By Jocelyn Kaiser Parkinson’s disease, a brain disorder that gradually leads to difficulty moving, tremors, and usually dementia by the end, is often difficult to diagnose early in its yearslong progression. That makes testing experimental treatments challenging and slows people from getting existing drugs, which can’t stop the ongoing death of brain cells but temporarily improve many of the resulting symptoms. Now, a study using rodents and tissue from diagnosed Parkinson’s patients suggests DNA damage spotted in blood samples offers a simple way to diagnose the disease early. Although the potential test needs to be validated in clinical studies, the detected DNA damage joins a “flurry” of other biomarkers recently identified for Parkinson’s and “adds to our ability to state confidently that an individual has Parkinson’s disease or not,” says neurodegeneration researcher Mark Cookson of the National Institute on Aging, whose grantmaking arm helped fund the new work, published today in Science Translational Medicine. A blood test based on the findings could also help patients go on existing treatments earlier and boost clinical trials evaluating new therapies, the study’s authors say. “It’s really exciting because it’s something [physicians] could use to detect [Parkinson’s] before the clinical symptoms emerge,” says neuroscientist Malú Tansey of the University of Florida, who also was not involved with the research. Parkinson’s occurs when the death of certain neurons in the brain causes levels of the neurotransmitter dopamine to drop, leading to muscle stiffness, balance problems, speech and cognitive problems, and other symptoms over time. The disorder, tied to both environmental and genetic factors, afflicts up to 1 million people in the United States.

Keyword: Parkinsons
Link ID: 28897 - Posted: 09.07.2023

By R. Douglas Fields One day, while threading a needle to sew a button, I noticed that my tongue was sticking out. The same thing happened later, as I carefully cut out a photograph. Then another day, as I perched precariously on a ladder painting the window frame of my house, there it was again! What’s going on here? I’m not deliberately protruding my tongue when I do these things, so why does it keep making appearances? After all, it’s not as if that versatile lingual muscle has anything to do with controlling my hands. Right? Yet as I would learn, our tongue and hand movements are intimately interrelated at an unconscious level. This peculiar interaction’s deep evolutionary roots even help explain how our brain can function without conscious effort. A common explanation for why we stick out our tongue when we perform precision hand movements is something called motor overflow. In theory, it can take so much cognitive effort to thread a needle (or perform other demanding fine motor skills) that our brain circuits get swamped and impinge on adjacent circuits, activating them inappropriately. It’s certainly true that motor overflow can happen after neural injury or in early childhood when we are learning to control our bodies. But I have too much respect for our brains to buy that “limited brain bandwidth” explanation. How, then, does this peculiar hand-mouth cross-talk really occur? Tracing the neural anatomy of tongue and hand control to pinpoint where a short circuit might happen, we find first of all that the two are controlled by completely different nerves. This makes sense: A person who suffers a spinal cord injury that paralyzes their hands does not lose their ability to speak. That’s because the tongue is controlled by a cranial nerve, but the hands are controlled by spinal nerves. Simons Foundation

Keyword: Language; Emotions
Link ID: 28894 - Posted: 08.30.2023

By Simon Makin Rats are extremely playful creatures. They love playing chase, and they literally jump for joy when tickled. Central to this playfulness, a new study finds, are cells in a specific region of rats’ brains. Neurons in the periaqueductal gray, or PAG, are active in rats during different kinds of play, scientists report July 28 in Neuron. And blocking the activity of those neurons makes the rodents much less playful. The results give insight into a poorly understood behavior, particularly in terms of how play is controlled in the brain. “There are prejudices that it’s childish and not important, but play is an underrated behavior,” says Michael Brecht, a neuroscientist at Humboldt University in Berlin. Scientists think play helps animals develop resilience. Some even relate it to optimal functioning. “When you’re playing, you’re being your most creative, thoughtful, interactive self,” says Jeffrey Burgdorf, a neuroscientist at Northwestern University in Evanston, Ill., who was not involved in the new study. This is the opposite of depressive states, and Burgdorf’s own research aims to turn understanding the neuroscience of play into new therapies for mood disorders. For the new study, Brecht and colleagues got rats used to lab life and being tickled and played with in a game of chase-the-hand. When rats play, they squeal with glee at a frequency of 50 kilohertz, which humans can’t hear. The researchers recorded these ultrasonic giggles as a way of measuring when the rats were having fun. To explore how a specific brain region in rats might relate to their well-documented play behavior, researchers tickled rats on their bellies and backs and played chase-the-hand. Rats also played together, chasing and play-fighting. Ultrasonic giggles, processed to make them audible to humans, coordinate social play and show that the rats are having fun. © Society for Science & the Public 2000–2023.

Keyword: Emotions; Evolution
Link ID: 28864 - Posted: 08.02.2023

By Claudia López Lloreda When someone loses a hand or leg, they don’t just lose the ability to grab objects or walk—they lose the ability to touch and sense their surroundings. Prosthetics can restore some motor control, but they typically can’t restore sensation. Now, a preliminary studyposted to the preprint server bioRxiv this month—shows that by mimicking the activity of nerves, a device implanted in the remaining part of the leg helps amputees “feel” as they walk, allowing them to move faster and with greater confidence. “It's a really elegant study,” says Jacob George, neuroengineer at the University of Utah who was not involved with the research. Because the experiments go from a computational model to an animal model and then, finally humans, he says, “This work is really impactful, because it's one of the first studies that's done in a holistic way.” Patients with prosthetics often have a hard time adapting. One big issue is that they can’t accurately control the device because they can’t feel the pressure that they’re exerting on an object. Hand and arm amputees, for example, are more prone to drop or break things. As a result, some amputees refuse to use such prosthetics. In the past few years, researchers have been working on prosthetic limbs that provide more natural sensory feedback both to help control the device better and give them back a sense of agency over their robotic limb. In a critical study in 2019, George and his team showed that so-called biomimetic feedback, sensory information that aims to resemble the natural signals that occur with touch, allowed a patient who’d lost his hand to more precisely grip fragile objects such as eggs and grapes. But such studies have been limited to single patients. They’ve also left many questions unanswered about how exactly this feedback helps with motor control and improves the use of the prosthetic. So in the new work, researchers used a computer model that re-creates how nerves in the foot respond to different inputs, such as feeling pressure. The goal was to create natural patterns of neural activity that might occur when sensing something with the foot or walking. © 2023 American Association for the Advancement of Science.

Keyword: Pain & Touch; Robotics
Link ID: 28863 - Posted: 08.02.2023

By Claudia Lopez Lloreda There are plenty of reasons to get off your duff and exercise—but is improving your brain one of them? The U.S. Centers for Disease Control and Prevention touts exercise as a way to “boost brain health,” while the World Health Organization suggests that about 2 hours of moderate activity or 75 minutes of vigorous activity per week can help improve thinking and memory skills. But new research reveals a more complex picture. One recent review of the literature suggests the studies tying exercise to brain health may have important limitations, including small sample sizes. Other studies suggest there is no one-size-fits-all approach to exercising as a way to boost cognition or prevent age-related cognitive decline. Still others indicate exercise may actually be harmful in people with certain medical conditions. Here’s the latest on what we know. What is the science linking exercise and improved brain function? Many studies correlate participants’ self-reported exercise with scores on cognitive tests, or track the effects of randomizing participants into groups that either exercise or remain sedentary. They typically find that the more physical activity a person does, the better their cognition. This result holds for healthy people, stroke survivors, and those with other neurological conditions such as Alzheimer’s disease. A study published earlier this year relied on genetic data to explore the effects of exercise. A team led by sports scientist Boris Cheval at the University of Geneva grouped about 350,000 people in the United Kingdom according to genetic variants associated with more or less physical activity. Those with an apparent genetic predisposition to be more active also tended to perform better on a set of cognitive tests, the researchers concluded in Scientific Reports. Other studies have focused on age-related cognitive decline. Research published in February in the Journal of Neurology, Neurosurgery & Psychiatry tracked more than 1400 people for 30 years, showing that more physical activity was associated with better cognitive performance at age 69.

Keyword: Development of the Brain; Alzheimers
Link ID: 28838 - Posted: 07.01.2023

Juana Summers On a recent crisp June night, as the Chicago Cubs prepare to take on the Pittsburgh Pirates, fans dressed in blue pack Wrigley Stadium's famous bleachers. Sitting in his wheelchair, 42-year-old Brian Wallach looks out over the park, rooting for a very particular outcome that has nothing to do with baseball. He has amyotrophic lateral sclerosis (ALS) — sometimes referred to as Lou Gehrig's disease, named for the baseball legend once dubbed the "iron horse" because of his durability, before the disease took his life. At the gates of the stadium, ballpark staff hand out bright blue T-shirts with the Cubs logo and the words, "End ALS for Lou." The night is part of a growing movement to highlight ALS and spread awareness of the toll it has wrought on people. Wallach and his wife Sandra Abrevaya watch a Cubs game at Wrigley Field in June. Jamie Kelter Davis for NPR For Wallach, a former assistant U.S. attorney who once worked for Barack Obama, his specialty is turning that goodwill into action in the ALS community, the halls of Congress and the Oval Office. And he has used his connections to change the face of medical advocacy in this country. Wallach was diagnosed six years ago, on the day that he and his wife, Sandra Abrevaya, brought the newborn second daughter home from the hospital. "Sandra and I cried and we held our family tight. We did so because being diagnosed with ALS today is a death sentence. There is no cure. I will not see my daughters grow up," Wallach told Congress during testimony he gave in 2019. © 2023 npr

Keyword: ALS-Lou Gehrig's Disease
Link ID: 28837 - Posted: 07.01.2023

By Charlotte Stoddart Charlotte Stoddart: Can a sugar pill make you feel better? What about the rituals surrounding a visit to the doctor? Can the care of a doctor or your trust in them reduce the amount of pain you feel? I’m Charlotte Stoddart and this is Knowable. This episode is all about the placebo effect. We’re going to look in detail at one key paper to learn how the placebo effect has been used in medicine and how it’s been understood and misunderstood. The paper is called “The Powerful Placebo.” It was written by Henry Beecher and published in JAMA, the Journal of the American Medical Association, in 1955. I chose this paper because it’s often referred to as a classic, and it’s still one of the most frequently cited papers on the placebo effect. I’ve enlisted the help of Ted Kaptchuk, who knows the paper well. Ted Kaptchuk: I enjoyed rereading it, actually. It’s a remarkable paper. I’ve read it probably 15 times in my life. Charlotte Stoddart: Ted is director of the Program in Placebo Studies at the Beth Israel Deaconess Medical Center in Boston and a professor of medicine at Harvard Medical School, where Henry Beecher also held a professorship. Beecher also worked at Massachusetts General Hospital. Charlotte Stoddart: During the Second World War, Beecher served in the US Army, and there’s a story about how that experience got him interested in the placebo effect. It goes like this: Beecher was working at a military hospital. One day, a badly injured soldier needed surgery, but the hospital had run out of morphine. So Beecher injected the soldier with saline solution instead. The soldier relaxed and Beecher carried out the operation without any real anesthetic. This, so the story goes, is when Beecher realized the power of the mind over the body. There are several different versions of this story, but Ted says it’s likely some version of it is true. © 2023 Annual Reviews

Keyword: Pain & Touch; Attention
Link ID: 28832 - Posted: 06.28.2023

Jon Hamilton Diseases like Alzheimer's, Parkinson's, and Huntington's are caused by toxic clumps of proteins that spread through the brain like a forest fire. Now scientists say they've figured out how the fire starts in at least one of these diseases. They've also shown how it can be extinguished. The finding involves Huntington's disease, a rare, inherited brain disorder that cut short the life of songwriter Woody Guthrie. But the study has implications for other degenerative brain diseases, including Alzheimer's. It "opens the path" to finding the initial event that leads to diseases like Alzheimer's and Parkinson's, says Corinne Lasmézas, who studies neurodegenerative diseases at the Wertheim UF Scripps Institute in Jupiter, Florida. She was not involved in the study. People with Huntington's "begin to lose control of their body movements, they have mental impediments over time, and eventually they die," says Randal Halfmann, an author of the study and a researcher at the Stowers Institute for Medical Research in Kansas City, Mo. Like other neurodegenerative diseases, Huntington's occurs when proteins in the brain fold into an abnormal shape and begin to stick together. Then these clumps of abnormal protein begin to cause nearby proteins to misfold and clump too. "As the disease progresses you're effectively watching a sort of a forest fire," Halfmann says. "And you're trying to figure out what started it." In essence, Halfmann's team wanted to find the molecular matchstick responsible for the lethal blaze. To do that, they needed to chronicle an event that is fleeting and usually invisible. It's called nucleation, the moment when a misfolded protein begins to aggregate and proliferate. © 2023 npr

Keyword: Huntingtons
Link ID: 28828 - Posted: 06.21.2023

Kari Paul and Maanvi Singh Elon Musk’s brain-implant company Neuralink last week received regulatory approval to conduct the first clinical trial of its experimental device in humans. But the billionaire executive’s bombastic promotion of the technology, his leadership record at other companies and animal welfare concerns relating to Neuralink experiments have raised alarm. “I was surprised,” said Laura Cabrera, a neuroethicist at Penn State’s Rock Ethics Institute about the decision by the US Food and Drug Administration to let the company go ahead with clinical trials. Musk’s erratic leadership at Twitter and his “move fast” techie ethos raise questions about Neuralink’s ability to responsibly oversee the development of an invasive medical device capable of reading brain signals, Cabrera argued. “Is he going to see a brain implant device as something that requires not just extra regulation, but also ethical consideration?” she said. “Or will he just treat this like another gadget?” Neuralink is far from the first or only company working on brain interface devices. For decades, research teams around the world have been exploring the use of implants and devices to treat conditions such as paralysis and depression. Already, thousands use neuroprosthetics like cochlear implants for hearing. But the broad scope of capabilities Musk is promising from the Neuralink device have garnered skepticism from experts. Neuralink entered the industry in 2016 and has designed a brain-computer interface (BCI) called the Link – an electrode-laden computer chip that can be sewn into the surface of the brain and connects it to external electronics – as well as a robotic device that implants the chip. © 2023 Guardian News & Media Limited

Keyword: Robotics; Learning & Memory
Link ID: 28816 - Posted: 06.07.2023

John Michael Streicher Opioid drugs such as morphine and fentanyl are like the two-faced Roman god Janus: The kindly face delivers pain relief to millions of sufferers, while the grim face drives an opioid abuse and overdose crisis that claimed nearly 70,000 lives in the U.S. in 2020 alone. Scientists like me who study pain and opioids have been seeking a way to separate these two seemingly inseparable faces of opioids. Researchers are trying to design drugs that deliver effective pain relief without the risk of side effects, including addiction and overdose. One possible path to achieving that goal lies in understanding the molecular pathways opioids use to carry out their effects in your body. How do opioids work? The opioid system in your body is a set of neurotransmitters your brain naturally produces that enable communication between neurons and activate protein receptors. These neurotransmitters include small proteinlike molecules like enkephalins and endorphins. These molecules regulate a tremendous number of functions in your body, including pain, pleasure, memory, the movements of your digestive system and more. Analysis of the world, from experts Opioid neurotransmitters activate receptors that are located in a lot of places in your body, including pain centers in your spinal cord and brain, reward and pleasure centers in your brain, and throughout the neurons in your gut. Normally, opioid neurotransmitters are released in only small quantities in these exact locations, so your body can use this system in a balanced way to regulate itself. The opioids your body produces and opioid drugs bind to the same receptors. The problem comes when you take an opioid drug like morphine or fentanyl, especially at high doses for a long time. These drugs travel through the bloodstream and can activate every opioid receptor in your body. You’ll get pain relief through the pain centers in your spinal cord and brain. But you’ll also get a euphoric high when those drugs hit your brain’s reward and pleasure centers, and that could lead to addiction with repeated use. When the drug hits your gut, you may develop constipation, along with other common opioid side effects. Targeting opioid signal transduction How can scientists design opioid drugs that won’t cause side effects? One approach my research team and I take is to understand how cells respond when they receive the message from an opioid neurotransmitter. Neuroscientists call this process opioid receptor signal transduction. Just as neurotransmitters are a communication network within your brain, each neuron also has a communication network that connects receptors to proteins within the neuron. When these connections are made, they trigger specific effects like pain relief. So, after a natural opioid neurotransmitter or a synthetic opioid drug activates an opioid receptor, it activates proteins within the cell that carry out the effects of the neurotransmitter or the drug. © 2010–2023, The Conversation US, Inc.

Keyword: Drug Abuse; Pain & Touch
Link ID: 28809 - Posted: 06.03.2023

By Linda Searing Getting regular exercise may reduce a woman’s chances of developing Parkinson’s disease by as much as 25 percent, according to research published in the journal Neurology. It involved 95,354 women, who were an average of age 49 and did not have Parkinson’s when the study began. The researchers compared the women’s physical exercise levels over nearly three decades, including such activities as walking, cycling, gardening, stair climbing, house cleaning and sports participation. In that time, 1,074 women developed Parkinson’s. The study found that as a woman’s exercise level increased, her risk for Parkinson’s decreased. Those who got the most exercise — based on timing and intensity — developed the disease at a 25 percent lower rate than those who exercised the least. The researchers wrote that the study’s findings “suggest that physical activity may help prevent or delay [Parkinson’s disease] onset.” Parkinson’s disease is a neurodegenerative disorder, meaning it is a progressive disease that affects the nervous system and parts of the body controlled by nerves. It is sometimes referred to as a movement disorder because of the uncontrollable tremors, muscle stiffness, and gait and balance problems it can cause, but people with Parkinson’s also may experience sleep problems, depression, memory issues, fatigue and more. The symptoms generally stem from the brain’s lack of production of dopamine, a chemical that helps control muscle movement. No cure exists for Parkinson’s, but treatments to relieve symptoms include medication, lifestyle adjustments and surgical procedures, such as deep brain stimulation.

Keyword: Parkinsons
Link ID: 28804 - Posted: 05.31.2023

By Oliver Whang Gert-Jan Oskam was living in China in 2011 when he was in a motorcycle accident that left him paralyzed from the hips down. Now, with a combination of devices, scientists have given him control over his lower body again. “For 12 years I’ve been trying to get back my feet,” Mr. Oskam said in a press briefing on Tuesday. “Now I have learned how to walk normal, natural.” In a study published on Wednesday in the journal Nature, researchers in Switzerland described implants that provided a “digital bridge” between Mr. Oskam’s brain and his spinal cord, bypassing injured sections. The discovery allowed Mr. Oskam, 40, to stand, walk and ascend a steep ramp with only the assistance of a walker. More than a year after the implant was inserted, he has retained these abilities and has actually showed signs of neurological recovery, walking with crutches even when the implant was switched off. “We’ve captured the thoughts of Gert-Jan, and translated these thoughts into a stimulation of the spinal cord to re-establish voluntary movement,” Grégoire Courtine, a spinal cord specialist at the Swiss Federal Institute of Technology, Lausanne, who helped lead the research, said at the press briefing. Jocelyne Bloch, a neuroscientist at the University of Lausanne who placed the implant in Mr. Oskam, added, “It was quite science fiction in the beginning for me, but it became true today.” A brave new world. A new crop of chatbots powered by artificial intelligence has ignited a scramble to determine whether the technology could upend the economics of the internet, turning today’s powerhouses into has-beens and creating the industry’s next giants. Here are the bots to know: © 2023 The New York Times Company

Keyword: Robotics; Brain imaging
Link ID: 28801 - Posted: 05.27.2023

By Jennie Erin Smith José Echeverría spends restless days in a metal chair reinforced with boards and padded with a piece of foam that his mother, Nohora Vásquez, adjusts constantly for his comfort. The chair is coming loose and will soon fall apart. Huntington’s disease, which causes José to move his head and limbs uncontrollably, has already left one bed frame destroyed. At 42, he is still strong. José’s sister Nohora Esther Echeverría, 37, lives with her mother and brother. Just two years into her illness, her symptoms are milder than his, but she is afraid to walk around her town’s steep streets, knowing she could fall. A sign on the front door advertises rum for sale that does not exist. The family’s scarce resources now go to food — José and Nohora Esther must eat frequently or they will rapidly lose weight — and medical supplies, like a costly cream for Jose’s skin. Huntington’s is a hereditary neurodegenerative disease caused by excess repetitions of three building blocks of DNA — cytosine, adenine, and guanine — on a gene called huntingtin. The mutation results in a toxic version of a key brain protein, and a person’s age at the onset of symptoms relates, roughly, to the number of repetitions the person carries. Early symptoms can include mood disturbances — Ms. Vásquez remembers how her late husband had chased the children out of their beds, forcing her to sleep with them in the woods — and subtle involuntary movements, like the rotations of Nohora Esther’s delicate wrists. The disease is relatively rare, but in the late 1980s a Colombian neurologist, Jorge Daza, began observing a striking number of cases in the region where Ms. Vásquez lives, a cluster of seaside and mountain towns near Barranquilla. Around the same time, American scientists led by Nancy Wexler were working with an even larger family with Huntington’s in neighboring Venezuela, gathering and studying thousands of tissue samples from them to identify the genetic mutation responsible. © 2023 The New York Times Company

Keyword: Huntingtons; Genes & Behavior
Link ID: 28796 - Posted: 05.23.2023

By Laura Sanders Scientists can see chronic pain in the brain with new clarity. Over months, electrodes implanted in the brains of four people picked up specific signs of their persistent pain. This detailed view of chronic pain, described May 22 in Nature Neuroscience, suggests new ways to curtail the devastating condition. The approach “provides a way into the brain to track pain,” says Katherine Martucci, a neuroscientist who studies chronic pain at Duke University School of Medicine. Chronic pain is incredibly common. In the United States from 2019 to 2020, more adults were diagnosed with chronic pain than with diabetes, depression or high blood pressure, researchers reported May 16 in JAMA Network Open. Chronic pain is also incredibly complex, an amalgam influenced by the body, brain, context, emotions and expectations, Martucci says. That complexity makes chronic pain seemingly invisible to an outsider, and very difficult to treat. One treatment approach is to stimulate the brain with electricity. As part of a clinical trial, researchers at the University of California, San Francisco implanted four electrode wires into the brains of four volunteers with chronic pain. These electrodes can both monitor and stimulate nerve cells in two brain areas: the orbitofrontal cortex, or OFC, and the anterior cingulate cortex, or ACC. The OFC isn’t known to be a key pain influencer in the brain, but this region has lots of neural connections to pain-related areas, including the ACC, which is thought to be involved in how people experience pain. But before researchers stimulated the brain, they needed to know how chronic pain was affecting it. For about 3 to 6 months, the implanted electrodes monitored brain signals of these people as they went about their lives. During that time, the participants rated their pain on standard scales two to eight times a day. © Society for Science & the Public 2000–2023.

Keyword: Pain & Touch; Brain imaging
Link ID: 28795 - Posted: 05.23.2023

By Priyanka Runwal Researchers have for the first time recorded the brain’s firing patterns while a person is feeling chronic pain, paving the way for implanted devices to one day predict pain signals or even short-circuit them. Using a pacemaker-like device surgically placed inside the brain, scientists recorded from four patients who had felt unremitting nerve pain for more than a year. The devices recorded several times a day for up to six months, offering clues for where chronic pain resides in the brain. The study, published on Monday in the journal Nature Neuroscience, reported that the pain was associated with electrical fluctuations in the orbitofrontal cortex, an area involved in emotion regulation, self-evaluation and decision making. The research suggests that such patterns of brain activity could serve as biomarkers to guide diagnosis and treatment for millions of people with shooting or burning chronic pain linked to a damaged nervous system. “The study really advances a whole generation of research that has shown that the functioning of the brain is really important to processing and perceiving pain,” said Dr. Ajay Wasan, a pain medicine specialist at the University of Pittsburgh School of Medicine, who wasn’t involved in the study. About one in five American adults experience chronic pain, which is persistent or recurrent pain that lasts longer than three months. To measure pain, doctors typically rely on patients to rate their pain, using either a numerical scale or a visual one based on emojis. But self-reported pain measures are subjective and can vary throughout the day. And some patients, like children or people with disabilities, may struggle to accurately communicate or score their pain. “There’s a big movement in the pain field to develop more objective markers of pain that can be used alongside self-reports,” said Kenneth Weber, a neuroscientist at Stanford University, who was not involved in the study. In addition to advancing our understanding of what neural mechanisms underlie the pain, Dr. Weber added, such markers can help validate the pain experienced by some patients that is not fully appreciated — or is even outright ignored — by their doctors. © 2023 The New York Times Company

Keyword: Pain & Touch; Brain imaging
Link ID: 28794 - Posted: 05.23.2023

Katharine Sanderson Researchers have developed an electronic skin that can mimic the same process that causes a finger, toe or limb to move when poked or scalded. The technology could lead to the development of a covering for prosthetic limbs that would give their wearers a sense of touch, or help to restore sensation in people whose skin has been damaged. The ‘e-skin’ was developed in the laboratory of chemical engineer Zhenan Bao at Stanford University in California. Her team has long been trying to make a prosthetic skin that is soft and flexible, but that can also transmit electrical signals to the brain to allow the wearer to ‘feel’ pressure, strain or changes in temperature. The latest work, published on 18 May in Science1, describes a thin, flexible sensor that can transmit a signal to part of the motor cortex in a rat’s brain that causes the animal’s leg to twitch when the e-skin is pressed or squeezed. “This current e-skin really has all the attributes that we have been dreaming about,” says Bao. “We have been talking about it for a long time.” In healthy living skin, mechanical receptors sense information and convert it into electrical pulses that are transmitted through the nervous system to the brain. To replicate this, an electronic skin needs sensors and integrated circuits, which are usually made from rigid semiconductors. Flexible electronic systems are already available, but they typically work only at high voltages that would be unsafe for wearable devices. To make a fully soft e-skin, Bao’s team developed a flexible polymer for use as a dielectric — a thin layer in a semiconductor device that determines the strength of the signal and the voltage needed to run the device. The researchers then used the dielectric to make stretchy, flexible arrays of transistors, combined into a sensor that was thin and soft like skin. © 2023 Springer Nature Limited

Keyword: Pain & Touch; Robotics
Link ID: 28790 - Posted: 05.21.2023

By Meredith Wadman A groundbreaking epidemiological study has produced the most compelling evidence yet that exposure to the chemical solvent trichloroethylene (TCE)—common in soil and groundwater—increases the risk of developing Parkinson’s disease. The movement disorder afflicts about 1 million Americans, and is likely the fastest growing neurodegenerative disease in the world; its global prevalence has doubled in the past 25 years. The report, published today in JAMA Neurology, involved examining the medical records of tens of thousands of Marine Corps and Navy veterans who trained at Marine Corps Base Camp Lejeune in North Carolina from 1975 to 1985. Those exposed there to water heavily contaminated with TCE had a 70% higher risk of developing Parkinson’s disease decades later compared with similar veterans who trained elsewhere. The Camp Lejeune contingent also had higher rates of symptoms such as erectile dysfunction and loss of smell that are early harbingers of Parkinson’s, which causes tremors; problems with moving, speaking, and balance; and in many cases dementia. Swallowing difficulties often lead to death from pneumonia. About 90% of Parkinson’s cases can’t be explained by genetics, but there have been hints that exposure to TCE may trigger it. The new study, led by researchers at the University of California, San Francisco (UCSF), represents by far the strongest environmental link between TCE and the disease. Until now, the entire epidemiological literature included fewer than 20 people who developed Parkinson’s after TCE exposure. The Camp Lejeune analysis “is exceptionally important,” says Briana De Miranda, a neurotoxicologist at the University of Alabama at Birmingham who studies TCE’s pathological impacts in the brains of rats. “It gives us an extremely large population to assess a risk factor in a very carefully designed epidemiological study.”

Keyword: Parkinsons; Neurotoxins
Link ID: 28785 - Posted: 05.18.2023

Scott Hensley In a split vote, advisers to the Food and Drug Administration recommended that the agency approve the first gene therapy for Duchenne muscular dystrophy, the most common form of the genetic illness. The vote, 8 to 6, came after a day of testimony from speakers for Sarepta Therapeutics, the maker of the gene therapy called SRP-9001, FDA scientists and families whose children have Duchenne muscular dystrophy. The question before the panel was whether the benefits for the treatment outweigh the risks. While the FDA is not bound by the recommendations of its outside advisers, it usually follows them. The agency is expected to decide by the end of May. Gene therapy for muscular dystrophy stirs hopes and controversy Duchenne muscular dystrophy is the most common inherited neuromuscular disorder among children. It affects an estimated 10,000 to 12,000 children in the U.S. The genetic condition mainly afflicts boys and leads to progressive muscle damage, loss of ability to movement and eventually death. Sarepta's treatment involves a single infusion of viruses that has been genetically modified to carry a gene to patients' muscles to produce a miniature version of a protein called dystrophin. Patients with Duchenne muscular dystrophy are missing the muscle-protecting protein or don't make enough of it. While not a cure, Sarepta argues that its "micro-dystrophin" treatment can help slow the progression of the disease. The company's request for approval rested mainly on how much micro-dystrophin the treatment produces in patients' muscles instead of waiting for clear, real-world evidence that it's actually helping patients. © 2023 npr

Keyword: Muscles; Movement Disorders
Link ID: 28780 - Posted: 05.13.2023

By Rebecca Robbins The Food and Drug Administration on Tuesday authorized the first drug for a rare genetic form of the neurological disorder A.L.S., despite uncertainty about the treatment’s effectiveness. The decision reflects the agency’s push toward greater flexibility in approving treatments for patients with devastating illnesses and few, if any, options. Biogen, the pharmaceutical company bringing the drug to market, said it would price the drug “within a range comparable to other recently launched A.L.S. treatments.” An A.L.S. therapy approved last year was priced at $158,000 annually. The drug, which is known scientifically as tofersen and will be sold under the brand name Qalsody, targets a mutation in a gene known as SOD1 that is present in about 2 percent of the roughly 6,000 cases of A.L.S. diagnosed in the United States each year. Fewer than 500 people in the United States at any given time are expected to be eligible. The agency authorized the treatment via a policy that allows a drug to be fast-tracked onto the market under certain circumstances before there is conclusive proof that it works. Biogen will be required to provide confirmatory evidence, from ongoing clinical research, to keep the drug on the market. The decision is the first conditional approval granted for a medication for A.L.S., or amyotrophic lateral sclerosis, which generally causes paralysis and death within a few years. Fewer than half the patients eligible for Qalsody survive more than three years after their diagnosis. The approval is based on evidence that the drug can significantly reduce levels of a protein that has been linked to damage to nerve cells. Biogen has argued that these results are reasonably likely to help patients, even though the drug, in a clinical trial, did not significantly slow the progression of the disease, as measured by patients’ ability to speak, swallow and perform other activities of daily living. © 2023 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 28753 - Posted: 04.26.2023

By Nora Bradford The classical view of how the human brain controls voluntary movement might not tell the whole story. That map of the primary motor cortex — the motor homunculus — shows how this brain region is divided into sections assigned to each body part that can be controlled voluntarily (SN: 6/16/15). It puts your toes next to your ankle, and your neck next to your thumb. The space each part takes up on the cortex is also proportional to how much control one has over that part. Each finger, for example, takes up more space than a whole thigh. A new map reveals that in addition to having regions devoted to specific body parts, three newfound areas control integrative, whole-body actions. And representations of where specific body parts fall on this map are organized differently than previously thought, researchers report April 19 in Nature. Research in monkeys had hinted at this. “There is a whole cohort of people who have known for 50 years that the homunculus isn’t quite right,” says Evan Gordon, a neuroscientist at Washington University School of Medicine in St. Louis. But ever since pioneering brain-mapping work by neurosurgeon Wilder Penfield starting in the 1930s, the homunculus has reigned supreme in neuroscience. Gordon and his colleagues study synchronized activity and communication between different brain regions. They noticed some spots in the primary motor cortex were linked to unexpected areas involved in action control and pain perception. Because that didn’t fit with the homunculus map, they wrote it off as a result of imperfect data. “But we kept seeing it, and it kept bugging us,” Gordon says. So the team gathered functional MRI data on volunteers as they performed various tasks. Two participants completed simple movements like moving just their eyebrows or toes, as well as complex tasks like simultaneously rotating their wrist and moving their foot from side to side. The fMRI data revealed which parts of the brain activated at the same time as each task was done, allowing the researchers to trace which regions were functionally connected to one another. Seven more participants were recorded while not doing any particular task in order to look at how brain areas communicate during rest. © Society for Science & the Public 2000–2023.

Keyword: Brain imaging
Link ID: 28748 - Posted: 04.22.2023