By Laura Sanders Like tiny, hairy Yodas raising X-wings from a swamp, rats can lift digital cubes and drop them near a target. But these rats aren’t using the Force. Instead, they are using their imagination. This telekinetic trick, described in the Nov. 3 Science, provides hints about how brains imagine new scenarios and remember past ones. “This is fantastic research,” says Mayank Mehta, a neurophysicist at UCLA. “It opens up a lot of exciting possibilities.” A deeper scientific understanding of the brain area involved in the feat could, for instance, help researchers diagnose and treat memory disorders, he says. Neuroscientist Albert Lee and his colleagues study how brains can go back in time by revisiting memories and jump ahead to imagine future scenarios. Those processes, sometimes called “mental time travel,” are “part of what makes our inner mental lives quite rich and interesting,” says Lee, who did the new study while at Howard Hughes Medical Institute’s Janelia Research Campus in Ashburn, Va. To dip into these complex questions, the researchers began with a simpler one: “Can you be in one place and think about another place?” says Lee, who is now an HHMI investigator at Beth Israel Deaconess Medical Center in Boston. “The rat isn’t doing anything fancier than that. We’re not asking them to recall their summer vacation.” Neuroscientist and engineer Chongxi Lai, also now at Beth Israel Deaconess, Lee and colleagues trained rats to move on a spherical treadmill in the midst of a 3-D virtual world projected onto a surrounding screen. While the rats poked around their virtual world, electrodes recorded signals from nerve cells in the rats’ hippocampi, brain structures known to hold complex spatial information, among other things (SN: 10/6/14). In this way, researchers matched patterns of brain activity with spots in the virtual world. © Society for Science & the Public 2000–2023.

Keyword: Attention
Link ID: 28988 - Posted: 11.04.2023

By Matt Richtel An Oxford University researcher and her team showed that digital wearable devices can track the progression of Parkinson’s disease in an individual more effectively than human clinical observation can, according to a newly published paper. By tracking more than 100 metrics picked up by the devices, researchers were able to discern subtle changes in the movements of subjects with Parkinson’s, a neurodegenerative disease that afflicts 10 million people worldwide. The lead researcher emphasized that the latest findings were not a treatment for Parkinson’s. Rather, they are a means of helping scientists gauge whether novel drugs and other therapies for Parkinson’s are slowing the progression of the disease. Quotable Quotes The sensors — six per subject, worn on the chest, at the base of the spine and one on each wrist and foot — tracked 122 physiological metrics. Several dozen metrics stood out as closely indicating the disease’s progression, including the direction a toe moved during a step and the length and regularity of strides. “We have the biomarker,” said Chrystalina Antoniades, a neuroscientist at the University of Oxford and the lead researcher on the paper, which was published earlier this month in the journal npj Parkinson’s Disease. “It’s super exciting. Now we hope to be able to tell you: Is a drug working?” Until now, Dr. Antoniades said, drug trials for Parkinson’s had relied on clinical assessment of whether a treatment was slowing the progression of the disease. But clinical observation can miss changes that happen day to day or that might not show up clearly in periodic visits to a doctor, she added. In the paper, the study’s authors concluded that the sensors proved more effective at tracking the disease progression “than the conventionally used clinical rating scales.” © 2023 The New York Times Company

Keyword: Parkinsons
Link ID: 28965 - Posted: 10.17.2023

Marlys Fassett Itching can be uncomfortable, but it’s a normal part of your skin’s immune response to external threats. When you’re itching from an encounter with poison ivy or mosquitoes, consider that your urge to scratch may have evolved to get you to swat away disease-carrying pests. However, for many people who suffer from chronic skin diseases like eczema, the sensation of itch can fuel a vicious cycle of scratching that interrupts sleep, reduces productivity and prevents them from enjoying daily life. This cycle is caused by sensory neurons and skin immune cells working together to promote itching and skin inflammation. But, paradoxically, some of the mechanisms behind this feedback loop also stop inflammation from getting worse. In our newly published research, my team of immunologists and neuroscientists and I discovered that a specific type of itch-sensing neuron can push back on the itch-scratch-inflammation cycle in the presence of a small protein. This protein, called interleukin-31, or IL-31, is typically involved in triggering itching. This negative feedback loop – like the vicious cycle – is only possible because the itch-sensing nerve endings in your skin are closely intertwined with the millions of cells that make up your skin’s immune system. The protein IL-31 is key to the connection between the nervous and immune systems. This molecule is produced by some immune cells, and like other members of this molecule family, it specializes in helping immune cells communicate with each other. © 2010–2023, The Conversation US, Inc.

Keyword: Pain & Touch; Neuroimmunology
Link ID: 28961 - Posted: 10.14.2023

Linda Geddes Science correspondent The former Premier League goalkeeper Brad Friedel once said that to be able to work well in the box, you have to be able to think outside the box. Now scientific data supports the idea that goalies’ brains really do perceive the world differently – their brains appear able to merge signals from the different senses more quickly, possibly underpinning their unique abilities on the football pitch. Goalkeeping is the most specialised position in football, with the primary objective of stopping the opposition from scoring. But while previous studies have highlighted differences in physiological and performance profiles between goalkeepers and other players, far less was known about whether they have different perceptual or cognitive abilities. “Unlike other football players, goalkeepers are required to make thousands of very fast decisions based on limited or incomplete sensory information,” said Michael Quinn, a former goalkeeper in the Irish Premiership, who is now studying for a master’s degree in behavioural neuroscience at University College Dublin. Suspecting that this ability might hinge on an enhanced capacity to combine information from different senses, Quinn and researchers at Dublin City University and University College Dublin recruited 60 professional goalkeepers, outfield players and age-matched non-players to do a series of tests, looking for differences in their ability to distinguish sounds and flashes as separate from one another. Doing so enabled them to estimate volunteers’ temporal binding windows – the timeframe in which different sensory signals are fused together in the brain. The study, published in Current Biology, found that goalkeepers had a narrower temporal binding window relative to outfielders and non-soccer players. © 2023 Guardian News & Media Limited

Keyword: Attention; Vision
Link ID: 28954 - Posted: 10.10.2023

Regina G. Barber Ever had an itch you can't scratch? Maybe it's out of reach, or your hands are full, or you don't want to damage your skin. It can be deeply frustrating. And even though the itch response, or what scientists refer to simply as "itch," has a purpose — it's one of our bodies' alert systems — it can also go very wrong. The importance of a regular itch Itch is evolution's way of drawing our attention to something on our skin that needs removing. This could be a stinging bug, a nesting parasite or an irritating plant (poison ivy, anyone?!). All these things urge us to scratch, which generally removes the threat and soothes the itch. "We know that itch can activate sensory neurons and the signal will be transmitted to the brain. When we scratch the skin, somehow other neural circuits will be activated. And these neural circuits will suppress the itch circuits and alleviate the itch sensation," says Qin Liu, a neuroscientist at the Washington University School of Medicine in St. Louis. Because the itch sensation has separate neural circuitry from temperature, pressure and pain, applying pressure or ice or scratching can relieve an itch. They're effective neural distractions. Oftentimes, when someone experiences hives or an insect bite, histamine is involved, a chemical released by our immune system that can contribute to itchiness. So relieving that itch only requires antihistamine medication. "But most other forms of itch, like atopic dermatitis, eczema, other conditions, they don't actually have a pathway for histamine as the itch mediator," says Kwatra. © 2023 npr

Keyword: Pain & Touch
Link ID: 28929 - Posted: 09.27.2023

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