Chapter 5. The Sensorimotor System

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By Lisa Sanders, M.D. It was dark by the time the 41-year-old woman was able to start the long drive from her father’s apartment in Washington, D.C., to her home in Westchester County, N.Y. She was eager to get back to her husband and three children. Somewhere after she crossed the border into Maryland, the woman suddenly developed a terrible itch all over her body. She’d been a little itchy for the past couple of weeks but attributed that to dry skin from her now-faded summertime tan. This seemed very different: much stronger, much deeper. And absolutely everywhere, all at the same time. The sensation was so intense it was hard for the woman to pay attention to the road. She found herself driving with one hand on the steering wheel and the other working to respond to her skin’s new need. There was no rash — or at least nothing she could feel — just the terrible itch, so deep inside her skin that she felt as if she couldn’t scratch hard enough to really get to it. By the light of the Baltimore Harbor Tunnel she saw that her nails and fingers were dark with blood. That scared her, and she tried to stop scratching, but she couldn’t. It felt as if a million ants were crawling all over her body. Not on her skin, but somehow under it. The woman had gone to Washington to help her elderly father move. His place was a mess. Many of his belongings hadn’t been touched in years. She figured that she was having a reaction to all the dust and dirt and who knows what else she encountered while cleaning. As soon as she got home, she took a long shower; the cool water soothed her excoriated skin. She lathered herself with moisturizer and sank gratefully into her bed. But the reprieve didn’t last, and from that night on she was tormented by an itch that no scratching could satisfy. © 2021 The New York Times Company

Keyword: Pain & Touch; Hormones & Behavior
Link ID: 27775 - Posted: 04.17.2021

by Peter Hess Dysfunction in a brain circuit that regulates movement may contribute to some of the motor learning difficulties associated with autism, according to a new mouse study. The mice lack one copy of a chromosomal region called 16p11.2. Up to about one-third of people with this deletion have autism, and some have speech and motor problems. Most autistic people have motor difficulties and show delays in developmental milestones such as standing and walking. The 16p mice, too, are slow to learn new motor tasks, such as balancing on a spinning rod. The explanation seems to be a shortage of the neurotransmitter noradrenaline in the motor cortex, which helps coordinate and execute movements. The dearth originates in the locus coeruleus, a part of the brainstem that serves as the brain’s main source of the chemical. “Noradrenaline is known to be involved in modulating the excitability of neurons,” says lead researcher Simon Chen, assistant professor of cellular and molecular medicine at the University of Ottawa in Ontario, Canada. “When there’s low noradrenaline in the motor cortex and the mouse is learning a movement, it takes them longer for the neural circuits to consolidate neurons that are important to control movement.” The learning process is similar for people, Chen says. When learning how to walk, for instance, a child loses her footing and falls many times. But once in a while, she will take a few more steps than she did in the previous attempt, and the brain remembers the movement that made that possible. © 2021 Simons Foundation

Keyword: Autism; Learning & Memory
Link ID: 27769 - Posted: 04.14.2021

Diana Kwon Susan was still a child when she first suspected something might be wrong with her mother. A cup or plate would often crash to the floor by accident when her mother was serving dinner or washing up dishes. “She was, she would have said, ‘clumsy’, but she wasn’t really clumsy,” says Susan. “Her hands had beautiful, glamorous movements, which I now recognize as early HD.” Huntington’s disease (HD) is an inherited condition that causes widespread deterioration in the brain and disrupts thinking, behaviour, emotion and movement. The disease usually begins in midlife, with subtle changes such as mood swings and difficulty in staying focused. As it progresses, people develop dementia and an inability to speak or move. Susan, who requested that her last name be withheld to protect her privacy, vividly remembers the day she learnt that her mother had the disease. It was the spring of 1982, and her mother had been admitted to a hospital because of her extreme exhaustion, frequent falls and irregular movements. There was no genetic test for the condition at the time, so she underwent a series of assessments. Her neurologist gathered the entire family into a room to break the news. “He told us that our mother had Huntington’s disease,” recalls Susan. “And that there’s no treatment and it can be wiped out in a generation if you just don’t breed.” Those blunt words had a profound impact on the lives of Susan and her siblings: her brother decided never to get married, and her sister chose to be sterilized. For Susan, however, those options were out of reach: she was pregnant when she received the news. © 2021 Springer Nature Limited

Keyword: Genes & Behavior; Movement Disorders
Link ID: 27762 - Posted: 04.08.2021

By Kathryn Schulz One of the most amazing things I have ever witnessed involved an otherwise unprepossessing house cat named Billy. This was some years ago, shortly after I had moved into a little rental house in the Hudson Valley. Billy, a big, bad-tempered old tomcat, belonged to the previous tenant, a guy by the name of Phil. Phil adored that cat, and the cat—improbably, given his otherwise unenthusiastic feelings about humanity—returned the favor. On the day Phil vacated the house, he wrestled an irate Billy into a cat carrier, loaded him into a moving van, and headed toward his new apartment, in Brooklyn. Thirty minutes down I-84, in the middle of a drenching rainstorm, the cat somehow clawed his way out of the carrier. Phil pulled over to the shoulder but found that, from the driver’s seat, he could neither coax nor drag the cat back into captivity. Moving carefully, he got out of the van, walked around to the other side, and opened the door a gingerly two inches—whereupon Billy shot out, streaked unscathed across two lanes of seventy-mile-per-hour traffic, and disappeared into the wide, overgrown median. After nearly an hour in the pouring rain trying to make his own way to the other side, Phil gave up and, heartbroken, continued onward to his newly diminished home. Some weeks later, at a little before seven in the morning, I woke up to a banging at my door. Braced for an emergency, I rushed downstairs. The house had double-glass doors flanked by picture windows, which together gave out onto almost the entire yard, but I could see no one. I was standing there, sleep-addled and confused, when up onto his hind legs and into my line of vision popped an extremely scrawny and filthy gray cat. I gaped. Then I opened the door and asked the cat, idiotically, “Are you Billy?” He paced, distraught, and meowed at the door. I retreated inside and returned with a bowl each of food and water, but he ignored them and banged again at the door. Flummoxed, I took a picture and texted it to my landlord with much the same question I had asked the cat: “Is this Billy?” © 2021 Condé Nast.

Keyword: Animal Migration
Link ID: 27752 - Posted: 03.31.2021

By Gretchen Reynolds Brisk walking improves brain health and thinking in aging people with memory impairments, according to a new, yearlong study of mild cognitive impairment and exercise. In the study, middle-aged and older people with early signs of memory loss raised their cognitive scores after they started walking frequently. Regular exercise also amplified the healthy flow of blood to their brains. The changes in their brains and minds were subtle but consequential, the study concludes, and could have implications not just for those with serious memory problems, but for any of us whose memories are starting to fade with age. Most of us, as we get older, will find that our ability to remember and think dulls a bit. This is considered normal, if annoying. But if the memory loss intensifies, it may become mild cognitive impairment, a medical condition in which the loss of thinking skills grows obvious enough that it becomes worrisome to you and others around you. Mild cognitive impairment is not dementia, but people with the condition are at heightened risk of developing Alzheimer’s disease later. Scientists have not yet pinpointed the underlying causes of mild cognitive impairment, but there is some evidence that changes in blood flow to the brain can contribute. Blood carries oxygen and nutrients to brain cells and if that stream sputters, so can the vitality of neurons. Unfortunately, many people experience declines in the flow of blood to their brains with age, when their arteries stiffen and hearts weaken. © 2021 The New York Times Company

Keyword: Alzheimers; Learning & Memory
Link ID: 27751 - Posted: 03.31.2021

By Veronique Greenwood There’s nothing quite like the peculiar, bone-jarring reaction of a damaged tooth exposed to something cold: a bite of ice cream, or a cold drink, and suddenly, that sharp, searing feeling, like a needle piercing a nerve. Researchers have known for years that this phenomenon results from damage to the tooth’s protective outer layer. But just how the message goes from the outside of your tooth to the nerves within it has been difficult to uncover. On Friday, biologists reported in the journal Science Advances that they have identified an unexpected player in this painful sensation: a protein embedded in the surface of cells inside the teeth. The discovery provides a glimpse of the connection between the outer world and the interior of a tooth, and could one day help guide the development of treatments for tooth pain. More than a decade ago, Dr. Katharina Zimmerman, now a professor at Friedrich-Alexander University in Germany, discovered that cells producing a protein called TRPC5 were sensitive to cold. When things got chilly, TRPC5 popped open to form a channel, allowing ions to flow across the cell’s membrane. Ion channels like TRPC5 are sprinkled throughout our bodies, Dr. Zimmerman said, and they are behind some surprisingly familiar sensations. For instance, if your eyes start to feel cold and dry in chilly air, it’s a result of an ion channel being activated in the cornea. She wondered which other parts of the body might make use of a cold receptor such as TRPC5. And it occurred to her that “the most sensitive tissue in the human body can be teeth” when it comes to cold sensations. © 2021 The New York Times Company

Keyword: Pain & Touch
Link ID: 27748 - Posted: 03.27.2021

By Erin Garcia de Jesús One defective gene might turn some bunnies’ hops into handstands, a new study suggests. To move quickly, a breed of domesticated rabbit called sauteur d’Alfort sends its back legs sky high and walks on its front paws. That strange gait may be the result of a gene tied to limb movement, researchers report March 25 in PLOS Genetics. Sauteur d’Alfort rabbits aren’t the only animal to adopt an odd scamper if there’s a mutation to this gene, known as RORB. Mice with a mutation to the gene also do handstands if they start to run, says Stephanie Koch, a neuroscientist at University College London who was not involved with the rabbit work. And even while walking, the mice hike their back legs up to waddle forward, almost like a duck. “I spent four years looking at these mice doing little handstands, and now I get to see a rabbit do the same handstand,” says Koch, who led a 2017 study published in Neuron that explored the mechanism behind the “duck gait” in mice. “It’s amazing.” Understanding why the rabbits move in such a strange way could help researchers learn more about how the spinal cord works. The study is “contributing to our basic knowledge about a very important function in humans and all animals — how we are able to move,” says Leif Andersson, a molecular geneticist at Uppsala University in Sweden. © Society for Science & the Public 2000–2021.

Keyword: Genes & Behavior; Movement Disorders
Link ID: 27747 - Posted: 03.27.2021

By Karen J. Bannan Hayley Gudgin of Sammamish, Wash., got her first migraine in 1991 when she was a 19-year-old nursing student. “I was convinced I was having a brain hemorrhage,” she says. “There was no way anything could be that painful and not be really serious.” She retreated to her bed and woke up feeling better the next day. But it wasn’t long until another migraine hit. And another. Taking a pill that combines caffeine with the pain relievers acetaminophen and codeine made life manageable until she got pregnant and had to stop taking her medication. After her son was born, the migraines came back. She started taking the drugs again, but they didn’t work and actually made her attacks worse. By the time Gudgin gave birth to her second son in 1997, she was having about 15 attacks a month. Her symptoms worsened over time and included severe pain, nausea, sensitivity to light, swollen hands, difficulty speaking, vomiting and diarrhea so intense she often wound up dehydrated in the emergency room. “It hit me [that] I had to do something when I was vomiting in the toilet, and my 3-year-old came and pulled my hair back,” she says. “It was no way to live — and not just because of the pain. You go to sleep every night not knowing how you’re going to wake up. You make plans knowing you might have to cancel them.” A headache specialist prescribed several preventive medicines, but each caused side effects for Gudgin, including weight gain and kidney stones. Then, in 2018, Gudgin read about a new type of treatment for frequent migraine sufferers. Her neurologist agreed it was worth a try. After much wrangling with her insurance company — the drug is costly, and she had to prove that two other drugs had failed to help her — she got approval to take it. © Society for Science & the Public 2000–2021.

Keyword: Pain & Touch
Link ID: 27743 - Posted: 03.23.2021

By Kelly Servick The most advanced mind-controlled devices being tested in humans rely on tiny wires inserted into the brain. Now researchers have paved the way for a less invasive option. They’ve used ultrasound imaging to predict a monkey’s intended eye or hand movements—information that could generate commands for a robotic arm or computer cursor. If the approach can be improved, it may offer people who are paralyzed a new means of controlling prostheses without equipment that penetrates the brain. “This study will put [ultrasound] on the map as a brain-machine interface technique,” says Stanford University neuroscientist Krishna Shenoy, who was not involved in the new work. “Adding this to the toolkit is spectacular.” Doctors have long used sound waves with frequencies beyond the range of human hearing to create images of our innards. A device called a transducer sends ultrasonic pings into the body, which bounce back to indicate the boundaries between different tissues About a decade ago, researchers found a way to adapt ultrasound for brain imaging. The approach, known as functional ultrasound, uses a broad, flat plane of sound instead of a narrow beam to capture a large area more quickly than with traditional ultrasound. Like functional magnetic resonance imaging (fMRI), functional ultrasound measures changes in blood flow that indicate when neurons are active and expending energy. But it creates images with much finer resolution than fMRI and doesn’t require participants to lie in a massive scanner. The technique still requires removing a small piece of skull, but unlike implanted electrodes that read neurons’ electrical activity directly, it doesn’t involve opening the brain’s protective membrane, notes neuroscientist Richard Andersen of the California Institute of Technology (Caltech), a co-author of the new study. Functional ultrasound can read from regions deep in the brain without penetrating the tissue. © 2021 American Association for the Advancement of Science.

Keyword: Brain imaging
Link ID: 27741 - Posted: 03.23.2021

Ariana Remmel A gene-silencing technique based on CRISPR can relieve pain in mice, according to a study1. Although the therapy is still a long way from being used in humans, scientists say it is a promising approach for squelching chronic pain that lasts for months or years. Chronic pain is typically treated with opioids such as morphine, which can lead to addiction. “It’s a real challenge that the best drugs we have to treat pain give us another disease,” says Margarita Calvo, a pain physician at the Pontifical Catholic University of Chile, in Santiago, who wasn’t involved in the research. That’s why the CRISPR-based technique is exciting, she says. Scientists are already evaluating CRISPR therapies that edit a person’s genome as treatments for blood diseases and some forms of hereditary blindness. The new version of CRISPR doesn’t edit genes directly — it stops them from being expressed — and so shouldn’t cause permanent changes, although it’s unclear how long its effects last for. Some studies estimate that a large proportion of the population in Europe and the United States — as high as 50% — experiences chronic pain2,3. This pain can become debilitating over time by limiting a person’s activity and having a negative effect on their mental health. Despite the prevalence of the condition, few options exist for providing long-term relief without side effects. Even so, doctors have been moving away from prescribing opioids owing to addiction risk, and that has pared down their options even further.

Keyword: Pain & Touch; Genes & Behavior
Link ID: 27728 - Posted: 03.13.2021

By Kelly Servick Swallowing an oxycodone pill might quiet nerves and blunt pain, but the drug makes other unwanted visits in the brain—to centers that can drive addiction and suppress breathing. Now, a study in mice shows certain types of pain can be prevented or reversed without apparent side effects by silencing a gene involved in pain signaling. If the approach weathers further testing, it could give chronic pain patients a safer and longer lasting option than opioids. “It’s a beautiful piece of work,” says Rajesh Khanna, a neuroscientist who studies pain mechanisms and potential treatments at the University of Arizona. Despite successes of gene therapy against rare and life-threatening disorders, few teams have explored genetic approaches to treating pain, he says. That’s in part because of reluctance to permanently change the genome to address conditions that, although disabling, aren’t always permanent or fatal. But the new approach doesn’t alter the DNA sequence itself and is theoretically reversible, Khanna notes. “I think this study is going to be our benchmark.” A prick of the finger or a punch in the gut causes pain because nerves branching through our bodies reach into the spinal cord to relay messages to the brain. Those messages can persist even after the initial injury has healed, causing chronic pain. To fire their electrical signals, pain-sensing nerves rely on the flow of ions across protein channels in their membranes. One such channel, called Nav1.7, stands out for the remarkable pain disorders that arise when it malfunctions. People with genetic mutations that make Nav1.7 overactive are prone to attacks of burning pain. Those with mutations that deactivate Nav1.7 feel no pain at all. © 2021 American Association for the Advancement of Science.

Keyword: Pain & Touch
Link ID: 27726 - Posted: 03.11.2021

By Lisa Sanders, M.D. The voice on the phone was kind but firm: “You need to go to the emergency room. Now.” Her morning was going to be busy, replied the 68-year-old woman, and she didn’t feel well. Could she go later today or maybe tomorrow? No, said Dr. Benison Keung, her neurologist. She needed to go now; it was important. As she hung up the phone, tears blurred the woman’s already bad vision. She’d been worried for a while; now she was terrified. She was always healthy, until about four months earlier. It was a Saturday morning when she noticed that something seemed wrong with her right eye. She hurried to the bathroom mirror, where she saw that her right eyelid was drooping, covering the top half of the brown of her iris. On Monday morning, when she met her eye doctor, she was seeing double. Since then she’d had tests — so many tests — but received no answers. The woman walked to the bedroom where her 17-year-old granddaughter was still asleep. She woke her and asked for help getting dressed. Her hands were too weak for her to button her own clothes or tie her shoes. When she was completely dressed, she sent the girl to get her mother. She would need a ride to the hospital. She hadn’t been able to drive since she started seeing double. The events of the past few months had left the woman exhausted. First, she had seen her eye doctor. He took one look at her and told her that she had what’s called a third-nerve palsy. The muscles of the face and neck, he explained, are controlled by nerves that line up at the top of the spine. The nerve that controlled the eyelid, called the oculomotor nerve, was the third in this column. But he didn’t know what was affecting it or how to fix the problem. She needed to see a neuro-ophthalmologist, a doctor who specialized in the nerves that control the eyes. © 2021 The New York Times Company

Keyword: Movement Disorders; Neuroimmunology
Link ID: 27720 - Posted: 03.06.2021

By Erin Garcia de Jesus A whiff of catnip can make mosquitoes buzz off, and now researchers know why. The active component of catnip (Nepeta cataria) repels insects by triggering a chemical receptor that spurs sensations such as pain or itch, researchers report March 4 in Current Biology. The sensor, dubbed TRPA1, is common in animals — from flatworms to people — and responds to environmental irritants such as cold, heat, wasabi and tear gas. When irritants come into contact with TRPA1, the reaction can make people cough or an insect flee. Catnip’s repellent effect on insects — and its euphoric effect on felines — has been documented for millennia. Studies have shown that catnip may be as effective as the widely used synthetic repellent diethyl-m-toluamide, or DEET (SN: 9/5/01). But it was unknown how the plant repelled insects. So researchers exposed mosquitoes and fruit flies to catnip and monitored the insects’ behavior. Fruit flies were less likely to lay eggs on the side of a petri dish that was treated with catnip or its active component, nepetalactone. Mosquitoes were also less likely to take blood from a human hand coated with catnip. Insects that had been genetically modified to lack TRPA1, however, had no aversion to the plant. That behavior — coupled with experiments in lab-grown cells that show catnip activates TRPA1 — suggests that insect TRPA1 senses catnip as an irritant. Puzzling out how the plant deters insects could help researchers design potent repellents that may be easier to obtain in developing countries hit hard by mosquito-borne diseases. “Oil extracted from the plant or the plant itself could be a great starting point,” says study coauthor Marco Gallio, a neuroscientist at Northwestern University in Evanston, Ill. © Society for Science & the Public 2000–2021

Keyword: Pain & Touch; Evolution
Link ID: 27719 - Posted: 03.06.2021

Linda Geddes Four scientists who discovered a key mechanism that causes migraines, paving the way for new preventive treatments, have won the largest prize for neuroscience in the world, sharing £1.1m. The Lundbeck Foundation in Denmark announced on Thursday that the British researcher Peter Goadsby, Michael Moskowitz of the US, Lars Edvinsson of Sweden and Jes Olesen of Denmark had won the Brain prize. Speaking at a press briefing ahead of the announcement, Goadsby, a professor of neurology at King’s College London, said: “I’m excited that migraine research is getting this award and that migraine – this disabling problem that is a brain disorder – is being recognised in an appropriate way.” Formally known as the Grete Lundbeck European brain research prize, the annual award recognises highly original and influential advances in any area of brain research. The award ceremony will take place in Copenhagen on 25 October, where the prize will be presented by Crown Prince Frederik of Denmark. The prize-winning research revolves around unpicking the neural basis of migraine, a crippling neurological condition characterised by episodes of throbbing head pain, as well as nausea, vomiting, dizziness, extreme sensitivity to sound, light, touch and smell. It affects about one in seven people globally and is about three times more common in women than men. In the UK, it is estimated that migraines result in the loss of 25m work or school days each year at an economic cost of £2.3bn. © 2021 Guardian News & Media Limited

Keyword: Pain & Touch
Link ID: 27717 - Posted: 03.06.2021

By Elizabeth Anne Brown Forget the soul — it turns out the eyes may be the best window to the brain. Changes to the retina may foreshadow Alzheimer’s and Parkinson’s diseases, and researchers say a picture of your eye could assess your future risk of neurodegenerative disease. Pinched off from the brain during embryonic development, the retina contains layers of neurons that seem to experience neurodegenerative disease along with their cousins inside the skull. The key difference is that these retinal neurons, right against the jellylike vitreous of the eyeball, live and die where scientists can see them. Early detection “is sort of the holy grail,” said Ron Petersen, director of Mayo Clinic’s Alzheimer’s Disease Research Center and the Mayo Clinic Study of Aging. By the time a patient complains of memory problems or tremors, the machinery of neurodegenerative disease has been at work probably for years or decades. Experts liken it to a cancer that only manifests symptoms at Stage 3 or 4. When patients begin to feel neurodegenerative disease’s impact on their daily life, it’s almost too late for treatment. Catching the warning signs of neurodegenerative disease earlier could give patients more time to plan for the future — whether that’s making caregiving arrangements, spending more time with family or writing the Great American novel. In the longer term, researchers hope the ability to notice brain changes before symptoms begin could eventually lead to early treatments more successful at slowing or stopping the progress of Parkinson’s and Alzheimer’s, since no such treatment is currently available. The hope is that “the sooner we intervene, the better we will be” at preventing cognitive impairment, Petersen said © 1996-2021 The Washington Post

Keyword: Alzheimers; Parkinsons
Link ID: 27713 - Posted: 02.28.2021

By Cara Giaimo Platypuses do it. Opossums do it. Even three species of North American flying squirrel do it. Tasmanian devils, echidnas and wombats may also do it, although the evidence is not quite so robust. And, breaking news: Two species of rabbit-size rodents called springhares do it. That is, they glow under black light, that perplexing quirk of certain mammals that is baffling biologists and delighting animal lovers all over the world. Springhares, which hop around the savannas of southern and eastern Africa, weren’t on anyone’s fluorescence bingo card. Like the other glowing mammals, they are nocturnal. But unlike the other creatures, they are Old World placental mammals, an evolutionary group not previously represented. Their glow, a unique pinkish-orange the authors call “funky and vivid,” forms surprisingly variable patterns, generally concentrated on the head, legs, rear and tail. Fluorescence is a material property rather than a biological one. Certain pigments can absorb ultraviolet light and re-emit it as a vibrant, visible color. These pigments have been found in amphibians and some birds, and are added to things like white T-shirts and party supplies. But mammals, it seems, don’t tend to have these pigments. A group of researchers, many associated with Northland College in Ashland, Wis., has been chasing down exceptions for the past few years — ever since one member, the biologist Jonathan Martin, happened to wave a UV flashlight at a flying squirrel in his backyard. It glowed eraser pink. © 2021 The New York Times Company

Keyword: Vision; Evolution
Link ID: 27697 - Posted: 02.19.2021

In a study led by National Institutes of Health researchers, scientists found that five genes may play a critical role in determining whether a person will suffer from Lewy body dementia, a devastating disorder that riddles the brain with clumps of abnormal protein deposits called Lewy bodies. Lewy bodies are also a hallmark of Parkinson’s disease. The results, published in Nature Genetics, not only supported the disease’s ties to Parkinson’s disease but also suggested that people who have Lewy body dementia may share similar genetic profiles to those who have Alzheimer’s disease. “Lewy body dementia is a devastating brain disorder for which we have no effective treatments. Patients often appear to suffer the worst of both Alzheimer’s and Parkinson’s diseases. Our results support the idea that this may be because Lewy body dementia is caused by a spectrum of problems that can be seen in both disorders,” said Sonja Scholz, M.D., Ph.D., investigator at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS) and the senior author of the study. “We hope that these results will act as a blueprint for understanding the disease and developing new treatments.” The study was led by Dr. Scholz’s team and researchers in the lab of Bryan J. Traynor, M.D., Ph.D., senior investigator at the NIH’s National Institute on Aging (NIA). Lewy body dementia usually affects people over 65 years old. Early signs of the disease include hallucinations, mood swings, and problems with thinking, movements, and sleep. Patients who initially have cognitive and behavioral problems are usually diagnosed as having dementia with Lewy bodies, but are sometimes mistakenly diagnosed with Alzheimer’s disease. Alternatively, many patients, that are initially diagnosed with Parkinson’s disease, may eventually have difficulties with thinking and mood caused by Lewy body dementia. In both cases, as the disease worsens, patients become severely disabled and may die within eight years of diagnosis.

Keyword: Alzheimers; Parkinsons
Link ID: 27694 - Posted: 02.17.2021

By Isobel Whitcomb It began with a pulled muscle. Each day after school, as the sun sank dusky purple over the hills of my hometown, I’d run with my track teammates. Even on our easy days, I’d bound ahead, leaving them behind. It wasn’t that I thought myself better than them—it’s that when I ran fast, and focused on nothing but the cold air burning my lungs and my feet pounding, my normally anxious thoughts turned to white noise. Until, one day, something popped in my leg. I stopped. I limped a little, and then tried running again: sharp, hot pain radiated down my thigh. Panic flooded me, as I imagined weeks without running: weeks without a predictable break from my own thoughts, weeks immersed in adolescent loneliness. I was 14. Pain was about to define a decade of my life. Advertisement First, I took a break from the sport—five months of stretching, icing, and waiting for the leg to heal. I returned to running, but soon after, I developed a throbbing pain in my back. The cycle repeated. Less than a year later, the pain showed up again, this time in my foot. My focus on healing my body became singular: I tried physical therapy and massage and acupuncture. I researched conditions that could lead to repeat injury. Maybe I had a rare soft-tissue disorder, I thought, or maybe early-onset rheumatoid arthritis. I let an osteopath stick a giant needle into my spinal ligaments, and inject me with sugar water, which is just as painful as it sounds. After a chiropractor recommended an anti-inflammatory diet, I subsisted on only meat and vegetables. I’d get a few good months—a joyful summer, a successful cross-country season. Then the pain would return again. As I prepared to leave home for college, my knees and ankles throbbed. For several months, my hip hurt so badly I dreaded even walking to the dining hall. Then, while scrambling to finish my senior thesis, neck spasms prevented me from leaving my bed for days. When I saw doctors, I hoped that they would discover something terribly wrong. They never did. “Have you tried psychotherapy?” one asked me. I had. I’d been in therapy for years. © 2021 The Slate Group LLC.

Keyword: Pain & Touch; Attention
Link ID: 27693 - Posted: 02.15.2021

The earliest eye damage from prion disease takes place in the cone photoreceptor cells, specifically in the cilia and the ribbon synapses, according to a new study of prion protein accumulation in the eye by National Institutes of Health scientists. Prion diseases originate when normally harmless prion protein molecules become abnormal and gather in clusters and filaments in the human body and brain. Understanding how prion diseases develop, particularly in the eye because of its diagnostic accessibility to clinicians, can help scientists identify ways to slow the spread of prion diseases. The scientists say their findings, published in the journal Acta Neuropathologica Communications, may help inform research on human retinitis pigmentosa, an inherited disease with similar photoreceptor degeneration leading to blindness. Prion diseases are slow, degenerative and usually fatal diseases of the central nervous system that occur in people and some other mammals. Prion diseases primarily involve the brain, but also can affect the eyes and other organs. Within the eye, the main cells infected by prions are the light-detecting photoreceptors known as cones and rods, both located in the retina. In their study, the scientists, from NIH’s National Institute of Allergy and Infectious Diseases at Rocky Mountain Laboratories in Hamilton, Montana, used laboratory mice infected with scrapie, a prion disease common to sheep and goats. Scrapie is closely related to human prion diseases, such as variant, familial and sporadic Creutzfeldt-Jakob disease (CJD). The most common form, sporadic CJD, affects an estimated one in one million people annually worldwide. Other prion diseases include chronic wasting disease in deer, elk and moose, and bovine spongiform encephalopathy in cattle.

Keyword: Prions; Vision
Link ID: 27674 - Posted: 02.03.2021

By Mitch Leslie Spitting cobras protect themselves by shooting jets of venom into the eyes of their attackers. A new study suggests that over the course of several million years, all three groups of spitters independently tailored the chemistry of their toxins in the same way to cause pain to a would-be predator. The work provides a novel example of convergent evolution that “deepens our understanding of this unique system” for delivering venom, says Timothy Jackson, an evolutionary toxinologist at the University of Melbourne. Like other cobras, spitting cobras will bite attackers in self-defense. Spitting is their signature move, however, and the snakes are crack shots. They can direct a stream of venom into an attacker’s face from more than 2 meters away, aiming for the eyes. The behavior is such a formidable defense that it evolved independently three times: in Asian cobras, African cobras, and a cobra cousin called the rinkhals (Hemachatus haemachatus) that lives in southern Africa. Scientists previously found the venom of some other snakes evolved to better subdue their prey. By analyzing the venoms of 17 spitting and nonspitting species—and measuring their effects—venom biologist Nicholas Casewell of the Liverpool School of Tropical Medicine and colleagues tested whether the makeup of spitting cobra venom had also changed over time to become a more effective defense. © 2021 American Association for the Advancement of Science.

Keyword: Pain & Touch; Evolution
Link ID: 27659 - Posted: 01.23.2021