Chapter 11. Motor Control and Plasticity

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Links 1 - 20 of 1933

By Miryam Naddaf Moving a prosthetic arm. Controlling a speaking avatar. Typing at speed. These are all things that people with paralysis have learnt to do using brain–computer interfaces (BCIs) — implanted devices that are powered by thought alone. These devices capture neural activity using dozens to hundreds of electrodes embedded in the brain. A decoder system analyses the signals and translates them into commands. Although the main impetus behind the work is to help restore functions to people with paralysis, the technology also gives researchers a unique way to explore how the human brain is organized, and with greater resolution than most other methods. Scientists have used these opportunities to learn some basic lessons about the brain. Results are overturning assumptions about brain anatomy, for example, revealing that regions often have much fuzzier boundaries and job descriptions than was thought. Such studies are also helping researchers to work out how BCIs themselves affect the brain and, crucially, how to improve the devices. “BCIs in humans have given us a chance to record single-neuron activity for a lot of brain areas that nobody’s ever really been able to do in this way,” says Frank Willett, a neuroscientist at Stanford University in California who is working on a BCI for speech. The devices also allow measurements over much longer time spans than classical tools do, says Edward Chang, a neurosurgeon at the University of California, San Francisco. “BCIs are really pushing the limits, being able to record over not just days, weeks, but months, years at a time,” he says. “So you can study things like learning, you can study things like plasticity, you can learn tasks that require much, much more time to understand.” © 2024 Springer Nature Limited

Keyword: Brain imaging; Robotics
Link ID: 29159 - Posted: 02.22.2024

By Angie Voyles Askham The primary visual cortex carries, well, visual information — or so scientists thought until early 2010. That’s when a team at the University of California, San Francisco first described vagabond activity in the brain area, called V1, in mice. When the animals started to run on a treadmill, some neurons more than doubled their firing rate. The finding “was kind of mysterious,” because V1 was thought to represent only visual signals transmitted from the retina, says Anne Churchland, professor of neurobiology at the University of California, Los Angeles, who was not involved in that work. “The idea that running modulated neural activity suggested that maybe those visual signals were corrupted in a way that, at the time, felt like it would be really problematic.” The mystery grew over the next decade, as a flurry of mouse studies from Churchland and others built on the 2010 results. Both arousal and locomotion could shape the firing of primary visual neurons, those newer findings showed, and even subtle movements such as nose scratches contribute to variance in population activity, all without compromising the sensory information. A consensus started to form around the idea that sensory cortical regions encode broader information about an animal’s physiological state than previously thought. At least until last year, when two studies threw a wrench into that storyline: Neither marmosets nor macaque monkeys show any movement-related increase in V1 signaling. Instead, running seems to slightly suppress V1 activity in marmosets, and spontaneous movements have no effect on the same cells in macaques. The apparent differences across species raise new questions about whether mice are a suitable model to study the primate visual system, says Michael Stryker, professor of physiology at the University of California, San Francisco, who led the 2010 work. “Maybe the primate’s V1 is not working the same as in the mouse,” he says. “As I see it, it’s still a big unanswered question.” © 2024 Simons Foundation

Keyword: Vision
Link ID: 29153 - Posted: 02.20.2024

Nancy S. Jecker & Andrew Ko Putting a computer inside someone’s brain used to feel like the edge of science fiction. Today, it’s a reality. Academic and commercial groups are testing “brain-computer interface” devices to enable people with disabilities to function more independently. Yet Elon Musk’s company, Neuralink, has put this technology front and center in debates about safety, ethics and neuroscience. In January 2024, Musk announced that Neuralink implanted its first chip in a human subject’s brain. The Conversation reached out to two scholars at the University of Washington School of Medicine – Nancy Jecker, a bioethicst, and Andrew Ko, a neurosurgeon who implants brain chip devices – for their thoughts on the ethics of this new horizon in neuroscience. How does a brain chip work? Neuralink’s coin-size device, called N1, is designed to enable patients to carry out actions just by concentrating on them, without moving their bodies. Subjects in the company’s PRIME study – short for Precise Robotically Implanted Brain-Computer Interface – undergo surgery to place the device in a part of the brain that controls movement. The chip records and processes the brain’s electrical activity, then transmits this data to an external device, such as a phone or computer. The external device “decodes” the patient’s brain activity, learning to associate certain patterns with the patient’s goal: moving a computer cursor up a screen, for example. Over time, the software can recognize a pattern of neural firing that consistently occurs while the participant is imagining that task, and then execute the task for the person. © 2010–2024, The Conversation US, Inc.

Keyword: Robotics; Learning & Memory
Link ID: 29151 - Posted: 02.20.2024

By Claudia López Lloreda By squirting cells from a 3D printer, researchers have created tissue that looks—and acts—like a chunk of brain. In recent years, scientists have learned how to load up 3D printers with cells and other scaffolding ingredients to create living tissues, but making realistic brainlike constructs has been a challenge. Now, one team has shown that, by modifying its printing techniques, it can print and combine multiple subtypes of cells that better mimic signaling in the human brain. “It’s remarkable that [the researchers] can replicate” how brain cells work, says Riccardo Levato, a regenerative medicine researcher at Utrecht University who was not involved with the study. “It’s the first demonstration that, with some simple organization [of cells], you can start getting some interesting functional [responses].” The new technology, described last week in Cell Stem Cell, could offer advantages over existing techniques that neuroscientists use to create 3D brain tissues in the lab. One common approach involves using stem cells to grow miniature brainlike blobs called organoids. But researchers can’t control the types of cells or their precise location in these constructs. Each organoid “is unique,” making it difficult to reproduce research results, says neuroscientist Su-Chun Zhang of the University of Wisconsin–Madison, an author of the new study. With the right kind of 3D printing, however, “you can control where different cell types are placed,” says developmental biologist Francis Szele of the University of Oxford. Past studies have used 3D printers to construct brain tissues that allowed researchers to study how the cells matured and made connections, and even integrate printed tissue into mouse brains. But those constructs had limited functionality. And efforts that produced more functional printed tissue used rat cells, not human cells. © 2024 American Association for the Advancement of Science.

Keyword: Development of the Brain; Robotics
Link ID: 29145 - Posted: 02.10.2024

By Ben Guarino Billionaire technologist Elon Musk announced this week that his company Neuralink has implanted its brain-computer interface into a human for the first time. The recipient was “recovering well,” Musk wrote on his social media platform X (formerly Twitter) on Monday evening, adding that initial results showed “promising neuron spike detection”—a reference to brain cells’ electrical activity. Each wireless Neuralink device contains a chip and electrode arrays of more than 1,000 superthin, flexible conductors that a surgical robot threads into the cerebral cortex. There the electrodes are designed to register thoughts related to motion. In Musk’s vision, an app will eventually translate these signals to move a cursor or produce text—in short, it will enable computer control by thinking. “Imagine if Stephen Hawking could communicate faster than a speed typist or auctioneer. That is the goal,” Musk wrote of the first Neuralink product, which he said is named Telepathy. The U.S. Food and Drug Administration had approved human clinical trials for Neuralink in May 2023. And last September the company announced it was opening enrollment in its first study to people with quadriplegia. Monday’s announcement did not take neuroscientists by surprise. Musk, the world’s richest man, “said he was going to do it,” says John Donoghue, an expert in brain-computer interfaces at Brown University. “He had done the preliminary work, built on the shoulders of others, including what we did starting in the early 2000s.” Neuralink’s original ambitions, which Musk outlined when he founded the company in 2016, included meshing human brains with artificial intelligence. Its more immediate aims seem in line with the neural keyboards and other devices that people with paralysis already use to operate computers. The methods and speed with which Neuralink pursued those goals, however, have resulted in federal investigations into dead study animals and the transportation of hazardous material. © 2024 SCIENTIFIC AMERICAN

Keyword: Robotics
Link ID: 29124 - Posted: 01.31.2024

By Ben Guarino Billionaire technologist Elon Musk announced this week that his company Neuralink has implanted its brain-computer interface into a human for the first time. The recipient was “recovering well,” Musk wrote on his social media platform X (formerly Twitter) on Monday evening, adding that initial results showed “promising neuron spike detection”—a reference to brain cells’ electrical activity. Each wireless Neuralink device contains a chip and electrode arrays of more than 1,000 superthin, flexible conductors that a surgical robot threads into the cerebral cortex. There the electrodes are designed to register thoughts related to motion. In Musk’s vision, an app will eventually translate these signals to move a cursor or produce text—in short, it will enable computer control by thinking. “Imagine if Stephen Hawking could communicate faster than a speed typist or auctioneer. That is the goal,” Musk wrote of the first Neuralink product, which he said is named Telepathy. The U.S. Food and Drug Administration had approved human clinical trials for Neuralink in May 2023. And last September the company announced it was opening enrollment in its first study to people with quadriplegia. Monday’s announcement did not take neuroscientists by surprise. Musk, the world’s richest man, “said he was going to do it,” says John Donoghue, an expert in brain-computer interfaces at Brown University. “He had done the preliminary work, built on the shoulders of others, including what we did starting in the early 2000s.” Neuralink’s original ambitions, which Musk outlined when he founded the company in 2016, included meshing human brains with artificial intelligence. Its more immediate aims seem in line with the neural keyboards and other devices that people with paralysis already use to operate computers. The methods and speed with which Neuralink pursued those goals, however, have resulted in federal investigations into dead study animals and the transportation of hazardous material. © 2024 SCIENTIFIC AMERICAN

Keyword: Robotics
Link ID: 29123 - Posted: 01.31.2024

James O’Brien for Quanta Magazine In recent decades, neuroscience has seen some stunning advances, and yet a critical part of the brain remains a mystery. I am referring to the cerebellum, so named for the Latin for “little brain,” which is situated like a bun at the back of the brain. This is no small oversight: The cerebellum contains three-quarters of all the brain’s neurons, which are organized in an almost crystalline arrangement, in contrast to the tangled thicket of neurons found elsewhere. Encyclopedia articles and textbooks underscore the fact that the cerebellum’s function is to control body movement. There is no question that the cerebellum has this function. But scientists now suspect that this long-standing view is myopic. Or so I learned in November in Washington, D.C., while attending the Society for Neuroscience annual meeting, the largest meeting of neuroscientists in the world. There, a pair of neuroscientists organized a symposium on newly discovered functions of the cerebellum unrelated to motor control. New experimental techniques are showing that in addition to controlling movement, the cerebellum regulates complex behaviors, social interactions, aggression, working memory, learning, emotion and more. The connection between the cerebellum and movement has been known since the 19th century. Patients suffering trauma to the brain region had obvious difficulties with balance and movement, leaving no doubt that it was critical for coordinating motion. Over the decades, neuroscientists developed a detailed understanding of how the cerebellum’s unique neural circuitry controls motor function. The explanation of how the cerebellum worked seemed watertight. Then, in 1998, in the journal Brain, neurologists reported on wide-ranging emotional and cognitive disabilities in patients with damage to the cerebellum. For example, in 1991, a 22-year-old female college student had fallen while ice skating; a CT scan revealed a tumor in her cerebellum. After it was removed surgically, she was a completely different person. The bright college student had lost her ability to write with proficiency, do mental arithmetic, name common objects or copy a simple diagram. Her mood flattened. She hid under covers and behaved inappropriately, undressing in the corridors and speaking in baby talk. Her social interactions, including recognizing familiar faces, were also impaired.

Keyword: Emotions; Movement Disorders
Link ID: 29118 - Posted: 01.27.2024

By David Levin It can start small: a peculiar numbness; a subtle facial tic; an inexplicably stiff muscle. But then time goes by — and eventually, the tremors set in. Roughly a million people in the United States (and roughly 10 million people worldwide) live with Parkinson’s disease, a potent neurological disorder that progressively kills neurons in the brain. As it does so, it can trigger a host of crippling symptoms, from violent tremors to excruciating muscle cramps, terrifying nightmares and constant brain fog. While medical treatments can alleviate some of these effects, researchers still don’t know exactly what causes the disease to occur in the first place. A growing number of studies, however, are suggesting that it may be tied to an unlikely culprit: bacteria living inside our guts. Every one of us has hundreds or thousands of microbial species in our stomach, small intestine and colon. These bacteria, collectively called our gut microbiome, are usually considerate guests: Although they survive largely on food that passes through our insides, they also give back, cranking out essential nutrients like niacin (which helps our body convert food into energy) and breaking down otherwise indigestible plant fiber into substances our bodies can use. As Parkinson’s advances in the brain, researchers have reported that the species of bacteria present in the gut also shift dramatically, hinting at a possible cause for the disease. A 2022 paper published in the journal Nature Communications recorded those differences in detail. After sequencing the mixed-together genomes of fecal bacteria from 724 people — a group with Parkinson’s and another without — the authors saw a number of distinct changes in the guts of people who suffered from the disease. The Parkinson’s group had dramatically lower amounts of certain species of Prevotella, a type of bacterium that helps the body break down plant-based fiber (changes like this in gut flora could explain why people with Parkinson’s disease often experience constipation). At the same time, the study found, two harmful species of Enterobacteriaceae, a family of microbes that includes Salmonella, E. coli and other bugs, proliferated. Those bacteria may be involved in a chain of biochemical events that eventually kill brain cells in Parkinson’s patients, says Tim Sampson, a biologist at Emory University School of Medicine and coauthor of the study.

Keyword: Parkinsons
Link ID: 29098 - Posted: 01.13.2024

By Mark MacNamara The notion of boxing as the “sweet science” is often thought to have been coined in 1956 by the great New Yorker writer A.J. Liebling. He used the term as the title of his definitive book on the sport, but he took it—with much appreciation—from a British sportswriter, Pierce Egan. In 1813, Egan wrote about the “sweet science of bruising” in his master work, Boxiana. The book is a collection of magazine pieces set in a bloody, bare-knuckled world opposite Jane Austen’s. As for the “sweet science,” no one ever really defines it. A carefully thrown knockout punch to a sweet spot on the chin is one possible derivation. There’s also the play on a science with so little apparent sweetness. But that’s not it. The sweet science Liebling and Egan describe had more to do with British principles of “stoic virtues,” “generosity,” and “true courage”—altogether, life in a contradictory place. It’s a square ring, after all, where sometimes hope transcends the specter of an awful inevitability. Or so I’ve come to think, on a journey I’ve begun in the past year, exploring how the sweet science can be used as a treatment for Parkinson’s disease—that increasingly common degenerative disorder of the nervous system, tied to a loss of the brain chemical dopamine, which is involved in movement, memory, motivation, and cognition. Someone told her she moved like a wavy wind sock outside a used car lot. “Exactly how I feel,” she said. In October 2022, a longtime tennis partner noticed something “strange” in my stride, along with a noisy shuffle. “Fatigue,” I replied with pique. The truth is I’m 75 and had known something might not be right for years, particularly the ominous hand tremors, as well as the night-of-the-living-dead gait and a facial expression to match. Add severe anxiety in public places and bizarre nightmares, some quite disturbing. © 2023 NautilusNext Inc.,

Keyword: Parkinsons
Link ID: 29055 - Posted: 12.19.2023

By Esther Landhuis Dropping an ice crystal into a bottle of near-frozen water produces a dramatic effect: very quickly, the liquid crystallizes into a block of ice. At the molecular level, an ice crystal has a distinct shape—a lattice structure. As incoming water molecules reshape to join the lattice, the crystal grows. Some researchers think an analogous process underlies Alzheimer’s disease, Parkinson’s disease and other neurodegenerative illnesses. According to this theory, these diseases begin when a particular protein misfolds, or fails to assume the proper shape for its intended role. That misshapen molecule ensnares normal versions of the protein, causing them to similarly misfold, and over time, these rogue proteins clump into toxic clusters that spread through the brain. In mad cow disease—a brain disorder in cattle that can spread to people who eat meat from ill animals —the toxic proteins, called prions, ravage the mind quickly, leading to dementia and death within months. Prion diseases are rare. About 350 cases of the most common type, Creutzfeldt-Jakob disease, are reported each year in the U.S. By comparison, each year, nearly 500,000 people in the U.S. are diagnosed with Alzheimer’s, which develops more gradually. Plaques made up of abnormal beta-amyloid proteins can accumulate in the brain for years or even decades before a person notices signs of mental decline. While the time lines for toxicity differ, “the mechanism of misfolding is the same,” says Mathias Jucker, a neuroscientist at the Hertie Institute for Clinical Brain Research at the University of Tübingen in Germany. Just as all of the water in a bottle freezes after a “‘misfolded’ water molecule” slips into the vessel, if “you have one misfolded protein, all the other ones will take the same shape.” The idea that many diseases could arise from a common prionlike process raises an intriguing and troubling question: Under certain circumstances, could neurodegenerative disorders be transmitted from person to person? © 2023 SCIENTIFIC AMERICAN,

Keyword: Alzheimers; Prions
Link ID: 29032 - Posted: 12.06.2023

By Sandra G. Boodman The first sign of trouble was difficulty reading. In late 2014 Cathy A. Haft, a New York real estate broker who divides her time between Brooklyn and Long Island, thought she needed new glasses. But an eye exam found that her prescription was largely unchanged. Bladder problems came next, followed by impaired balance, intermittent dizziness and unexplained falls. By 2018 Haft, unable to show properties because she was too unsteady on her feet, was forced to retire. For the next four years specialists evaluated her for neuromuscular and balance-related ear problems in an attempt to explain her worsening condition, which came to include cognitive changes her husband feared was Alzheimer’s disease. In August 2022 Haft, by then dependent on a walker, consulted a Manhattan neurosurgeon. After observing her gait and reviewing images from a recent brain scan, he sent her to a colleague. Less than eight weeks later Haft underwent brain surgery for a condition that is frequently unrecognized or misdiagnosed. The operation succeeded in restoring skills that had gradually slipped away, stunting Haft’s life. “It’s pretty astonishing that this disorder is not that uncommon and no one put the pieces together,” she said. In her case a confluence of confounding symptoms, a complex medical history and the possible failure to take a holistic approach may have led doctors to overlook a condition that can sometimes be reversed — with dramatic results.

Keyword: Movement Disorders; Alzheimers
Link ID: 29020 - Posted: 11.26.2023

By Tina Hesman Saey WASHINGTON — Scientists have uncovered a clue about why it takes so long for Huntington’s disease to develop. And they may have a lead on how to stop the fatal brain disease. Huntington’s is caused by a mistakenly repeated bit of a gene called HTT. Until recently, researchers thought the number of repeats a person is born with doesn’t change, though repeats may expand when passed to future generations. But in some brain cells, the repeats can grow over time to hundreds of copies, geneticist Bob Handsaker reported November 2 at the annual meeting of the American Society of Human Genetics. Once the number of repeats passes a certain point, the activity of thousands of other genes in the brain cells changes drastically, leading the cells to die. These findings suggest that adding repeats to the HTT gene in vulnerable brain cells is what is driving Huntington’s disease, says Handsaker, of the Broad Institute of MIT and Harvard in Cambridge, Mass. The research also suggests that preventing the repeats from growing may stop the development of the disease. The new work gives “serious insight into the disease mechanism,” says Russell Snell, a geneticist at the University of Auckland in New Zealand who was not involved in the work. About 41,000 people in the United States have symptomatic Huntington’s disease, and another 200,000 are at risk of developing it. Inheriting just one copy of a repeat-riddled HTT gene produces symptoms. Even though individuals are born with the disease-causing gene, symptoms don’t usually appear until people are in their 30s to 50s. Those symptoms include depression, mood swings, forgetfulness, balance problems, involuntary movements and slurred speech. Eventually, a person with the disease may be paralyzed and can die from complications such as pneumonia or heart failure. © Society for Science & the Public 2000–2023.

Keyword: Huntingtons
Link ID: 29008 - Posted: 11.15.2023

Liam Drew In a laboratory in San Francisco, California, a woman named Ann sits in front of a huge screen. On it is an avatar created to look like her. Thanks to a brain–computer interface (BCI), when Ann thinks of talking, the avatar speaks for her — and in her own voice, too. In 2005, a brainstem stroke left Ann almost completely paralysed and unable to speak. Last year, neurosurgeon Edward Chang, at the University of California, San Francisco, placed a grid of more than 250 electrodes on the surface of Ann’s brain, on top of the regions that once controlled her body, face and larynx. As Ann imagined speaking certain words, researchers recorded her neural activity. Then, using machine learning, they established the activity patterns corresponding to each word and to the facial movements Ann would, if she could, use to vocalize them. The system can convert speech to text at 78 words per minute: a huge improvement on previous BCI efforts and now approaching the 150 words per minute considered average for regular speech1. Compared with two years ago, Chang says, “it’s like night and day”. In an added feat, the team programmed the avatar to speak aloud in Ann’s voice, basing the output on a recording of a speech she made at her wedding. “It was extremely emotional for Ann because it was the first time that she really felt that she was speaking for almost 20 years,” says Chang. This work was one of several studies in 2023 that boosted excitement about implantable BCIs. Another study2 also translated neural activity into text at unprecedented speed. And in May, scientists reported that they had created a digital bridge between the brain and spinal cord of a man paralysed in a cycling accident3. A BCI decoded his intentions to move and directed a spinal implant to stimulate the nerves of his legs, allowing him to walk. © 2023 Springer Nature Limited

Keyword: Brain imaging; Language
Link ID: 28997 - Posted: 11.11.2023

Emily Waltz A highly experimental implant that delivers electrical stimulation to the spinal cord has substantially improved mobility for one man with advanced Parkinson’s disease, according to a report published today in Nature Medicine1. Stimulating spinal cord helps paralysed people to walk again The technology, developed by researchers at the Swiss Federal Institute of Technology in Lausanne (EPFL), enables the man to walk fluidly and to navigate terrain without falling — something he couldn’t do before the treatment. Parkinson’s causes uncontrollable movements and difficulty with coordination that worsens over time. The effects of the treatment have lasted for two years. “There are no therapies to address the severe gait problems that occur at a later stage of Parkinson’s, so it’s impressive to see him walking,” says Jocelyne Bloch, a neurosurgeon at the EPFL and a lead author of the paper. But with only one individual tested, it remains unclear whether the approach will work for other people with the disease. The next step “would be to do a randomized, controlled trial”, says Susan Harkema, a neuroscientist at the University of Louisville in Kentucky who works on stimulation therapy in people with spinal cord injuries. Spinal cord stimulation involves surgically implanting a neuroprosthetic device that delivers pulses of electricity to specific regions of the spinal cord in an effort to activate dysfunctional neural circuits. The technique has been used experimentally to enable people paralysed by spinal cord injury to stand on their own, and even to walk short distances. © 2023 Springer Nature Limited

Keyword: Parkinsons; Robotics
Link ID: 28994 - Posted: 11.08.2023

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

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