Chapter 11. Motor Control and Plasticity

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By Nancy Clanton, Studies have shown COVID-19 can cause brain complications in some patients’ brains, from memory problems to strokes. A new study has found the brains of people who died from COVID-19 were remarkably similar to the brains of people who die from Alzheimer’s and Parkinson’s, showing inflammation and disrupted circuitry, researchers reported. “The brains of patients who died from severe COVID-19 showed profound molecular markers of inflammation, even though those patients didn’t have any reported clinical signs of neurological impairment,” study co-senior author Tony Wyss-Coray, a professor of neurology and neurological sciences at Stanford University, said in a press release. According to Wyss-Coray, about a third of hospitalized COVID-19 patients report neurological symptoms, such as fuzzy thinking, forgetfulness, difficulty concentrating and depression, and these problems continue for long haul patients even when they’ve recovered from COVID. For their study, his team analyzed brain tissue from eight people who died of COVID-19 and 14 who died of other causes. The researchers found significant inflammation in the brains of the deceased COVID-19 patients. However, their brain tissue showed no signs of SARS-CoV-2, the virus that causes COVID-19. Wyss-Coray added that scientists disagree about whether the virus is present in COVID-19 patients’ brains. © 2021 The Atlanta Journal-Constitution.

Keyword: Parkinsons; Alzheimers
Link ID: 27871 - Posted: 06.23.2021

Adrienne Matei Asked about the future of Parkinson’s disease in the US, Dr Ray Dorsey says, “We’re on the tip of a very, very large iceberg.” Dorsey, a neurologist at the University of Rochester Medical Center and author of Ending Parkinson’s Disease, believes a Parkinson’s epidemic is on the horizon. Parkinson’s is already the fastest-growing neurological disorder in the world; in the US, the number of people with Parkinson’s has increased 35% the last 10 years, says Dorsey, and “We think over the next 25 years it will double again.” Most cases of Parkinson’s disease are considered idiopathic – they lack a clear cause. Yet researchers increasingly believe that one factor is environmental exposure to trichloroethylene (TCE), a chemical compound used in industrial degreasing, dry-cleaning and household products such as some shoe polishes and carpet cleaners. Advertisement Employers think the pandemic was a time for earnest self-improvement. Screw that | Jessa Crispin To date, the clearest evidence around the risk of TCE to human health is derived from workers who are exposed to the chemical in the work-place. A 2008 peer-reviewed study in the Annals of Neurology, for example, found that TCE is “a risk factor for parkinsonism.” And a 2011 study echoed those results, finding “a six-fold increase in the risk of developing Parkinson’s in individuals exposed in the workplace to trichloroethylene (TCE).” Dr Samuel Goldman of The Parkinson’s Institute in Sunnyvale, California, who co-led the study, which appeared in the Annals of Neurology journal, wrote: “Our study confirms that common environmental contaminants may increase the risk of developing Parkinson’s, which has considerable public health implications.” It was off the back of studies like these that the US Department of Labor issued a guidance on TCE, saying: “The Board recommends [...] exposures to carbon disulfide (CS2) and trichloroethylene (TCE) be presumed to cause, contribute, or aggravate Parkinsonism.” © 2021 Guardian News & Media Limited

Keyword: Parkinsons
Link ID: 27856 - Posted: 06.16.2021

Ian Sample Science editor Regular strenuous exercise raises the risk of developing motor neurone disease (MND) in people who are genetically predisposed to the condition, researchers say. Scientists at the University of Sheffield found a causal relationship between high intensity physical activity and the disorder among those already susceptible to the disease. They believe the work marks a major step towards understanding the link between intense exercise, which may contribute to motor neurone injury in certain people, and the neurodegenerative disease, which affects about 5,000 individuals in the UK. “We have suspected for some time that exercise was a risk factor for MND, but until now this link was considered controversial,” said Dr Johnathan Cooper-Knoc, a neurologist at Sheffield. “This study confirms that in some people, frequent strenuous exercise leads to an increase in the risk of MND.” The life-time risk of developing MND is about 1 in 400, but previous studies have suggested it is six times greater in professional football players compared with the general population. A number of high-profile British sportsmen have shared their experience with MND in recent years, including rugby league’s Rob Burrow, rugby union’s Doddie Weir and the the footballer Stephen Darby. The Sheffield researchers emphasise that the vast majority of people who undertake vigorous exercise do not develop MND, and that their next step is to develop tests that identify people most at risk. © 2021 Guardian News & Media Limited

Keyword: ALS-Lou Gehrig's Disease
Link ID: 27848 - Posted: 06.11.2021

By Nayef Al-Rodhan o In Chile, the National Commission for Scientific and Technological Research has begun to debate a “neurorights” bill to be written into the country’s constitution. The world, and most importantly the OECD, UNESCO and the United Nations, should be watching closely. The Chilean bill sets out to protect the right to personal identity, free will, mental privacy, equitable access to technologies that augment human capacities, and the right to protection against bias and discrimination. The landmark bill would be the first of its kind to pioneer a regulatory framework which protects human rights from the manipulation of brain activity. The relatively nascent concept of neurorights follows a number of recent medical innovations, most notably brain-computer interface technology (BCI), which has the potential to revolutionize the field of neuroscience. BCI-based therapy may be useful for poststroke motor rehabilitation and may be a potential method for the accurate detection and treatment of neurological diseases such as Alzheimer’s. Advocates claim there is therefore a moral imperative to use the technology, given the benefits it could bring; others worry about its ethical, moral and societal consequences. Many (mistakenly) see this process as being potentially undermined by premature governance restrictions, or accuse any mention of brake mechanisms as an exaggerated reaction to an unlikely science-fiction scenario. © 2021 Scientific American

Keyword: Robotics; Consciousness
Link ID: 27841 - Posted: 06.02.2021

By Richard Sima An elephant’s trunk is a marvel of biology. Devoid of any joints or bone, the trunk is an appendage made of pure muscle that is capable of both uprooting trees and gingerly plucking individual leaves and also boasts a sense of smell more powerful than a bomb-sniffing dog’s. Elephants use their trunks in a variety of ways. They use it to drink, store and spray water, and they also blow air through it to communicate — their 110-decibel bellows can be heard for miles. “It’s like a muscular multitool,” said Andrew Schulz, a mechanical engineering doctoral student at the Georgia Institute of Technology. In a study published Wednesday in The Journal of the Royal Society Interface, Mr. Schulz and his colleagues reported on how elephants can use their trunks for yet another function: applying suction to grab food, a behavior previously thought to be exclusive to fishes. Despite the ubiquity of elephants in children’s books and nature documentaries, there are numerous gaps in scientific knowledge about the biomechanics of their trunks that the new study helps fill. For example, the most recent detailed account of elephant trunk anatomy is a hand-drawn monograph that was published in 1908, Mr. Schulz said. Contrary to popular belief, the trunk does not act like a straw. “What they do is actually drink water into their trunk and they store it,” Mr. Schulz said. “So the elephant trunk is actually like a trunk.” Mr. Schulz completed his research in the lab of David Hu, which studies how animals move and function with an eye toward applying the discoveries toward human engineering problems. He said one reason elephants’ anatomy is poorly understood is because they are difficult to work with. © 2021 The New York Times Company

Keyword: Evolution; Learning & Memory
Link ID: 27840 - Posted: 06.02.2021

By Charles Q. Choi Precise control of the tongue is often vital in life, from the way frogs capture flies to human speech (SN: 1/31/17). But much remains unknown about how the brain controls the tongue, given how its quick motions are difficult to track. Now, experiments show that the brain circuits in mice that help the tongue lick water may be the same ones that help primates reach out to grasp objects, scientists report online May 19 in Nature. Using high-speed video, neuroscientist Tejapratap Bollu and colleagues recorded the sides and bottoms of mouse tongues as the rodents drank from a waterspout. With the help of artificial intelligence to develop 3-D simulations of the appendages, the researchers discovered that successful licks required previously unknown corrective movements, too fast to be seen in standard video. These adjustments came after the tongue missed unseen or distant droplets, or when the spout was unexpectedly retracted a millimeter or more. Inhibiting a brain region that controls the body’s voluntary motions impaired these corrections, suggesting this brain area was behind these movements. These newfound corrective motions are similar to ones that primates use when reaching out with their limbs for uncertain targets, the researchers say. Those primate adjustments are also controlled by similar brain circuits as those used by the mice. “This to me shows that mammalian brains use similar principles to control the tongue and the limb,” says Bollu, now at the Salk Institute for Biological Studies in La Jolla, Calif. “Everything we know about reaching in the primates can also be used to understand how the brain controls [tongue] movements.” © Society for Science & the Public 2000–2021.

Keyword: Movement Disorders
Link ID: 27828 - Posted: 05.27.2021

R. Douglas Fields The raging bull locked its legs mid-charge. Digging its hooves into the ground, the beast came to a halt just before it would have gored the man. Not a matador, the man in the bullring standing eye-to-eye with the panting toro was the Spanish neuroscientist José Manuel Rodriguez Delgado, in a death-defying public demonstration in 1963 of how violent behavior could be squelched by a radio-controlled brain implant. Delgado had pressed a switch on a hand-held radio transmitter to energize electrodes implanted in the bull’s brain. Remote-controlled brain implants, Delgado argued, could suppress deviant behavior to achieve a “psychocivilized society.” Unsurprisingly, the prospect of manipulating the human mind with brain implants and radio beams ignited public fears that curtailed this line of research for decades. But now there is a resurgence using even more advanced technology. Laser beams, ultrasound, electromagnetic pulses, mild alternating and direct current stimulation and other methods now allow access to, and manipulation of, electrical activity in the brain with far more sophistication than the needlelike electrodes Delgado stabbed into brains. Billionaires Elon Musk of Tesla and Mark Zuckerberg of Facebook are leading the charge, pouring millions of dollars into developing brain-computer interface (BCI) technology. Musk says he wants to provide a “superintelligence layer” in the human brain to help protect us from artificial intelligence, and Zuckerberg reportedly wants users to upload their thoughts and emotions over the internet without the bother of typing. But fact and fiction are easily blurred in these deliberations. How does this technology actually work, and what is it capable of? All Rights Reserved © 2021

Keyword: Robotics; Attention
Link ID: 27827 - Posted: 05.19.2021

By Lisa Sanders, M.D. “I can’t move my legs,” the 26-year-old man told his younger brother, who towered above him as he lay sprawled on the floor. He’d been on his computer for hours, he explained, and when he tried to stand up, he couldn’t. His legs looked normal, felt normal, yet they wouldn’t move. At first, he figured his legs must have fallen asleep. He pulled himself up, leaning on his desk, and slowly straightened until he was standing. He could feel the weight on his feet and knees. He let go of the desk and commanded his legs to move. Instead, they buckled, and he landed on the floor with a thud. His brother awkwardly pulled him onto the bed. Then they waited. Surely this weird paralysis would disappear just as suddenly as it came. An hour passed, then two. I’m calling an ambulance, the younger brother announced finally. Reluctantly, the elder agreed. He was embarrassed to be this helpless but worried enough to want help. When the E.M.T.s arrived, they were as confused as the brothers. The medics asked what the young man had been up to. Nothing bad, he assured them. For the past few weeks he had been getting back into shape. He changed his diet, cut out the junk and was drinking a protein concoction that was supposed to help him build muscle. And he was working out hard every day. He’d lost more than 20 pounds, he added proudly. © 2021 The New York Times Company

Keyword: Movement Disorders; Hormones & Behavior
Link ID: 27813 - Posted: 05.12.2021

Diana Kwon Two pharmaceutical companies have halted clinical trials of gene-targeting therapies for Huntington’s disease (HD), following the drugs’ disappointing performance. Researchers had hoped that the treatments — known as antisense oligonucleotides (ASOs) — would be a game changer for HD, an incurable genetic condition that affects cognition, behaviour and movement. But back-to-back announcements from Roche, headquartered in Basel, Switzerland, and Wave Life Sciences, in Cambridge, Massachusetts, have dealt a crushing blow to those affected by the disease. “I was really shocked, really tearful,” says Marion, a woman in London with HD, who was part of one of the trials. “We didn’t see it coming at all. I felt really frightened and worried about my future.” Marion requested that her last name be withheld to protect her privacy. In mid-March, Roche announced that it was halting a phase III study of its ASO drug, tominersen. A week later, Wave Life Sciences said that it would discontinue the development of two of its HD ASOs that were in phase I/II clinical trials. “The Roche trial in particular left the community quite devastated,” says Cath Stanley, chief executive of the Huntington’s Disease Association, a UK advocacy group supporting people with the disease. “There has been so much positive noise around it, both from researchers and clinicians and from the drug company themselves. I think the community was really swept up by that hope.” © 2021 Springer Nature Limited

Keyword: Huntingtons
Link ID: 27811 - Posted: 05.08.2021

By Christine Kenneally The first thing that Rita Leggett saw when she regained consciousness was a pair of piercing blue eyes peering curiously into hers. “I know you, don’t I?” she said. The man with the blue eyes replied, “Yes, you do.” But he didn’t say anything else, and for a while Leggett just wondered and stared. Then it came to her: “You’re my surgeon!” It was November, 2010, and Leggett had just undergone neurosurgery at the Royal Melbourne Hospital. She recalled a surge of loneliness as she waited alone in a hotel room the night before the operation and the fear she felt when she entered the operating room. She’d worried about the surgeon cutting off her waist-length hair. What am I doing in here? she’d thought. But just before the anesthetic took hold, she recalled, she had said to herself, “I deserve this.” Leggett was forty-nine years old and had suffered from epilepsy since she was born. During the operation, her surgeon, Andrew Morokoff, had placed an experimental device inside her skull, part of a brain-computer interface that, it was hoped, would be able to predict when she was about to have a seizure. The device, developed by a Seattle company called NeuroVista, had entered a trial stage known in medical research as “first in human.” A research team drawn from three prominent epilepsy centers based in Melbourne had selected fifteen patients to test the device. Leggett was Patient 14. © 2021 Condé Nast.

Keyword: Robotics; Epilepsy
Link ID: 27791 - Posted: 04.28.2021

By Kathiann Kowalski On most mornings, Jeremy D. Brown eats an avocado. But first, he gives it a little squeeze. A ripe avocado will yield to that pressure, but not too much. Brown also gauges the fruit’s weight in his hand and feels the waxy skin, with its bumps and ridges. “I can’t imagine not having the sense of touch to be able to do something as simple as judging the ripeness of that avocado,” says Brown, a mechanical engineer who studies haptic feedback — how information is gained or transmitted through touch — at Johns Hopkins University. Many of us have thought about touch more than usual during the COVID-19 pandemic. Hugs and high fives rarely happen outside of the immediate household these days. A surge in online shopping has meant fewer chances to touch things before buying. And many people have skipped travel, such as visits to the beach where they might sift sand through their fingers. A lot goes into each of those actions. “Anytime we touch anything, our perceptual experience is the product of the activity of thousands of nerve fibers and millions of neurons in the brain,” says neuroscientist Sliman Bensmaia of the University of Chicago. The body’s natural sense of touch is remarkably complex. Nerve receptors detect cues about pressure, shape, motion, texture, temperature and more. Those cues cause patterns of neural activity, which the central nervous system interprets so we can tell if something is smooth or rough, wet or dry, moving or still. © Society for Science & the Public 2000–2021.

Keyword: Pain & Touch; Robotics
Link ID: 27787 - Posted: 04.24.2021

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 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 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 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

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 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

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

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