Chapter 11. Motor Control and Plasticity

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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

Michelle Andrews Once the rules for implementing it are worked out, a bill signed into federal law in December will eliminate the required five-month waiting period for diagnosed ALS patients to begin disability benefits, enabling quicker Medicare coverage as well. LumiNola/Getty Images Anita Baron first noticed something was wrong in August 2018, when she began to drool. Her dentist chalked it up to a problem with her jaw. Then her speech became slurred. She managed to keep her company going — it offers financing to small businesses — but working became increasingly difficult for her as her speech worsened. Finally, nine months, four neurologists and countless tests later, Baron, now 66, got a diagnosis: amyotrophic lateral sclerosis. ALS, often called Lou Gehrig's disease after the New York Yankees first baseman who died of the disease in 1941, destroys motor neurons, causing people to lose control of their limbs, their speech and, ultimately, their ability to breathe. It's usually fatal in two to five years, though about 10% of people survive ten years or more. People with ALS often must quit their jobs — and sometimes their spouses do, too, to provide care — leaving families in financial distress. A decade-long campaign by advocates highlighting this predicament notched a victory last month when Congress passed a bill opening key support programs earlier for ALS patients. © 2021 npr

Keyword: ALS-Lou Gehrig's Disease
Link ID: 27652 - Posted: 01.20.2021

By Nicholas Bakalar People who consume a diet rich in vitamins C and E may be at reduced risk for Parkinson’s disease. Researchers followed 41,058 Swedish men and women for an average of 18 years, gathering data on their health and diet. They assessed intake of vitamins C and E as well as beta-carotene and a measure called NEAC, which takes into account all antioxidants from food and their interactions with each other. Over the course of the study, published in Neurology, there were 465 cases of Parkinson’s disease. After adjusting for age, sex, B.M.I., education, smoking, alcohol consumption and other characteristics, they found that compared with the one-third of people with the lowest intake of vitamin C or E, the one-third with the highest intake had a 32 percent reduced risk for Parkinson’s disease. Those in the highest one-third in consumption of both vitamins together had a 38 percent reduced risk. There was no effect for beta-carotene or the NEAC measure. The lead author, Essi Hantikainen, who was a researcher at the University of Milano-Bicocca when the work was done, said that more research needs to be done before drawing definitive conclusions or offering advice about diet or supplement use and the risk of Parkinson’s. Still, she said, “Implementation of a diet that includes foods rich in vitamins C and E might help protect against the development of Parkinson’s later in life. In any case, it’s never wrong to implement a healthy diet.” © 2021 The New York Times Company

Keyword: Parkinsons
Link ID: 27643 - Posted: 01.15.2021

A study led by researchers at the National Institutes of Health has made a surprising connection between frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS), two disorders of the nervous system, and the genetic mutation normally understood to cause Huntington’s disease. This large, international project, which included a collaboration between the National Institute of Neurological Disorders and Stroke (NINDS) and the National Institute on Aging (NIA), opens a potentially new avenue for diagnosing and treating some individuals with FTD or ALS. Several neurological disorders have been linked to “repeat expansions,” a type of mutation that results in abnormal repetition of certain DNA building blocks. For example, Huntington’s disease occurs when a sequence of three DNA building blocks that make up the gene for a protein called huntingtin repeats many more times than normal. These repeats can be used to predict whether someone will develop the illness and even when their symptoms are likely to appear, because the more repeats in the gene, the earlier the onset of disease. “It has been recognized for some time that repeat expansion mutations can give rise to neurological disorders,” said Sonja Scholz, M.D., Ph.D., investigator, NINDS Intramural Research Program. “But screening for these mutations throughout the entire genome has traditionally been cost-prohibitive and technically challenging.” Taking advantage of technology available at NIH, the researchers screened the entire genomes from large cohorts of FTD/ALS patients and compared them to those of age-matched healthy individuals. While several patients had a well-established genetic marker for FTD/ALS, a small subset surprisingly had the same huntingtin mutation normally associated with Huntington’s disease. Remarkably, these individuals did not show the classical symptoms of Huntington’s but rather those of ALS or FTD.

Keyword: ALS-Lou Gehrig's Disease ; Huntingtons
Link ID: 27604 - Posted: 12.05.2020

By Concepción de León Pat Quinn, who helped raise $220 million to fight amyotrophic lateral sclerosis, or A.L.S., by promoting the Ice Bucket Challenge in 2014, died on Sunday, seven years after he learned he had the disease. He was 37. His death, at St. John’s Riverside Hospital in Yonkers, N.Y., was confirmed by the A.L.S. Association and in a post on his official Facebook page. Mr. Quinn did not create the challenge, in which people dumped buckets of ice water on their heads while pledging to donate money to fight A.L.S. But he and his friend Pete Frates, who also had A.L.S., are credited with amplifying it and helping to make it a sensation in the summer and fall of 2014, raising tens of millions of dollars for research and, perhaps nearly as important, wider awareness of the disease. “Pat changed the trajectory of the fight against A.L.S. forever,” Calaneet Balas, the president and chief executive of the A.L.S. Association, said in a statement on Sunday. “He inspired millions to get involved and care about people who are living with A.L.S.” A.L.S., also called Lou Gehrig’s disease, is a progressive neurodegenerative disorder that attacks the nerve cells that control voluntary muscle movements and leads to full paralysis. People with the disease typically live three to five years from the time of diagnosis, according to the National Institute of Neurological Disorders and Stroke. Shortly after Mr. Quinn learned he had A.L.S. in 2013, he created Quinn for the Win, a Facebook group, to raise awareness of the disease and to raise money to fight for a cure. Mr. Frates created his own page, Team Frate Train, with the same goal. In July 2014, Mr. Quinn and Mr. Frates saw another A.L.S. patient, Anthony Senerchia, do the Ice Bucket Challenge online. They created their own ice-bucket videos and shared the challenge with their followers. (Mr. Frates died last year at age 34.) In Her Words: Where women rule the headlines. From there, the campaign spread wildly, with Lady Gaga, Oprah Winfrey, LeBron James and scores of other celebrities participating and donating to the cause. The challenge raised $115 million for the A.L.S. Association and $220 million around the world for A.L.S. research in the span of just six weeks, the A.L.S. Association said. © 2020 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 27596 - Posted: 11.30.2020

By Lisa Sanders, M.D. It started to drizzle just moments after the 24-year-old man crossed the finish line of the 2017 New York City Marathon. It was his first marathon, and he felt both elated and exhausted as the medal given for completing the brutal race was draped around his neck. A goody bag containing an energy drink was put in his left hand. It felt strangely heavy. His whole body ached and trembled with fatigue, but somehow that left arm felt even more tired. Unconcerned, he switched the bag to his right hand and went in search of his partner. Recovery took longer than he expected. It was a day and a half before his legs were strong enough for him to walk down stairs facing forward, rather than the sideways shuffle that his tired muscles insisted on. But by the end of the week he felt mostly normal. Only that left shoulder remained tired, sore and stiff. He went to a nearby walk-in clinic just south of City Hall. The nurse practitioner who examined him thought he had a rotator-cuff injury. She recommended a nonsteroidal anti-inflammatory like ibuprofen, physical therapy and time. The ibuprofen didn’t help much; neither did the physical therapy. That weekend he headed to the gym — his first workout since the race. He did his usual set of reps on his right biceps and triceps. But when he transferred the 25-pound dumbbell to his left hand, it seemed heavier. He struggled through two curls, but on the third the muscles in his arm turned wobbly. He grabbed the weight with his right hand and lowered it to the ground. By the time he got home, straightening his aching arm was excruciating, as if the muscles were too short to allow a full extension. That scared him. And it only got worse. The next day his whole arm was achy and tight. He couldn’t even work on his computer. Thinking back, the young runner questioned the assumption — shared by both him and the nurse practitioner — that the injury had occurred during the race. Now he suspected it started weeks earlier. © 2020 The New York Times Company

Keyword: Movement Disorders; Neuroimmunology
Link ID: 27587 - Posted: 11.21.2020

By Elisabeth Egan Two years ago, Michael J. Fox had surgery to remove a benign tumor on his spinal cord. The actor and activist, who had been living with Parkinson’s disease for nearly three decades, had to learn to walk all over again. Four months later, he fell in the kitchen of his Upper East Side home and fractured his arm so badly that it had to be stabilized with 19 pins and a plate. Mired in grueling, back-to-back recoveries, he started to wonder if he had oversold the idea of hope in his first three memoirs, “Lucky Man,” “Always Looking Up” and “A Funny Thing Happened on the Way to the Future.” “I had this kind of crisis of conscience,” Fox said during a video interview last month from his Manhattan office, where pictures of Tracy Pollan, his wife of 31 years, and his dog, Gus, hung behind him. “I thought, what have I been telling people? I tell people it’s all going to be OK — and it might suck!” His solution was to channel that honesty into a fourth memoir, “No Time Like the Future,” which Flatiron is publishing on Nov. 17. For an example of his new outlook, consider his perspective on traveling by wheelchair. “It can be a frustrating and isolating experience, allowing someone else to determine the direction I’m going and the rate of speed I can travel. The pusher is in charge,” Fox writes. “From the point of view of the occupant of the chair, it’s a world of asses and elbows. No one can hear me. To compensate, I raise my voice and suddenly feel like Joan Crawford in ‘What Ever Happened to Baby Jane?,’ barking out orders.” He continues: “Generally the person in control is a stranger, an airport or hotel employee. I’m sure that if we could look each other in the eye, we’d recognize our mutual humanity. But often in the wheelchair, I’m luggage. I’m not expected to say much. Just sit still.” Later, he adds, “No one listens to luggage.” Before the spinal surgery, Fox was working on a book about golf. “Then life happened,” he said. “I started thinking about what it meant to be able to move and express myself physically, to have that taken away. And then dealing with the surrender it takes to lie down and say, ‘Cut me open.’ I don’t know what that’s like for anybody else, but I can figure out what it’s like for me and write it down.” © 2020 The New York Times Company

Keyword: Parkinsons
Link ID: 27580 - Posted: 11.14.2020

By Giorgia Guglielmi, Spectrum A small clinical trial of a gene therapy for Angelman syndrome—a rare genetic condition related to autism—is on hold after two participants temporarily lost the ability to walk. The safety issue is important to resolve, experts say, given that the therapy otherwise appears to be effective, and the trial could guide treatment strategies for similar brain conditions. Biopharmaceutical company Ultragenyx in Novato, California, in collaboration with Florida-based biotech startup GeneTx, launched the trial in February to assess the safety of a therapy for Angelman syndrome, a neurodevelopmental condition characterized by intellectual disability, balance and motor problems, seizures, sleep problems and, in some cases, autism. Angelman syndrome results from the mutation or absence of a gene called UBE3A. People inherit two copies of UBE3A. Typically, only the maternal copy is active in neurons and the paternal copy is silent. But in people with Angelman syndrome, the maternal copy is mutated or missing, so their brain cells express no active UBE3A protein. The drug developed by Ultragenyx and GeneTx, called GTX-102, is a short snippet of RNA called an antisense oligonucleotide that activates the paternal copy of UBE3A and aims to restore the protein to typical levels. Three other companies—Roche, Biogen, and Ionis—are pursuing similar therapies for the syndrome. On 26 October, Ultragenyx and GeneTx reported that the clinical trial had enrolled five individuals with Angelman syndrome, aged 5 to 15. The plan had been to administer to each participant a dose of GTX-102 once a month over four months. Researchers injected the drug directly into the nutrient-rich solution that envelops the brain and spinal cord through a site in the lower back. © 2020 American Association for the Advancement of Science

Keyword: Autism
Link ID: 27572 - Posted: 11.07.2020

By Gretchen Reynolds Roiled by concerns about the pandemic and politics? Lifting weights might help, according to a timely new study of anxiety and resistance training. The study, which involved healthy young adults, barbells and lunges, indicates that regular weight training substantially reduces anxiety, a finding with particular relevance during these unsettling, bumpy days. We already have plenty of evidence that exercise helps stave off depression and other mental ills, and that exercise can elevate feelings of happiness and contentment. But most past studies of exercise and moods have looked at the effects of aerobic exercise, like running on a treadmill or riding a stationary bike. Scientists only recently have begun to investigate whether and how weight training might also affect mental health. A 2018 review of studies, for instance, concluded that adults who lift weights are less likely to develop depression than those who never lift. In another study, women with clinical anxiety disorders reported fewer symptoms after taking up either aerobic or weight training. But many of these studies involved frequent and complicated sessions of resistance exercise performed under the eyes of researchers, which is not how most of us are likely to work out. They also often focused on somewhat narrow groups, such as men or women with a diagnosed mental health condition like depression or an anxiety disorder, limiting their applicability. So for the new study, which was published in October in Scientific Reports, researchers at the University of Limerick in Ireland and other institutions decided to see if a simple version of weight training could have benefits for mood in people who already were in generally good mental health. © 2020 The New York Times Company

Keyword: Stress
Link ID: 27568 - Posted: 11.07.2020

By Sam Roberts Chris Pendergast, a Long Island teacher who defied the odds by surviving 27 years with Lou Gehrig’s disease, leading marathon “rides for life” for hundreds of miles from his motorized wheelchair to publicize the plight of fellow patients and raise $10 million for research, died on Oct. 14 at his home in Miller Place, N.Y. He was 71. His wife, Christine Pendergast, said the cause was complications of amyotrophic lateral sclerosis, the medical term for the disease that ended the career of Gehrig, the Yankee first baseman who, after playing in 2,130 consecutive games, proclaimed himself “the luckiest man on the face of the earth.” Gehrig died two years later, shortly before his 38th birthday. Mr. Pendergast was a 44-year-old teacher of gifted students at Dickinson Avenue elementary school in East Northport, on Long Island, when his eyes and hands began twitching and he started getting muscle spasms. On Oct. 13, 1993, he received the diagnosis: He had A.L.S., a degenerative disease, which diminishes muscle function and eventually the ability to breathe. The prognosis: He had three to five years to live. But Mr. Pendergast proved to be indomitable. He recast himself as the disease’s self-described squeaky wheel — “Since there’s no surviving constituency for A.L.S., there’s no squeaky wheel,” he told The New York Times in 2008. He founded the A.L.S. Ride for Life in 1997. The following year it mounted a 350-mile, two-week cavalcade from Yankee Stadium in the Bronx to Washington, with Mr. Pendergast leading it from his wheelchair. Subsequent annual rides went from Long Island’s East End to Manhattan with a small group of fellow patients. “We are dying men riding for life,” he told The Baltimore Sun in 2000. © 2020 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 27557 - Posted: 10.31.2020

By Pam Belluck A potential therapy for amyotrophic lateral sclerosis, a fatal neurological disorder, may allow patients to live several months longer than they otherwise would have, according to a study published Friday. The two-drug combination, dreamed up by two college students, is one of several potential treatments raising the hopes of patients with A.L.S., also known as Lou Gehrig’s disease. The paralytic condition steals people’s ability to walk, speak, eat and ultimately breathe, typically causing death within two to five years. There are only two approved A.L.S. medications, neither tremendously effective. But advocacy efforts by patients and organizations, along with the Ice Bucket Challenge, a highly successful fundraising campaign, have galvanized research into more than 20 therapies that are currently in clinical trials. The two-drug combination, called AMX0035, was conceived seven years ago by Joshua Cohen and Justin Klee, then a junior and senior at Brown University, with the goal of preventing the destruction of neurons that occurs in many brain disorders. It is a combination of an existing supplement and a medication for a pediatric urea disorder. Last month, a study of 137 patients reported that AMX0035 slowed progression of A.L.S. paralysis by about 25 percent more than a placebo. Measuring patients using a scale of physical function, researchers found that those receiving a placebo declined in 18 weeks to a level that patients receiving the treatment didn’t reach until 24 weeks, according to the study’s principal investigator, Dr. Sabrina Paganoni. But because that trial was conducted for only 24 weeks, it left unanswered a crucial question of whether the treatment extended survival for the patients receiving the therapy. After that study ended, 98 of the participants, who had not been told whether they had received placebo or therapy, were given the option of taking the therapy for up to 30 months, a format called an open-label extension study. © 2020 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 27533 - Posted: 10.19.2020

By Gunjan Sinha Light therapy can help lift moods, heal wounds, and boost the immune system. Can it improve symptoms of Parkinson’s disease, too? A first-of-its-kind trial scheduled to launch this fall in France aims to find out. In seven patients, a fiber optic cable implanted in their brain will deliver pulses of near-infrared (NIR) light directly to the substantia nigra, a region deep in the brain that degenerates in Parkinson’s disease. The team, led by neurosurgeon Alim- Louis Benabid of the Clinatec Institute—a partnership between several government-funded research institutes and industry—hopes the light will protect cells there from dying. The study is one of several set to explore how Parkinson’s patients might benefit from light. “I am so excited,” says neuropsychologist Dawn Bowers of the University of Florida College of Medicine, who is recruiting patients for a trial in which NIR will be beamed into the skull instead of delivered with an implant. Small tests in people with Parkinson’s and animal models of the disease have already suggested benefits, but some mainstream Parkinson’s researchers are skeptical. No one has shown exactly how light might protect the key neurons—or why it should have any effect at all on cells buried deep in the brain that never see the light of day. Much or all of the encouraging hints seen so far in people may be the result of the placebo effect, skeptics say. Because there are no biomarkers that correlate well with changes in Parkinson’s symptoms, “we are reliant on observing behavior,” says neurobiologist David Sulzer of Columbia University Irving Medical Center, an editor of the journal npj Parkinson’s Disease. “It’s not easy to guard against placebo effects.” © 2020 American Association for the Advancement of Science

Keyword: Parkinsons
Link ID: 27482 - Posted: 09.19.2020

By Laura J. Snyder I’m an inveterate storyteller,” confesses the celebrated neurologist and writer Oliver Sacks at the start of Oliver Sacks: His Own Life. “I tell many stories, some comic, some tragic.” Tales of both types abound in this elegiac yet lighthearted film based on director Ric Burns’s interviews with Sacks and his friends, colleagues, family members, and patients in the months before and after the physician’s death in 2015 at the age of 82. The result is a vivid portrait of an ebullient, provocative, brilliant man who transformed the practice of medicine and spearheaded the neurodiversity movement. Born into an upper-middle-class Jewish family in northwest London in 1933, Sacks was the youngest of four sons. He was an outsider: one of only three Jews at his elite prep school; a gay adolescent at a time when gay sex was illegal; an introverted, dreamy, chemistry-obsessed boy in a family of accomplished physicians. His father was a general practitioner who made house calls, and his mother was one of the first female surgeons in England. His two eldest brothers were already studying medicine when he was in high school. Sacks dutifully followed his expected career path and was drawn to neurology when his third brother, Michael, developed schizophrenia. But after completing medical training, Sacks fled the homophobic confines of his nation and family—his mother had called him “an abomination.” Paul Theroux tells Burns that Sacks’s “great luck” was ending up in Los Angeles in 1960, where he found ample “guys, weights, drugs, and hospitals.” © 2020 American Association for the Advancement of Science

Keyword: Parkinsons
Link ID: 27477 - Posted: 09.19.2020

By Gretchen Reynolds Exercise makes it easier to bounce back from too much stress, according to a fascinating new study with mice. It finds that regular exercise increases the levels of a chemical in the animals’ brains that helps them remain psychologically resilient and plucky, even when their lives seem suddenly strange, intimidating and filled with threats. The study involved mice, but it is likely to have implications for our species, too, as we face the stress and discombobulation of the ongoing pandemic and today’s political and social disruptions. Stress can, of course, be our ally. Emergencies and perils require immediate responses, and stress results in a fast, helpful flood of hormones and other chemicals that prime our bodies to act. “If a tiger jumps out at you, you should run,” says David Weinshenker, a professor of human genetics at Emory University School of Medicine in Atlanta and the senior author of the new study. The stress response, in that situation, is appropriate and valuable. But if, afterward, we “jump at every little noise” and shrink from shadows, we are overreacting to the original stress, Dr. Weinshenker continues. Our response has become maladaptive, because we no longer react with appropriate dread to dreadful things but with twitchy anxiety to the quotidian. We lack stress resilience. In interesting past research, scientists have shown that exercise seems to build and amplify stress resilience. Rats that run on wheels for several weeks, for instance, and then experience stress through light shocks to their paws, respond later to unfamiliar — but safe — terrain with less trepidation than sedentary rats that also experience shocks. But the physiological underpinnings of the animals’ relative buoyancy after exercise remain somewhat mysterious. And, rats are just one species. Finding similar relationships between physical activity and resilience in other animals would bolster the possibility that a similar link exists in people. © 2020 The New York Times Company

Keyword: Stress; Hormones & Behavior
Link ID: 27461 - Posted: 09.09.2020

By Tanya Lewis During Musk’s demonstration, he strolled near a pen containing several pigs, some of which had Neuralink implants. One animal, named Gertrude, had hers for two months. The device’s electrodes were situated in a part of Gertrude’s cortex that connected to neurons in her snout. And for the purposes of the demo, her brain signals were converted to audible bleeps that became more frequent as she sniffed around the pen and enjoyed some tasty treats. Musk also showed off a pig whose implant had been successfully removed to show that the surgery was reversible. Some of the other displayed pigs had multiple implants. Neuralink implantable device Neuralink implantable device, v0.9. Credit: Neuralink Neuralink, which was founded by Musk and a team of engineers and scientists in 2016, unveiled an earlier, wired version of its implant technology in 2019. It had several modules: the electrodes were connected to a USB port in the skull, which was intended to be wired to an external battery and a radio transmitter that were located behind the ear. The latest version consists of a single integrated implant that fits in a hole in the skull and relays data through the skin via a Bluetooth radio. The wireless design makes it seem much more practical for human use but limits the bandwidth of data that can be sent, compared with state-of-the-art brain-computer interfaces. The company’s goal, Musk said in the demo, is to “solve important spine and brain problems with a seamlessly implanted device”—a far cry from his previously stated, much more fantastic aim of allowing humans to merge with artificial intelligence. This time Musk seemed more circumspect about the device’s applications. As before, he insisted the demonstration was purely intended as a recruiting event to attract potential staff. Neuralink’s efforts build on decades of work from researchers in the field of brain-computer interfaces. Although technically impressive, this wireless brain implant is not the first to be tested in pigs or other large mammals.] © 2020 Scientific American,

Keyword: Robotics; Movement Disorders
Link ID: 27457 - Posted: 09.07.2020

By Pam Belluck Seven years ago, Joshua Cohen, then a junior at Brown University majoring in biomedical engineering, was captivated by the question of why people develop brain disorders. “How does a neuron die?” he wondered. After poring over scientific studies, he sketched out his ideas for a way to treat them. “I was sitting in my dorm room and I had kind of written out the research on these crazy-looking diagrams,” he recalled. A study published on Wednesday in the New England Journal of Medicine reported that the experimental treatment he and another Brown student, Justin Klee, conceived might hold promise for slowing progression of amyotrophic lateral sclerosis, the ruthless disease that robs people of their ability to move, speak, eat and ultimately breathe. More than 50 clinical trials over 25 years have failed to find effective treatments for A.L.S., also called Lou Gehrig’s disease, which often causes death within two to five years. But now, scientific advances and an influx of funding are driving clinical trials for many potential therapies, generating hope and intense discussion among patients, doctors and researchers. The new study reported that a two-drug combination slowed progression of A.L.S. paralysis by about six weeks over about six months, approximately 25 percent more than a placebo. On average, patients on a placebo declined in 18 weeks to a level that patients receiving the treatment didn’t reach until 24 weeks, said the principal investigator, Dr. Sabrina Paganoni, a neuromuscular medicine specialist at Massachusetts General Hospital’s Healey & AMG Center for A.L.S. “It’s such a terrible disease and as you can imagine, for the folks who have it or the family members, it’s just desperation that something’s going to work,” said Dr. Walter Koroshetz, director of the National Institute of Neurological Disorders and Stroke, who wasn’t involved in the new study. “Any kind of slowing of progression for a patient with A.L.S. might be valuable even though it’s not a big effect.” © 2020 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 27455 - Posted: 09.05.2020

Ian Sample Science editor Brain scans of cosmonauts have revealed the first clear evidence of how the organ adapts to the weird and often sickness-inducing challenge of moving around in space. Analysis of scans taken from 11 cosmonauts, who spent about six months each in orbit, found increases in white and grey matter in three brain regions that are intimately involved in physical movement. The changes reflect the “neuroplasticity” of the brain whereby neural tissue, in this case the cells that govern movement or motor activity, reconfigures itself to cope with the fresh demands of life in orbit. “With the techniques we used, we can clearly see there are microstructural changes in three major areas of the brain that are involved in motor processing,” said Steven Jillings, a neuroscientist at the University of Antwerp in Belgium. Visitors to the International Space Station face a dramatic shock to the system for a whole host of reasons, but one of the most striking is weightlessness. While the space station and its occupants are firmly in the grip of gravity – they are constantly falling around the planet – the body must recalibrate its senses to cope with the extreme environment. Images of the cosmonauts’ brains, taken before and after missions lasting on average 171 days, and again seven months later, confirmed that the cerebrospinal fluid that bathes the brain redistributes itself in orbit, pushing the brain up towards the top of the skull. This also expands fluid-filled cavities called ventricles, which may be linked to a loss of sharpness in the cosmonauts’ vision, a condition called spaceflight-associated neuro-ocular syndrome or Sans. © 2020 Guardian News & Media Limited

Keyword: Learning & Memory
Link ID: 27453 - Posted: 09.05.2020