Links for Keyword: Parkinsons

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

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 28362 - Posted: 06.09.2022

By Laura Sanders Deep in the human brain, a very specific kind of cell dies during Parkinson’s disease. For the first time, researchers have sorted large numbers of human brain cells in the substantia nigra into 10 distinct types. Just one is especially vulnerable in Parkinson’s disease, the team reports May 5 in Nature Neuroscience. The result could lead to a clearer view of how Parkinson’s takes hold, and perhaps even ways to stop it. The new research “goes right to the core of the matter,” says neuroscientist Raj Awatramani of Northwestern University Feinberg School of Medicine in Chicago. Pinpointing the brain cells that seem to be especially susceptible to the devastating disease is “the strength of this paper,” says Awatramani, who was not involved in the study. Parkinson’s disease steals people’s ability to move smoothly, leaving balance problems, tremors and rigidity. In the United States, nearly 1 million people are estimated to have Parkinson’s. Scientists have known for decades that these symptoms come with the death of nerve cells in the substantia nigra. Neurons there churn out dopamine, a chemical signal involved in movement, among other jobs (SN: 9/7/17). But those dopamine-making neurons are not all equally vulnerable in Parkinson’s, it turns out. “This seemed like an opportunity to … really clarify which kinds of cells are actually dying in Parkinson’s disease,” says Evan Macosko, a psychiatrist and neuroscientist at Massachusetts General Hospital in Boston and the Broad Institute of MIT and Harvard. © Society for Science & the Public 2000–2022.

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 28320 - Posted: 05.07.2022

Jon Hamilton Paul knew his young grandson was in danger. "Out of the corner of my eye I could see this little figure moving," he says. The figure was heading for a steep flight of stairs. But what could he do? Paul was sitting down. And after more than a decade of living with Parkinson's disease, getting out of a chair had become a long and arduous process. But not on this day. "Paul jumped up from the chair and ran to my grandson," says his wife, Rose. (The couple asked to be identified by only their first names to protect their medical privacy.) "I mean, he just got up like there was nothing and ran to pick up Max." Amazing. But it's also the kind of story that's become familiar to Peter Strick, professor and chair of neurobiology at the University of Pittsburgh and scientific director of the University of Pittsburgh Brain Institute. "It was a great example of what people call paradoxical kinesia," Strick says. "It was a description of just what we are studying." Article continues after sponsor message Paradoxical kinesia refers to the sudden ability of a person with Parkinson's to move quickly and fluidly, the way they did before the disease eroded a brain area involved in movement. The phenomenon is a variation of the placebo effect. But instead of being induced by the belief that a sugar pill is really medicine, it tends to appear in situations that involve stress or a strong emotion. For Paul, "it was the fear of his grandson falling down the stairs," says Strick, who learned about the event in an email from Rose. A treatment that's "all in your head" © 2022 npr

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 11: Emotions, Aggression, and Stress
Link ID: 28193 - Posted: 02.09.2022

By Linda Searing For people with early-stage Parkinson’s disease, four hours a week of moderate exercise may help slow the progression of the disease. Symptoms of Parkinson’s, which is a movement disorder, generally start gradually but worsen over time. FAQ: What to know about the omicron variant of the coronavirus But research published in the journal Neurology found that those who were regularly active for at least that amount of time — whether with traditional exercise or such physical activity as walking, gardening or dancing — had less decline in balance and walking ability, were better able to maintain daily activities and did better on cognitive tests five years later than those who exercised less. The researchers noted that the key to achieving these benefits was maintaining regular exercise over time, rather than how active people had been when their disease started. Parkinson’s, which is more common in men than women, usually begins about age 60 as nerve cells in the brain (neurons) become weak or damaged. Symptoms may include trembling or shaking (tremor), muscle stiffness (rigidity), slow movement (bradykinesia) and poor balance and coordination. As symptoms get worse, people may have trouble walking, talking or continuing to do routine daily activities. Although no cure exists for Parkinson’s, treatment — medication, surgery or electrical stimulation — can sometimes help ease some symptoms for a while. The researchers wrote, however, that “there is still no disease-modifying treatment to slow the disease’s progression.”

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 28157 - Posted: 01.19.2022

Meredith Wadman Progress in treating Parkinson’s disease—a progressive neurological illness that causes tremors, muscle rigidity, and dementia—has been painfully slow, in large part because scientists still don’t fully understand the molecular events that kill select brain cells. What they do know is Parkinson’s leaves behind a telltale mark: clumps of the misfolded alpha synuclein (αS) protein in the brains and guts of patients at autopsy. In its normal form, the protein is widely thought to help brain cells communicate, but researchers have now uncovered another role—αS plays an essential part in immune and inflammatory responses in the gut. The new work is “extremely well done and very exciting,” says physician-scientist Michael Schlossmacher, who studies Parkinson’s disease at the Ottawa Hospital Research Institute but was not involved with the study. He adds that the protein’s “pivotal role” in immunity may help explain why chronic infection or inflammation can lead to a higher risk of Parkinson’s. Others in the field, however, question the work’s relevance to the brain disorder. The dominant view among researchers is that misfolded αS aggregates and takes on new toxic properties, and some say the natural role of the protein, although interesting, may be irrelevant to pursuing needed treatments. Parkinson’s disease, the second most common neurodegenerative ailment after Alzheimer’s, affects one in 331, or about 1 million, people in the United States and at least 7 million people globally. Many patients are diagnosed in their 60s, as brain cells that make the neurotransmitter dopamine die and lead to symptoms. But the disease can also strike the young—including those who produce too much αS, or fail to break it down—because of rare genetic mutations. Other risk factors include sex—prevalence is 40% to 50% higher in men than in women—and some chronic inflammatory diseases, such as inflammatory bowel disease and chronic hepatitis C. Oral dopamine can mitigate symptoms, but the 60-year-old treatment isn’t a cure and ultimately fails to prevent worsening symptoms and death. © 2022 American Association for the Advancement of Science.

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 28155 - Posted: 01.15.2022

By Nicholas Bakalar Need more incentive to get a flu shot, or to keep taking extra precautions this flu season? A new study suggests there may be a link between influenza infection and an increased risk for Parkinson’s disease. For decades, neurologists have suspected there may be a link between the flu and Parkinson’s disease, a chronic and progressive disorder of the nervous system marked by problems with movement, cognitive changes and a range of other symptoms. Several earlier studies, for example, reported a sharp increase in Parkinson’s cases following the 1918 influenza pandemic. Some cases of Parkinson’s have been linked to environmental exposures to pesticides and other toxic chemicals, and genetics may also play a role, but most cases of Parkinson’s have no known cause. Treatments for Parkinson’s can help delay its progression, but there is no known cure. The new study, using Danish health care databases, included 10,231 men and women who had been diagnosed with Parkinson’s between 2000 and 2016. Researchers compared them with 51,196 controls who were matched for age and sex. The researchers tracked influenza infections beginning in 1977 using hospital and outpatient discharge records. The report appeared in JAMA Neurology. Parkinson’s takes years, if not decades, to develop, and initially may produce only subtle symptoms like a hand tremor. It may take years for doctors to diagnose the condition, so any connection between a flu infection and the disease would be evident only many years later. The researchers found that compared with people who had not had a flu infection, those who had the flu had a 70 percent higher risk of Parkinson’s 10 years later, and a 90 percent higher risk 15 years after. © 2021 The New York Times Company

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 28127 - Posted: 12.29.2021

By Marlene Cimons J. William Langston, who has been studying and treating Parkinson’s disease for nearly 40 years, always has found it striking that so many more men than women show up in his clinic. His observation is not anecdotal. It is grounded in science and shared by many physicians: Men are roughly 1.5 times more likely than women to develop Parkinson’s, a progressive disorder of the nervous system that impairs movement and can erode mental acuity. “It’s a big difference that is quite real,” says Langston, clinical professor of neurology, neuroscience and of pathology at the Stanford University School of Medicine and associate director of the Stanford Udall Center. “It’s pretty dramatic. I think anyone who sees a lot of Parkinson’s will tell you that.” While the disproportionate impact is clear, the reasons for it are not. “It’s a great mystery,” Langston says. Researchers still don’t know what it is that makes men more susceptible to Parkinson’s, or what it is about women that may protect them — or both. But they are trying to find out. “We in the research community have been working for decades to sort this out, but the answers are still elusive,” says Caroline Tanner, a neurology professor in the Weill Institute for Neurosciences at the University of California at San Francisco. “Nevertheless, it’s important to keep at it. We need to understand the mechanisms that underlie the specific differences between men and women so we can apply them to trying to prevent Parkinson’s.” Parkinson’s results from the death of key neurons in the substantia nigra region of the brain that produce the chemical messenger dopamine. Over time, the loss of these nerve cells disrupts movement, diminishes cognition, and can cause other symptoms, such as slurred speech and depression. © 1996-2021 The Washington Post

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 8: Hormones and Sex
Link ID: 27892 - Posted: 07.06.2021

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.

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 13: Memory and Learning
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

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 27856 - Posted: 06.16.2021

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

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 27643 - Posted: 01.15.2021

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

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 27580 - Posted: 11.14.2020

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

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
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

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 27477 - Posted: 09.19.2020

By Jane E. Brody Michael Richard Clifford, a 66-year-old retired astronaut living in Cary, N.C., learned before his third spaceflight that he had Parkinson’s disease. He was only 44 and in excellent health at the time, and had no family history of this disabling neurological disorder. What he did have was years of exposure to numerous toxic chemicals, several of which have since been shown in animal studies to cause the kind of brain damage and symptoms that afflict people with Parkinson’s. As a youngster, Mr. Clifford said, he worked in a gas station using degreasers to clean car engines. He also worked on a farm where he used pesticides and in fields where DDT was sprayed. Then, as an aviator, he cleaned engines readying them for test flights. But at none of these jobs was he protected from exposure to hazardous chemicals that are readily inhaled or absorbed through the skin. Now Mr. Clifford, a lifelong nonsmoker, believes that his close contact with these various substances explains why he developed Parkinson’s disease at such a young age. Several of the chemicals have strong links to Parkinson’s, and a growing body of evidence suggests that exposure to them may very well account for the dramatic rise in the diagnosis of Parkinson’s in recent decades. To be sure, the medical literature is replete with associations between people’s habits and exposures and their subsequent risk of developing various ailments, from allergies to heart disease and cancer. Such linkages do not — and cannot by themselves — prove cause and effect. Sometimes, though, the links are so strong and the evidence so compelling that there can be little doubt that one causes the other. The link of cigarette smoking to lung cancer is a classic example. Despite tobacco industry claims that there was no definitive proof, the accumulation of evidence, both experimental and epidemiological, eventually made it impossible to deny that years of smoking can cause cancer even long after a person has quit. © 2020 The New York Times Company

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 27378 - Posted: 07.21.2020

Ruth Williams Turning off just one factor in the brain’s astrocyte cells is sufficient to convert them into neurons in live mice, according to a paper published in Nature today (June 24) and one this spring by another research team in Cell. By flipping this cellular identity switch, researchers have, to some extent, been able to reverse the neuron loss and motor deficits caused by a Parkinson’s-like illness. Not everyone is entirely convinced by the claims. “I think this is very exciting work,” says Pennsylvania State University’s Gong Chen of the Nature paper. It reaffirms that “using the brain’s internal glial cells to regenerate new neurons is a really new avenue for the treatment of brain disorders,” he continues. Chen, who is also based at Jinan University and is the chief scientific officer for NeuExcell—a company developing astrocyte-to-neuron conversion therapies—has performed such conversions in the living mouse brain by a different method but was not involved in the new study. In Parkinson’s disease, dopaminergic neurons within the brain’s substantia nigra—a region in the midbrain involved in movement and reward—gradually die. This results in a deterioration of motor control, characterized by tremors and other types of dyskinesia, with other faculties such as cognition and mood sometimes affected too, especially at later stages of the disease. While treatments to boost diminishing dopamine levels, such as the drug levodopa, can ameliorate symptoms, none can stop the underlying disease process that relentlessly eats away at the patient’s neurological functions and quality of life. © 1986–2020 The Scientist.

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 1: Cells and Structures: The Anatomy of the Nervous System
Link ID: 27324 - Posted: 06.26.2020

By Sam Roberts Oleh Hornykiewicz, a Polish-born pharmacologist whose breakthrough research on Parkinson’s disease has spared millions of patients the tremors and other physical impairments it can cause, died on May 27 in Vienna. He was 93. His death was confirmed by his longtime colleague, Professor Stephen J. Kish of the University of Toronto, where Professor Hornykiewicz (pronounced whor-nee-KEE-eh-vitch) taught from 1967 until his retirement in 1992. Professor Hornykiewicz was among several scientists who were considered instrumental in first identifying a deficiency of the neurotransmitter dopamine as a cause of Parkinson’s disease, and then in perfecting its treatment with L-dopa, an amino acid found in fava beans. The Nobel laureate Dr. Arvid Carlsson and his colleagues had earlier shown that dopamine played a role in motor function. Drawing on that research, Professor Hornykiewicz and his assistant, Herbert Ehringer, discovered in 1960 that the brains of patients who had died of Parkinson’s had very low levels of dopamine. He persuaded another one of his collaborators, the neurologist Walther Birkmayer, to inject Parkinson’s patients with L-dopa, the precursor of dopamine, which could cross the barrier between blood vessels and the brain and be converted into dopamine by enzymes in the body, thus replenishing those depleted levels. The treatment alleviated symptoms of the disease, and patients who had been bedridden started walking. The initial results of this research were published in 1961 and presented at a meeting of the Medical Society of Vienna. The “L-dopa Miracle,” as it was called, inspired Dr. Oliver Sacks’s memoir “Awakenings” (1973) and the fictionalized movie of the same name in 1990. © 2020 The New York Times Company

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 27299 - Posted: 06.13.2020

Sandra G. Boodman First she toppled off a ladder. Then Carol Hardy-Fanta tripped on a step outside her western Massachusetts home while gazing at her cellphone. Next she fell three times during a five-mile hike after catching her left foot on a rock or tree root. At first, Hardy-Fanta thought her repeated stumbles had a simple cause: She was distracted. But when she racked up more than 30 falls in a three-year period — some for no apparent reason — she repeatedly asked her doctors whether an undiagnosed medical problem might be causing her to “drop like a log.” The 10 doctors she consulted between 2016 and 2019 — four orthopedists, three neurologists, a rheumatologist, a podiatrist and her internist — reached disparate conclusions. One suggested she was clumsy. Others suspected her problem was primarily orthopedic or could find no clear explanation. It wasn't until September 2019 that a scan revealed what Hardy-Fanta had come to suspect — a diagnosis she said several of her doctors had brushed off. “These are the smartest people,” said Hardy-Fanta, now 71, whose husband is a Boston physician. “They really wanted to help” but appeared to be misled by her symptoms. “If someone’s falling that much, they should really pay attention.” The falls started in 2016, shortly after Hardy-Fanta and her husband sold their house in a Boston suburb and began splitting their time between a condo in the city and what she described as their “dream home” in the Berkshires. Hardy-Fanta had retired as director of a university think tank. Her fourth book on women and politics had just been published. She was in excellent health, which she regarded as a legacy from her mother, who remained mentally sharp and physically able until shortly before her death at age 100. Hardy-Fanta said she was looking forward to traveling with her husband and taking long bike rides along the scenic rural roads that snake through the Berkshires.

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 9: Hearing, Balance, Taste, and Smell
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 27216 - Posted: 04.27.2020

By E. Ray Dorsey, Todd Sherer, Michael S. Okun, Bastiaan R. Bloem The number of people with Parkinson’s disease more than doubled from 1990 to 2015 and could double again by 2040. An aging population alone does not account for this rise. Air pollution, metal production, certain industrial chemicals, and some synthetic pesticides are linked to Parkinson’s. Yet we are doing little to manage known risk factors. Neither our increased awareness of the disease nor our lengthening life spans can fully account for the upsurge in diagnoses that we now face. Our knowledge of another neurological disorder, multiple sclerosis, has increased too, and we have improved diagnostic tools for it. Rates for multiple sclerosis have indeed gone up, but that increase is nothing like the exponential rise of Parkinson’s (see figure below). As for aging, more people are, of course, living longer. For example, from 1900 to 2014, the number of individuals over age 65 in the United Kingdom increased about sixfold. However, over that same period, the number of deaths due to Parkinson’s disease increased almost three times faster. Parkinson’s disease is characterized by tremors, slowness in movement, stiffness, and difficulties with balance and walking. It can also cause a wide range of symptoms that are not visible—loss of smell, constipation, sleep disorders, and depression. Most people with Parkinson’s are diagnosed in their fifties or later. But it is not just a disease of the elderly. Up to 10 percent of those with the condition develop the disease in their forties or younger. © 2020 Sigma Xi, The Scientific Research Honor Society

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 27213 - Posted: 04.24.2020

By Denise Grady A lifelong swimmer leapt into deep water near his lakeside home, and was horrified to find himself completely unable to swim. Had his wife not rescued him, he might have drowned. He had recently received an electronic brain implant to control tremors and other symptoms of Parkinson’s disease, and somehow the signals from the device had knocked out his ability to coordinate his arms and legs for swimming. He was one of nine patients, all good swimmers despite having Parkinson’s, who had the same strange, dangerous side effect from deep brain stimulators. Three of them tried turning off the stimulators, and immediately could swim again, according to an article in the journal Neurology by a medical team from the University of Zurich. At first, doctors thought the case of the man in the lake was an isolated event, Dr. Christian R. Baumann, an author of the paper, said in an interview. But when the same thing happened to another patient, one who had been a competitive swimmer, Dr. Baumann and his colleagues began to ask other patients about swimming. They found seven more cases among about 250 patients. About 150,000 people worldwide have brain implants made by Medtronic, the leading manufacturer, the company said. Most had the implants for relief of Parkinson’s symptoms. The swimming problem is not that common Dr. Baumann said, adding: “I think it’s a minority of patients. We find many who are still wonderfully able to swim and we don’t know why. We have no clue. They are treated in the same region of the brain. But this is life-threatening, and we need to pay more attention in the future.” Now, Dr. Baumann warns all patients with stimulators never to go into deep water alone. © 2019 The New York Times Company

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 26860 - Posted: 11.29.2019

Maheen Mausoof Adamson, Ph.D. The 1982 science fiction film classic Blade Runner is a gritty detective story set in the dystopian future that raises questions about what it means to be human. In the film, Harrison Ford plays Rick Deckard, a police officer turned bounty hunter searching the streets of Los Angeles for a replicant (human-like androids) rebellion leader Roy Batty. Batty is presented as a technologically perfected being fitted with a human-template brain completely rewired to create an enemy to be deathly feared. Fear of the perfect altered brain is prominent in science fiction—and may be particularly prevalent today, amid growing concerns about genetic editing and artificial intelligence. The prospect of a fully artificial human brain remains very distant. However, we are in the midst of a neuromodulation revolution that will increase our ability to treat disease and optimize human performance. We must, however, carefully consider the benefits and risks of these techniques in fully evaluating their potential for society as well as the individual. A large number of patients suffering from neurological or psychiatric disorders—depression, pain, and post-traumatic stress disorder among them—are resistant to or can develop resistance to standard medication and psychotherapy, suggesting the need for new approaches. Neuromodulation may possibly be such an approach. The term (aka neurostimulation) refers to direct stimulation and modification of the nervous system through the use of electrical, chemical, or mechanical signals. Neuromodulation therapy is already used to treat many brain disorders, most commonly movement disorders, chronic pain, and depression. © 2019 The Dana Foundation.

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 26797 - Posted: 11.07.2019