By Tom Siegfried Survival of the fittest often means survival of the fastest. But fastest doesn’t necessarily mean the fastest moving. It might mean the fastest thinking. When faced with the approach of a powerful predator, for instance, a quick brain can be just as important as quick feet. After all, it is the brain that tells the feet what to do — when to move, in what direction, how fast and for how long. And various additional mental acrobatics are needed to evade an attacker and avoid being eaten. A would-be meal’s brain must decide whether to run or freeze, outrun or outwit, whether to keep going or find a place to hide. It also helps if the brain remembers where the best hiding spots are and recalls past encounters with similar predators. All in all, a complex network of brain circuitry must be engaged, and neural commands executed efficiently, to avert a predatory threat. And scientists have spent a lot of mental effort themselves trying to figure out how the brains of prey enact their successful escape strategies. Studies in animals as diverse as mice and crabs, fruit flies and cockroaches are discovering the complex neural activity — in both the primitive parts of the brain and in more cognitively advanced regions — that underlies the physical behavior guiding escape from danger and the search for safety. Lessons learned from such studies might not only illuminate the neurobiology of escape, but also provide insights into how evolution has shaped other brain-controlled behaviors. This research “highlights an aspect of neuroscience that is really gaining traction these days,” says Gina G. Turrigiano of Brandeis University, past president of the Society for Neuroscience. “And that is the idea of using ethological behaviors — behaviors that really matter for the biology of the animal that’s being studied — to unravel brain function.” © 2022 Annual Reviews

Keyword: Aggression; Attention
Link ID: 28609 - Posted: 12.24.2022

By Christina Jewett and Cade Metz A jumble of cords and two devices the size of soda cans protrude from Austin Beggin’s head when he undergoes testing with a team of researchers studying brain implants that are meant to restore function to those who are paralyzed. Despite the cumbersome equipment, it is also when Mr. Beggin feels the most free. He was paralyzed from the shoulders down after a diving accident eight years ago, and the brain device picks up the electrical surges that his brain generates as he envisions moving his arm. It converts those signals to cuffs on the major nerves in his arm. They allow him to do things he had not done on his own since the accident, like lift a pretzel to his mouth. “This is like the first time I’ve ever gotten the opportunity or I’ve ever been privileged and blessed enough to think, ‘When I want to open my hand, I open it,’” Mr. Beggin, 30, said. Days like that are always “a special day.” The work at the Cleveland Functional Electrical Stimulation Center represents some of the most cutting-age research in the brain-computer interface field, with the team connecting the brain to the arm to restore motion. It’s a field that Elon Musk wants to advance, announcing in a recent presentation that brain implants from his company Neuralink would someday help restore sight to the blind or return people like Mr. Beggin to “full-body functionality.” Mr. Musk also said the Neuralink device could allow anyone to use phones and other machines with new levels of speed and efficiency. Neuroscientists and Mr. Beggin alike see such giant advances as decades away, though. Scientists who have approval to test such devices in humans are inching toward restoring normal function in typing, speaking and limited movements. Researchers caution that the goal is much harder and more dangerous than it may seem. And they warn that Mr. Musk’s goals may never be possible — if it is even worth doing in the first place. © 2022 The New York Times Company

Keyword: Robotics
Link ID: 28591 - Posted: 12.13.2022

By Kevin Hartnett A mouse is running on a treadmill embedded in a virtual reality corridor. In its mind’s eye, it sees itself scurrying down a tunnel with a distinctive pattern of lights ahead. Through training, the mouse has learned that if it stops at the lights and holds that position for 1.5 seconds, it will receive a reward — a small drink of water. Then it can rush to another set of lights to receive another reward. This setup is the basis for research published in July in Cell Reports by the neuroscientists Elie Adam, Taylor Johns and Mriganka Sur of the Massachusetts Institute of Technology. It explores a simple question: How does the brain — in mice, humans and other mammals — work quickly enough to stop us on a dime? The new work reveals that the brain is not wired to transmit a sharp “stop” command in the most direct or intuitive way. Instead, it employs a more complicated signaling system based on principles of calculus. This arrangement may sound overly complicated, but it’s a surprisingly clever way to control behaviors that need to be more precise than the commands from the brain can be. Control over the simple mechanics of walking or running is fairly easy to describe: The mesencephalic locomotor region (MLR) of the brain sends signals to neurons in the spinal cord, which send inhibitory or excitatory impulses to motor neurons governing muscles in the leg: Stop. Go. Stop. Go. Each signal is a spike of electrical activity generated by the sets of neurons firing. The story gets more complex, however, when goals are introduced, such as when a tennis player wants to run to an exact spot on the court or a thirsty mouse eyes a refreshing prize in the distance. Biologists have understood for a long time that goals take shape in the brain’s cerebral cortex. How does the brain translate a goal (stop running there so you get a reward) into a precisely timed signal that tells the MLR to hit the brakes? Simons Foundation, All Rights Reserved © 2022

Keyword: Movement Disorders
Link ID: 28573 - Posted: 11.30.2022

By Sidney Perkowitz In 2019, Edward Chang, a neurosurgeon at the University of California, San Francisco, opened the skull of a 36-year-old man, nicknamed “Pancho,” and placed a thin sheet of electrodes on the surface of his brain.1 The electrodes gather electrical signals from the motor neurons that control the movement of the mouth, larynx, and other body parts to produce speech. A small port, implanted on top of Pancho’s head, relayed the brain signals to a computer. This “brain-computer interface,” or BCI, solved an intractable medical problem. In 2003, Pancho, a field worker in California’s vineyards, was involved in a car crash. Days after undergoing surgery, he suffered a brainstem stroke, reported the New York Times Magazine.2 The stroke robbed Poncho of the power of speech. He could communicate only by laboriously spelling out words one letter at a time with a pointing device. After training with the computer outfitted with deep-learning algorithms that interpreted his brain activity, Pancho could think the words that he wanted to say, and they would appear on the computer screen. Scientists called the results “groundbreaking”; Pancho called them “life-changing.” The clinical success of BCIs (there are other stories to go along with Pancho’s) appear to vindicate the futurists who claim that BCIs may soon enhance the brains of healthy people. Most famously, Ray Kurzweil, author of The Singularity Is Near, has asserted that exponentially rapid developments in neuroscience, bioscience, nanotechnology, and computation will coalesce and allow us to transcend the limitations of our bodies and brains. A major part of this huge shift will be the rise of artificial intelligences that are far more capable than human brains. It is an inevitability of human evolution, Kurzweil thinks, that the two kinds of intelligence will merge to form powerful hybrid brains, which will define the future of humanity. This, he predicted, would happen by 2045. While futuristic scenarios like Kurzweil’s are exciting to ponder, they are brought back down to Earth by the technological capabilities of brain-computer hybrids as they exist today. BCIs are impressive, but the path from helping stroke victims to giving people superpowers is neither direct nor inevitable. © 2022 NautilusThink Inc,

Keyword: Brain imaging; Robotics
Link ID: 28570 - Posted: 11.30.2022

By Elizabeth Preston Ryan Grant was in his 20s and serving in the military when he learned that the numbness and tingling in his hands and feet, as well as his unshakeable fatigue, were symptoms of multiple sclerosis. Like nearly a million other people with MS in the United States, Grant had been feeling his immune system attack his central nervous system. The insulation around his nerves was crumbling, weakening the signals between his brain and body. The disease can have a wide range of symptoms and outcomes. Now 43, Grant has lost the ability to walk, and he has moved into a veterans’ home in Oregon, so that his wife and children don’t have to be his caretakers. He’s all too familiar with the course of the illness and can name risk factors he did and didn’t share with other MS patients, three-quarters of whom are female. But until recently, he hadn’t heard that many scientists now believe the most important factor behind MS is a virus.  For decades, researchers suspected that Epstein-Barr virus, a common childhood infection, is linked to multiple sclerosis. In January, the journal Science pushed that connection into headlines when it published the results of a two-decade study of people who, like Grant, have served in the military. The study’s researchers concluded that EBV infection is “the leading cause” of MS.  Bruce Bebo, executive vice president of research at the nonprofit National Multiple Sclerosis Society, which helped fund the study, said he believes the findings fall just short of proving causation. They do, however, provide “probably the strongest evidence to date of that link between EBV and MS,” he said. Epstein-Barr virus has infected about 95 percent of adults. Yet only a tiny fraction of them will develop multiple sclerosis. Other factors are also known to affect a person’s MS risk, including genetics, low vitamin D, smoking, and childhood obesity. If this virus that infects nearly everyone on Earth causes multiple sclerosis, it does so in concert with other actors in a choreography that scientists don’t yet understand.

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 28565 - Posted: 11.23.2022

Dyani Lewis Neuroscientists have identified the nerve cells responsible for helping paralysed people to walk again, opening up the possibility of targeted therapies that could benefit a wider range of people with spinal-cord injuries1. Severe spinal-cord injuries can disrupt the connection between the brain and the networks of nerve cells in the lower spine that control walking. In 2018, neuroscientist Grégoire Courtine at the Swiss Federal Institute of Technology in Lausanne and his colleagues showed that delivering electrical pulses to those lower-spine nerves — a technique known as epidural electrical stimulation (EES) — could, when combined with intensive training, get people with this kind of spinal-cord injury walking again2. All three participants in a trial went from having severe or complete motor paralysis and minimal sensation in their legs to being able to take steps on their own, or with a walker or crutches. Two other teams showed similar results that year3,4. Courtine’s team has now extended the work, showing that the system works in people who have lost all sensation in their legs. The group reports in Nature today that nine participants in the same trial — three of whom had complete paralysis and no sensation in their legs — regained the ability to walk after training paired with EES delivered by devices implanted in their spines. Five months into the trial, all participants could bear their own weight and take steps, using a walker for stability. Four no longer need the EES to be switched on to walk. This sustained recovery suggests that the stimulation triggers remodelling of the spinal neurons to bring the locomotion network back on line. “The amount of hope that it gives to people with spinal-cord injury is incredible,” says Marc Ruitenberg, a neurologist at the University of Queensland in Brisbane, Australia, who studies spinal-cord injury. © 2022 Springer Nature Limited

Keyword: Regeneration
Link ID: 28546 - Posted: 11.13.2022

Nina Lakhani The mystery behind the astronomical rise in neurological disorders like Parkinson’s disease and Alzheimer’s could be caused by exposure to environmental toxins that are omnipresent yet poorly understood, leading doctors warn. At a conference on Sunday, the country’s leading neurologists and neuroscientists will highlight recent research efforts to fill the gaping scientific hole in understanding of the role environmental toxins – air pollution, pesticides, microplastics, forever chemicals and more – play in increasingly common diseases like dementias and childhood developmental disorders. Humans may encounter a staggering 80,000 or more toxic chemicals as they work, play, sleep and learn – so many that it is almost impossible to determine their individual effects on a person, let alone how they may interact or the cumulative impacts on the nervous system over a lifespan. Some contact with environmental toxins is inevitable given the proliferation of plastics and chemical pollutants, as well as America’s hands off regulatory approach, but exposure is unequal. In the US, communities of color, Indigenous people and low income families are far more likely to be exposed to a myriad of pollutants through unsafe housing and water, manufacturing and agricultural jobs, and proximity to roads and polluting industrial plants, among other hazards. It’s likely genetic makeup plays a role in how susceptible people are to the pathological effects of different chemicals, but research has shown higher rates of cancers and respiratory disease in environmentally burdened communities. © 2022 Guardian News & Media Limited

Keyword: Alzheimers; Parkinsons
Link ID: 28526 - Posted: 10.26.2022

by Carey Gillam and Aliya Uteuova For decades, Swiss chemical giant Syngenta has manufactured and marketed a widely used weed-killing chemical called paraquat, and for much of that time the company has been dealing with external concerns that long-term exposure to the chemical may be a cause of the incurable brain ailment known as Parkinson’s disease. Syngenta has repeatedly told customers and regulators that scientific research does not prove a connection between its weedkiller and the disease, insisting that the chemical does not readily cross the blood-brain barrier, and does not affect brain cells in ways that cause Parkinson’s. But a cache of internal corporate documents dating back to the 1950s reviewed by the Guardian suggests that the public narrative put forward by Syngenta and the corporate entities that preceded it has at times contradicted the company’s own research and knowledge. And though the documents reviewed do not show that Syngenta’s scientists and executives accepted and believed that paraquat can cause Parkinson’s, they do show a corporate focus on strategies to protect product sales, refute external scientific research and influence regulators. In one defensive tactic, the documents indicate that the company worked behind the scenes to try to keep a highly regarded scientist from sitting on an advisory panel for the US Environmental Protection Agency (EPA). The agency is the chief US regulator for paraquat and other pesticides. Company officials wanted to make sure the efforts could not be traced back to Syngenta, the documents show. And the documents show that insiders feared they could face legal liability for long-term, chronic effects of paraquat as long ago as 1975. One company scientist called the situation “a quite terrible problem” for which “some plan could be made … ”

Keyword: Parkinsons; Neurotoxins
Link ID: 28522 - Posted: 10.22.2022

By Diana Kwon A Scottish woman named Joy Milne made headlines in 2015 for an unusual talent: her ability to sniff out people afflicted with Parkinson’s disease, a progressive neurodegenerative illness that is estimated to affect nearly a million people in the U.S. alone. Since then a group of scientists in the U.K. has been working with Milne to pinpoint the molecules that give Parkinson’s its distinct olfactory signature. The team has now zeroed in on a set of molecules specific to the disease—and has created a simple skin-swab-based test to detect them. Milne, a 72-year-old retired nurse from Perth, Scotland, has hereditary hyperosmia, a condition that endows people with a hypersensitivity to smell. She discovered that she could sense Parkinson’s with her nose after noticing her late husband, Les, was emitting a musky odor that she had not detected before. Eventually, she linked this change in scent to Parkinson’s when he was diagnosed with the disease many years later. Les passed away in 2015. In 2012 Milne met Tilo Kunath, a neuroscientist at the University of Edinburgh in Scotland, at an event organized by the research and support charity Parkinson’s UK. Although skeptical at first, Kunath and his colleagues decided to put Milne’s claims to the test. They gave her 12 T-shirts, six from people with Parkinson’s and six from healthy individuals. She correctly identified the disease in all six cases—and the one T-shirt from a healthy person she categorized as having Parkinson’s belonged to someone who went on to be diagnosed with the disease less than a year later. Advertisement Subsequently, Kunath, along with chemist Perdita Barran of the University of Manchester in England and her colleagues, has been searching for the molecules responsible for the change in smell that Milne can detect. The researchers used mass spectrometry to identify types and quantities of molecules in a sample of sebum, an oily substance found on the skin’s surface. They discovered changes to fatty molecules known as lipids in people with Parkinson’s. © 2022 Scientific American

Keyword: Chemical Senses (Smell & Taste); Parkinsons
Link ID: 28510 - Posted: 10.13.2022

Ian Sample Science editor It was while watching University Challenge that the doctor first suspected something wrong with Jeremy Paxman. Normally highly animated, the TV presenter was less effusive and exuberant than usual. He had acquired what specialists in the field call the “Parkinson’s mask”. Paxman was formally diagnosed with Parkinson’s disease in hospital after he collapsed while walking his dog and found himself in hospital. There, Paxman recalled in an ITV documentary, the doctor walked in and said: “I think you’ve got Parkinson’s”. For Paxman, at least, the news came out of the blue. Parkinson’s was first described in medical texts more than 200 years ago, yet there is still no cure. It’s a common condition, particularly in the over-50s. About 1 in 37 people in the UK will be diagnosed at some point in their life. Existing drugs aim to manage patients’ symptoms, rather than slow down or stop the condition’s progression. But scientists have made progress in understanding the neurodegenerative disorder. The hope now is that gamechanging therapies are finally on the horizon. Advertisement “Parkinson’s is a hugely complex condition and there’s probably no single cure,” says Katherine Fletcher, a research communications manager at Parkinson’s UK. “It’s the progressive loss of dopamine-producing cells in the brain. If you want to slow or stop the condition, you somehow need to protect those cells or maybe even regrow those cells in the brain. That is the ultimate goal.” Why brain cells die off in Parkinson’s is still unknown. The condition strikes a brain region called the substantia nigra, where neurons make a chemical called dopamine. The loss of these brain cells causes dopamine to plunge, and this drives most of the problems patient’s experience. It is not a fast decline: typically, patients only become aware of symptoms when about 80% of nerve cells in the substantia nigra have failed. © 2022 Guardian News & Media Limited or its affiliated companies.

Keyword: Parkinsons
Link ID: 28507 - Posted: 10.08.2022

By Pam Belluck A new medication for A.L.S., the devastating neurological disorder that causes paralysis and death, will have a list price of $158,000 a year, its manufacturer disclosed Friday. The treatment, to be marketed as Relyvrio, is a combination of two existing drugs and will be available to patients in the United States in about four to six weeks, according to officials of the company, Amylyx Pharmaceuticals. Relyvrio was approved by the Food and Drug Administration on Thursday, even though the agency’s analysis concluded there was not yet sufficient evidence that the medication could help patients live longer or slow the rate at which they lose functions like muscle control, speaking or breathing without assistance. The F.D.A. decided to greenlight the drug instead of waiting until 2024 for results of a large clinical trial partly because the treatment is considered to be safe. The agency said that although the evidence of effectiveness was uncertain, “given the serious and life-threatening nature of A.L.S. and the substantial unmet need, this level of uncertainty is acceptable in this instance.” A.L.S., or amyotrophic lateral sclerosis — also called Lou Gehrig’s disease — often strikes patients in the prime of life and frequently causes death within two to five years. It is diagnosed in about 6,000 people worldwide each year, and Amylyx estimates that there are about 29,000 people living with the disease in the United States. Amylyx officials predicted that most patients would pay little or nothing for the treatment because the company expects insurers, both private and public, to cover it. Amylyx plans to provide it free to uninsured patients experiencing financial hardship. Still, the list price is much higher than that recommended by the Institute for Clinical and Economic Review, a nonprofit organization that evaluates the value of medicines. In a statement, the group’s chief medical officer, Dr. David Rind, said that while “there are clear benefits to patients with a rapidly fatal disease to have early access to a safe therapy,” his organization had concluded that “an annual price of $9,100 to $30,700 would be reasonable if the therapy actually works.” © 2022 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 28495 - Posted: 10.01.2022

By Jonathan Moens An artificial intelligence can decode words and sentences from brain activity with surprising — but still limited — accuracy. Using only a few seconds of brain activity data, the AI guesses what a person has heard. It lists the correct answer in its top 10 possibilities up to 73 percent of the time, researchers found in a preliminary study. The AI’s “performance was above what many people thought was possible at this stage,” says Giovanni Di Liberto, a computer scientist at Trinity College Dublin who was not involved in the research. Developed at the parent company of Facebook, Meta, the AI could eventually be used to help thousands of people around the world unable to communicate through speech, typing or gestures, researchers report August 25 at arXiv.org. That includes many patients in minimally conscious, locked-in or “vegetative states” — what’s now generally known as unresponsive wakefulness syndrome (SN: 2/8/19). Most existing technologies to help such patients communicate require risky brain surgeries to implant electrodes. This new approach “could provide a viable path to help patients with communication deficits … without the use of invasive methods,” says neuroscientist Jean-Rémi King, a Meta AI researcher currently at the École Normale Supérieure in Paris. King and his colleagues trained a computational tool to detect words and sentences on 56,000 hours of speech recordings from 53 languages. The tool, also known as a language model, learned how to recognize specific features of language both at a fine-grained level — think letters or syllables — and at a broader level, such as a word or sentence. © Society for Science & the Public 2000–2022.

Keyword: Language; Robotics
Link ID: 28470 - Posted: 09.10.2022

By Laurie McGinley Independent advisers to the Food and Drug Administration on Wednesday voted 7 to 2 to recommend approval of an experimental ALS drug with strong support from patients and advocates, making it likely the hotly debated treatment will be cleared by the agency within weeks. The vote was a stunning turnaround from late March when the panel voted 6 to 4 to recommend against FDA approval. At that meeting, the FDA’s Peripheral and Central Nervous System Drugs Advisory Committee concluded the evidence from a single clinical trial — with just 137 patients and some follow-up data — was not sufficient to show the drug, called AMX0035, slowed a degenerative disease that usually kills people within three to five years. But on Wednesday, after hours of discussion, several advisers said that additional analyses submitted by the drug’s manufacturer, Cambridge-based Amylyx, bolstered the case for approval, even though uncertainties remain. Advisers were also affected by the disease’s severity and the lack of effective treatments. A vow by a top Amylyx official to pull the drug from the market if a larger study, with 600 patients, fails to show effectiveness was also a factor in the vote. The FDA, which usually follows the recommendation of its outside advisers but is not required to, is expected to decide whether to approve the drug by Sept. 29. The improved fortunes of the medicine came despite criticism from FDA staff as recently as last week about the treatment’s effectiveness, the conduct of its clinical trial and the researchers’ interpretation of the data. But the medicine is considered safe, and the agency has been under intense pressure from ALS patients and physicians who say the treatment holds promise for a fatal disease that typically causes rapid deterioration and death.

Keyword: ALS-Lou Gehrig's Disease
Link ID: 28467 - Posted: 09.10.2022

Researchers have published two papers describing how they identified a potential new pathway for treating a sporadic form of amyotrophic lateral sclerosis (ALS). The studies were published as part of a cooperative research agreement between the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health, and the Switzerland-based biotechnology company GeNeuro Inc. One unusual side effect of hundreds of thousands of years of evolution is that the human genome now contains DNA sequences from ancient retroviruses—referred to as human endogenous retroviruses (HERVs). Though most remain dormant, reactivation of HERVs have been implicated in several neurodegenerative diseases, including ALS. The first of these papers shows that a specific HERV produces a protein that can be found in the cerebrospinal fluid (CSF) of people with ALS. This protein, called HERV-K ENV, is toxic when added to neurons grown in laboratory dishes. In addition, a special kind of mouse genetically designed to create HERV-K ENV develops symptoms very similar to ALS. Adding the CSF from people with ALS to lab-grown neurons resulted in damage to the cells. When a synthetic antibody designed specifically to recognize HERV-K ENV was added as well to those neurons, the toxic effects were reduced. These findings together suggest that the improper activation of the HERV-K ENV gene could be the cause of the symptoms seen in certain cases of sporadic ALS. The discovery that a synthetic antibody to HERV-K ENV could be protective led the researchers to look at whether the immune system of people with ALS produced any antibodies, as well. In the second paper, the authors show that indeed higher levels of antibodies against HERV-K ENV were seen in the blood of a group of people with ALS as compared to healthy donors. The pattern of antibodies against this viral protein was also more complex in persons with ALS. In addition, there was also a correlation between higher antibody levels against HERV-K ENV and longer overall survival.

Keyword: ALS-Lou Gehrig's Disease
Link ID: 28455 - Posted: 08.31.2022

By Pam Belluck An experimental therapy for A.L.S., the paralyzing and fatal neurological disorder, has been approved in Canada, adding a new treatment option for a disease for which there are few effective therapies. The approval, the first in the world for the treatment — AMX0035, to be marketed in Canada as Albrioza — comes with the condition that the drug company later provide better evidence that the treatment works. It is likely to be of major interest to patients with A.L.S. (amyotrophic lateral sclerosis) in the United States, where the same therapy is being evaluated by the Food and Drug Administration, which has raised questions about the treatment’s effectiveness. An F.D.A. review earlier this year found the treatment to be safe, but said there was not enough evidence that it was effective either in helping patients live longer or slowing the rate at which they lose functions like muscle control, speaking or breathing without assistance. A committee of independent advisers to the F.D.A. voted by a narrow margin in March that the therapy was not ready for approval. The F.D.A. had been scheduled to issue a final decision this month, but recently extended the deadline to Sept. 29, saying it needed more time to review additional analyses of data submitted by the company. In the meantime, Calaneet Balas, president and chief executive of the A.L.S. Association, one of several patient advocacy organizations pressing for F.D.A. approval, said, “We expect that Americans living with A.L.S. will try to access Albrioza in Canada, just as we have heard reports of people trying to buy the ingredients on Amazon.” © 2022 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 28369 - Posted: 06.14.2022

By Maria Temming The Terminator may be one step closer to reality. Researchers at the University of Tokyo have built a robotic finger that, much like Arnold Schwarzenegger’s titular cyborg assassin, is covered in living human skin. The goal is to someday build robots that look like real people — albeit for more altruistic applications. Super realistic-looking robots could more seamlessly interact with humans in medical care and service industries, say biohybrid engineer Shoji Takeuchi and his colleagues June 9 in Matter. (Whether cyborgs masked in living tissue would be more congenial or creepy is probably in the eye of the beholder.) To cover the finger in skin, Takeuchi and colleagues submerged the robotic digit in a blend of collagen and human skin cells called dermal fibroblasts. The mixture settled into a base layer of skin, or dermis, covering the finger. The team then poured a liquid containing human keratinocyte cells onto the finger, which formed an outer skin layer, or epidermis. After two weeks, skin covering the finger measured a few millimeters thick — comparable to the thickness of human skin. The lab-made skin was strong and stretchy enough to withstand the robotic finger bending. It could also heal itself: When researchers made a small cut on the robotic finger and covered it with a collagen bandage, the skin’s fibroblast cells merged the bandage with the rest of the skin within a week. Researchers at the University of Tokyo covered this robotic finger in living human skin to pave the way for ultrarealistic cyborgs. “This is very interesting work and an important step forward in the field,” says Ritu Raman, an MIT engineer who also builds machines with living components. “Biological materials are appealing because they can dynamically sense and adapt to their environments.” For instance, she’d like to see a future version of the living robot skin embedded with nerve cells to make robots more aware of their surroundings. © Society for Science & the Public 2000–2022.

Keyword: Pain & Touch; Robotics
Link ID: 28365 - Posted: 06.11.2022

ByRobert F. Service An experimental drug is raising new hopes for those with Parkinson’s disease. So far, the compound has only been tested in animals and in an initial safety assessment in humans. But results show it inhibits a cellular pathway that gives rise to the disease, which researchers have been working to target for nearly 20 years. Investigators are now launching expanded clinical trials. “This is a very, very important step forward,” says Patrick Lewis, a neuroscientist who studies the mechanisms of Parkinson’s at the University of London’s Royal Veterinary College. If further tests prove the compound is effective in humans, says Lewis, who was not involved with the new study, it would likely be given to patients as soon as they exhibit the first signs of developing the progressive disorder. “The hope is that [the new drug] would slow down the progression of disease.” Parkinson’s affects as many as 10 million people worldwide. It results when cells in the brain that produce the neurotransmitter dopamine stop working or die. Over time this causes a widespread decline in brain function, leading to shaking and loss of muscle control. Current drugs can help replace lost dopamine and reduce symptoms, but no therapies slow or halt disease progression itself. The new study focuses on a gene called leucine-rich repeat kinase 2 (LRRK2). People with mutations in this gene are at high risk for developing Parkinson’s. Among other roles, LRRK2 modifies a suite of proteins called Rab guanosine triphosphates, which act like air traffic controllers, orchestrating the flow of proteins in and out of cells. The mutations kick Rab into overdrive and reduce the efficiency of cellular structures called lysosomes, which chew up and recycle unwanted proteins. This creates a buildup of toxic byproducts that can kill neurons and lead to Parkinson’s, says Carole Ho, chief medical officer of Denali Therapeutics, a biotech startup in California. © 2022 American Association for the Advancement of Science.

Keyword: Parkinsons
Link ID: 28362 - Posted: 06.09.2022

By Lisa Sanders, M.D. “You have to take your husband to the hospital right now,” the doctor urged over the phone. “His kidneys aren’t working at all, and we need to find out why.” The woman looked at her 82-year-old spouse. He was so thin and pale. She thanked the doctor and called 911. For the past couple of months, every meal was a struggle. Swallowing food was strangely difficult. Liquids were even worse. Whatever he drank seemed to go down the wrong pipe, and he coughed and sputtered after almost every sip. It was terrifying. He saw an ear, nose and throat specialist, who scoped his mouth and esophagus. There wasn’t anything blocking the way. The doctor recommended that he get some therapy to help him strengthen the muscles he used to swallow, and until he did that, he should thicken his liquids to make drinking easier. The patient tried that once, but it was so disgusting he gave up on it. His wife was worried as she watched him eat and drink less and less. She could see that he was getting weaker every day. He had a stroke four months earlier, and since then his right foot dragged a little. But now she had to help him get out of his recliner. And he wasn’t able to drive — she had to make the 45-minute trip with him each day to his office. Finally, he agreed to see Dr. Richard Kaufman, their primary-care doctor. Kaufman was shocked by the man’s appearance, how the skin on his face hung in folds as if air had been let out of his cheeks. He’d lost nearly 40 pounds. He struggled to walk the few steps to the exam table. His right side, which was weakened by his stroke, was now matched by weakness on his left side. His stroke hadn’t done this. There was something else going on. Kaufman ordered some preliminary blood tests to try to see where the problem might lie. Those were the results that sent the couple to the emergency room. © 2022 The New York Times Company

Keyword: Neuroimmunology; Muscles
Link ID: 28339 - Posted: 05.28.2022

By Veronique Greenwood Lovebirds, small parrots with vibrant rainbow plumage and cheeky personalities, are popular pets. They swing from ropes, cuddle with companions and race for treats in a waddling gait with all the urgency of toddlers who spot a cookie. But, along with other parrots, they also do something strange: They use their faces to climb walls. Give these birds a vertical surface to clamber up, and they cycle between left foot, right foot and beak as if their mouths were another limb. In fact, a new analysis of the forces climbing lovebirds exert reveals that this is precisely what they are doing. Somehow, a team of scientists wrote in the journal Proceedings of the Royal Society B on Wednesday, the birds and perhaps other parrot species have repurposed the muscles in their necks and heads so they can walk on their beaks, using them the way rock climbers use their arms. Climbing with a beak as a third limb is peculiar because third limbs generally are not something life on Earth is capable of producing, said Michael Granatosky, an assistant professor of anatomy at the New York Institute of Technology and an author of the new paper. “There is this very deep, deep set aspect of our biology that everything is bilateral” in much of the animal kingdom, he said. The situation makes it developmentally unlikely to grow an odd numbers of limbs for walking. Some animals have developed workarounds. Kangaroos use their tails as a fifth limb when hopping slowly, pushing off from the ground with their posteriors the same way they push with their feet. To see if parrots were using their beaks in a similar way, Dr. Granatosky and a graduate student, Melody Young, as well as their colleagues brought six rosy-faced lovebirds from a pet store into the lab. They had the birds climb up a surface that was fitted with a sensor to keep track of how much force they were exerting and in what directions. The scientists found that the propulsive force the birds applied through their beaks was similar to what they provided with their legs. What had started as a way to eat had transformed into a way to walk, with beaks as powerful as their limbs. © 2022 The New York Times Company

Keyword: Evolution
Link ID: 28336 - Posted: 05.25.2022

Nicola Davis Science correspondent Mice with spinal cord injuries have shown remarkable recovery after being given a drug initially developed for people with lung disease, researchers have revealed, saying the treatment could soon be tested on humans. It is thought there are about 2,500 new spinal cord injuries in the UK every year, with some of those affected experiencing full loss of movement as a result. Despite a number of promising areas of research, at present damage to the spinal cord is not reversible. Now researchers at the University of Birmingham say a drug called AZD1236, initially developed to treat chronic obstructive pulmonary disease in humans, has shown promise in mice with spinal cord compression injuries, a type of injury often associated with motor accidents in humans, but which is also linked to conditions such as osteoarthritis. A similar drug, called AZD3342, showed comparable benefits in rats. The results, published in the journal Clinical and Translational Medicine, suggested the drugs block the action of enzymes known as MMP-9 and MMP-12 that rise after spinal cord injury. The upshot was that swelling of the spinal cord was reduced, levels of proteins linked to inflammation and pain were lowered, and breakdown of the blood-spinal cord barrier was limited. Scarring of connective tissue was also reduced. The team said that compared with injured mice not given AZD1236, those given the drug for three days showed 85% improvement in movement and sensation six weeks after the spinal injury, while their nerve function was 80% of that seen in uninjured mice. Furthermore, the benefits were similar whether the drug was given immediately after spinal injury or 24 hours later. © 2022 Guardian News & Media Limited

Keyword: Regeneration
Link ID: 28333 - Posted: 05.21.2022