration that occurs in the cerebellum. The uncertain and awkward way the patient moved made doctors at LincolnHealth worry that something — maybe a stroke, maybe a tumor — had injured that part of the brain. But two CT scans and an M.R.I. were unrevealing. When his doctors weren’t sure what to do next, the patient decided it was time to go home. His wife was supportive but worried. How could she help him get around? He was a big guy and outweighed her by 50 pounds. And they still needed to figure out what was wrong with him. Couldn’t they try another hospital? Maybe, he said, but first he wanted to go home. So that’s where she took him. Once there, it took only a day for the man to recognize, again, that he couldn’t just tough it out at home. There was another hospital, a larger one a couple of towns over in Brunswick: Mid Coast Hospital. His wife was happy to take him there. Those few steps he took from porch to car, supported by his wife, were the last he would take for weeks. © 2022 The New York Times Company

Keyword: Movement Disorders; Neuroimmunology
Link ID: 28204 - Posted: 02.16.2022

By Pallab Ghosh A paralysed man with a severed spinal cord has been able to walk again, thanks to an implant developed by a team of Swiss researchers. It is the first time someone who has had a complete cut to their spinal cord has been able to walk freely. The same technology has improved the health of another paralysed patient to the extent that he has been able to become a father. The research has been published in the journal Nature Medicine. Michel Roccati was paralysed after a motorbike accident five years ago. His spinal cord was completely severed - and he has no feeling at all in his legs. But he can now walk - because of an electrical implant that has been surgically attached to his spine. Someone this injured has never been able to walk like this before. The researchers stress that it isn't a cure for spinal injury and that the technology is still too complicated to be used in everyday life, but hail it nonetheless as a major step to improving quality of life. I met Michel at the lab where the implant was created. He told me that the technology "is a gift to me". "I stand up, walk where I want to, I can walk the stairs - it's almost a normal life." It was not the technology alone that drove Michel's recovery. The young Italian has a steely resolve. He told me that from the moment of his accident, he was determined to make as much progress as he could. "I used to box, run and do fitness training in the gym. But after the accident, I could not do the things that I loved to do, but I did not let my mood go down. I never stopped my rehabilitation. I wanted to solve this problem." The speed of Michel's recovery amazed the neurosurgeon who inserted the implant and expertly attached electrodes to individual nerve fibres, Prof Jocelyne Bloch at Lausanne University Hospital "I was extremely surprised," she told me. "Michel is absolutely incredible. He should be able to use this technology to progress and be better and better." © 2022 BBC.

Keyword: Robotics; Regeneration
Link ID: 28194 - Posted: 02.09.2022

Jon Hamilton Paul knew his young grandson was in danger. "Out of the corner of my eye I could see this little figure moving," he says. The figure was heading for a steep flight of stairs. But what could he do? Paul was sitting down. And after more than a decade of living with Parkinson's disease, getting out of a chair had become a long and arduous process. But not on this day. "Paul jumped up from the chair and ran to my grandson," says his wife, Rose. (The couple asked to be identified by only their first names to protect their medical privacy.) "I mean, he just got up like there was nothing and ran to pick up Max." Amazing. But it's also the kind of story that's become familiar to Peter Strick, professor and chair of neurobiology at the University of Pittsburgh and scientific director of the University of Pittsburgh Brain Institute. "It was a great example of what people call paradoxical kinesia," Strick says. "It was a description of just what we are studying." Article continues after sponsor message Paradoxical kinesia refers to the sudden ability of a person with Parkinson's to move quickly and fluidly, the way they did before the disease eroded a brain area involved in movement. The phenomenon is a variation of the placebo effect. But instead of being induced by the belief that a sugar pill is really medicine, it tends to appear in situations that involve stress or a strong emotion. For Paul, "it was the fear of his grandson falling down the stairs," says Strick, who learned about the event in an email from Rose. A treatment that's "all in your head" © 2022 npr

Keyword: Parkinsons; Emotions
Link ID: 28193 - Posted: 02.09.2022

by Holly Barker New software uses machine-learning to automatically detect and quantify gait and posture from videos of mice moving around their cage. The tool could accelerate research on how autism-linked mutations or drug treatments affect motor skills, says lead researcher Vivek Kumar, associate professor of mammalian genetics at The Jackson Laboratory in Bar Harbor, Maine. Most efforts to analyze motor behavior involve placing a mouse on a treadmill or training it to walk through a maze. These assays are a simple way of testing speed, but they restrict the animals’ movement and force mice to walk in an unnatural way. The algorithm processes footage from an overhead camera and tracks 12 key points on a mouse’s body as it freely explores its surroundings. As the animal wanders, the software detects the position of its limbs and other body parts, automatically generating data on its gait and posture. The researchers described their method in January in Cell Reports. Kumar’s group trained the software by feeding it about 8,000 video frames that had been manually annotated to tag key points on the animal’s body, such as the nose, ears and tip of the tail. They repeated the process with a variety of different strains to teach the algorithm to recognize mice of all shapes and sizes. The trained software learned to read the rodent’s pose, which was further analyzed to extract more detailed information, such as the speed and length of each stride and the width of the mouse’s stance. © 2022 Simons Foundation

Keyword: Autism; Movement Disorders
Link ID: 28186 - Posted: 02.05.2022

ByRodrigo Pérez Ortega A good workout doesn’t just boost your mood—it also boosts the brain’s ability to create new neurons. But exactly how this happens has puzzled researchers for years. “It’s been a bit of a black box,” says Tara Walker, a neuroscientist at the University of Queensland’s Brain Institute. Now, Walker and her colleagues think they have found a key: the chemical element selenium. During exercise, mice produce a protein containing selenium that helps their brains grow new neurons, the team reports today. Scientists may also be able to harness the element to help reverse cognitive decline due to old age and brain injury, the authors say. It’s a “fantastic” study, says Bárbara Cardoso, a nutritional biochemist at Monash University’s Victorian Heart Institute. Her own research has shown selenium—which is found in Brazil nuts, grains, and some legumes—improves verbal fluency and the ability to copy drawings correctly in older adults. “We could start thinking about selenium as a strategy” to treat or prevent cognitive decline in those who cannot exercise or are more vulnerable to selenium deficiency, she says, such as older adults, and stroke and Alzheimer’s disease patients. In 1999, researchers reported that running stimulates the brain to make new neurons in the hippocampus, a region involved in learning and memory. But which molecules were released into the bloodstream to spark this “neurogenesis” remained unclear. So 7 years ago, Walker and her colleagues screened the blood plasma of mice that had exercised on a running wheel in their cages for 4 days, versus mice that had no wheel. The team identified 38 proteins whose levels increased after the workout. © 2022 American Association for the Advancement of Science.

Keyword: Learning & Memory; Obesity
Link ID: 28185 - Posted: 02.05.2022

Rupert Neate The billionaire entrepreneur Elon Musk’s brain chip startup is preparing to launch clinical trials in humans. Musk, who co-founded Neuralink in 2016, has promised that the technology “will enable someone with paralysis to use a smartphone with their mind faster than someone using thumbs”. The Silicon Valley company, which has already successfully implanted artificial intelligence microchips in the brains of a macaque monkey named Pager and a pig named Gertrude, is now recruiting for a “clinical trial director” to run tests of the technology in humans. “As the clinical trial director, you’ll work closely with some of the most innovative doctors and top engineers, as well as working with Neuralink’s first clinical trial participants,” the advert for the role in Fremont, California, says. “You will lead and help build the team responsible for enabling Neuralink’s clinical research activities and developing the regulatory interactions that come with a fast-paced and ever-evolving environment.” Musk, the world’s richest person with an estimated $256bn fortune, said last month he was cautiously optimistic that the implants could allow tetraplegic people to walk. “We hope to have this in our first humans, which will be people that have severe spinal cord injuries like tetraplegics, quadriplegics, next year, pending FDA [Food and Drug Administration] approval,” he told the Wall Street Journal’s CEO Council summit. “I think we have a chance with Neuralink to restore full-body functionality to someone who has a spinal cord injury. Neuralink’s working well in monkeys, and we’re actually doing just a lot of testing and just confirming that it’s very safe and reliable and the Neuralink device can be removed safely.” © 2022 Guardian News & Media Limited

Keyword: Brain imaging; Robotics
Link ID: 28164 - Posted: 01.22.2022

By Linda Searing For people with early-stage Parkinson’s disease, four hours a week of moderate exercise may help slow the progression of the disease. Symptoms of Parkinson’s, which is a movement disorder, generally start gradually but worsen over time. FAQ: What to know about the omicron variant of the coronavirus But research published in the journal Neurology found that those who were regularly active for at least that amount of time — whether with traditional exercise or such physical activity as walking, gardening or dancing — had less decline in balance and walking ability, were better able to maintain daily activities and did better on cognitive tests five years later than those who exercised less. The researchers noted that the key to achieving these benefits was maintaining regular exercise over time, rather than how active people had been when their disease started. Parkinson’s, which is more common in men than women, usually begins about age 60 as nerve cells in the brain (neurons) become weak or damaged. Symptoms may include trembling or shaking (tremor), muscle stiffness (rigidity), slow movement (bradykinesia) and poor balance and coordination. As symptoms get worse, people may have trouble walking, talking or continuing to do routine daily activities. Although no cure exists for Parkinson’s, treatment — medication, surgery or electrical stimulation — can sometimes help ease some symptoms for a while. The researchers wrote, however, that “there is still no disease-modifying treatment to slow the disease’s progression.”

Keyword: Parkinsons
Link ID: 28157 - Posted: 01.19.2022

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