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

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 29098 - Posted: 01.13.2024

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

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 29055 - Posted: 12.19.2023

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

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 28994 - Posted: 11.08.2023

By Matt Richtel An Oxford University researcher and her team showed that digital wearable devices can track the progression of Parkinson’s disease in an individual more effectively than human clinical observation can, according to a newly published paper. By tracking more than 100 metrics picked up by the devices, researchers were able to discern subtle changes in the movements of subjects with Parkinson’s, a neurodegenerative disease that afflicts 10 million people worldwide. The lead researcher emphasized that the latest findings were not a treatment for Parkinson’s. Rather, they are a means of helping scientists gauge whether novel drugs and other therapies for Parkinson’s are slowing the progression of the disease. Quotable Quotes The sensors — six per subject, worn on the chest, at the base of the spine and one on each wrist and foot — tracked 122 physiological metrics. Several dozen metrics stood out as closely indicating the disease’s progression, including the direction a toe moved during a step and the length and regularity of strides. “We have the biomarker,” said Chrystalina Antoniades, a neuroscientist at the University of Oxford and the lead researcher on the paper, which was published earlier this month in the journal npj Parkinson’s Disease. “It’s super exciting. Now we hope to be able to tell you: Is a drug working?” Until now, Dr. Antoniades said, drug trials for Parkinson’s had relied on clinical assessment of whether a treatment was slowing the progression of the disease. But clinical observation can miss changes that happen day to day or that might not show up clearly in periodic visits to a doctor, she added. In the paper, the study’s authors concluded that the sensors proved more effective at tracking the disease progression “than the conventionally used clinical rating scales.” © 2023 The New York Times Company

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 28965 - Posted: 10.17.2023

By Jocelyn Kaiser Parkinson’s disease, a brain disorder that gradually leads to difficulty moving, tremors, and usually dementia by the end, is often difficult to diagnose early in its yearslong progression. That makes testing experimental treatments challenging and slows people from getting existing drugs, which can’t stop the ongoing death of brain cells but temporarily improve many of the resulting symptoms. Now, a study using rodents and tissue from diagnosed Parkinson’s patients suggests DNA damage spotted in blood samples offers a simple way to diagnose the disease early. Although the potential test needs to be validated in clinical studies, the detected DNA damage joins a “flurry” of other biomarkers recently identified for Parkinson’s and “adds to our ability to state confidently that an individual has Parkinson’s disease or not,” says neurodegeneration researcher Mark Cookson of the National Institute on Aging, whose grantmaking arm helped fund the new work, published today in Science Translational Medicine. A blood test based on the findings could also help patients go on existing treatments earlier and boost clinical trials evaluating new therapies, the study’s authors say. “It’s really exciting because it’s something [physicians] could use to detect [Parkinson’s] before the clinical symptoms emerge,” says neuroscientist Malú Tansey of the University of Florida, who also was not involved with the research. Parkinson’s occurs when the death of certain neurons in the brain causes levels of the neurotransmitter dopamine to drop, leading to muscle stiffness, balance problems, speech and cognitive problems, and other symptoms over time. The disorder, tied to both environmental and genetic factors, afflicts up to 1 million people in the United States.

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 28897 - Posted: 09.07.2023

By Linda Searing Getting regular exercise may reduce a woman’s chances of developing Parkinson’s disease by as much as 25 percent, according to research published in the journal Neurology. It involved 95,354 women, who were an average of age 49 and did not have Parkinson’s when the study began. The researchers compared the women’s physical exercise levels over nearly three decades, including such activities as walking, cycling, gardening, stair climbing, house cleaning and sports participation. In that time, 1,074 women developed Parkinson’s. The study found that as a woman’s exercise level increased, her risk for Parkinson’s decreased. Those who got the most exercise — based on timing and intensity — developed the disease at a 25 percent lower rate than those who exercised the least. The researchers wrote that the study’s findings “suggest that physical activity may help prevent or delay [Parkinson’s disease] onset.” Parkinson’s disease is a neurodegenerative disorder, meaning it is a progressive disease that affects the nervous system and parts of the body controlled by nerves. It is sometimes referred to as a movement disorder because of the uncontrollable tremors, muscle stiffness, and gait and balance problems it can cause, but people with Parkinson’s also may experience sleep problems, depression, memory issues, fatigue and more. The symptoms generally stem from the brain’s lack of production of dopamine, a chemical that helps control muscle movement. No cure exists for Parkinson’s, but treatments to relieve symptoms include medication, lifestyle adjustments and surgical procedures, such as deep brain stimulation.

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 28804 - Posted: 05.31.2023

By Meredith Wadman A groundbreaking epidemiological study has produced the most compelling evidence yet that exposure to the chemical solvent trichloroethylene (TCE)—common in soil and groundwater—increases the risk of developing Parkinson’s disease. The movement disorder afflicts about 1 million Americans, and is likely the fastest growing neurodegenerative disease in the world; its global prevalence has doubled in the past 25 years. The report, published today in JAMA Neurology, involved examining the medical records of tens of thousands of Marine Corps and Navy veterans who trained at Marine Corps Base Camp Lejeune in North Carolina from 1975 to 1985. Those exposed there to water heavily contaminated with TCE had a 70% higher risk of developing Parkinson’s disease decades later compared with similar veterans who trained elsewhere. The Camp Lejeune contingent also had higher rates of symptoms such as erectile dysfunction and loss of smell that are early harbingers of Parkinson’s, which causes tremors; problems with moving, speaking, and balance; and in many cases dementia. Swallowing difficulties often lead to death from pneumonia. About 90% of Parkinson’s cases can’t be explained by genetics, but there have been hints that exposure to TCE may trigger it. The new study, led by researchers at the University of California, San Francisco (UCSF), represents by far the strongest environmental link between TCE and the disease. Until now, the entire epidemiological literature included fewer than 20 people who developed Parkinson’s after TCE exposure. The Camp Lejeune analysis “is exceptionally important,” says Briana De Miranda, a neurotoxicologist at the University of Alabama at Birmingham who studies TCE’s pathological impacts in the brains of rats. “It gives us an extremely large population to assess a risk factor in a very carefully designed epidemiological study.”

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 4: Development of the Brain
Link ID: 28785 - Posted: 05.18.2023

By Diana Kwon Alan Alda was running for his life. The actor, best known for his role on the television series M*A*S*H, wasn’t on a set. This threat was real—or at least it felt that way. So when he saw a bag of potatoes in front of him, he grabbed it and threw it at his attacker. Suddenly, the scene shifted. He was in his bedroom, having lurched out of sleep, and the sack of potatoes was a pillow he’d just chucked at his wife. Acting out dreams marks a disorder that occurs during the rapid eye movement (REM) phase of sleep. Called RBD, for REM sleep behavior disorder, it affects an estimated 0.5 to 1.25 percent of the general population and is more commonly reported in older adults, particularly men. Apart from being hazardous to dreamers and their partners, RBD may foreshadow neurodegenerative disease, primarily synucleinopathies—conditions in which the protein α-synuclein (or alpha-synuclein) forms toxic clumps in the brain. Not all nocturnal behaviors are RBD. Sleepwalking and sleep talking, which occur more often during childhood and adolescence, take place during non-REM sleep. This difference is clearly distinguishable in a sleep laboratory, where clinicians can monitor stages of sleep to see when a person moves. Nor is RBD always associated with a synucleinopathy: it can also be triggered by certain drugs such as antidepressants or caused by other underlying conditions such as narcolepsy or a brain stem tumor. When RBD occurs in the absence of these alternative explanations, the chance of future disease is high. Some epidemiological studies suggest that enacted dreaming predicts a more than 80 percent chance of developing a neurodegenerative disease within the patient’s lifetime. It may also be the first sign of neurodegenerative disease, which on average shows up within 10 to 15 years after onset of the dream disorder. One of the most common RBD-linked ailments is Parkinson’s disease, characterized mainly by progressive loss of motor control. Another is Lewy body dementia, in which small clusters of α-synuclein called Lewy bodies build up in the brain, disrupting movement and cognition. A third type of synucleinopathy, multiple system atrophy, interferes with both movement and involuntary functions such as digestion. RBD is one of the strongest harbingers of future synucleinopathy, more predictive than other early markers such as chronic constipation and a diminished sense of smell.

Related chapters from BN: Chapter 14: Biological Rhythms, Sleep, and Dreaming; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 10: Biological Rhythms and Sleep; Chapter 5: The Sensorimotor System
Link ID: 28642 - Posted: 01.25.2023

by Carey Gillam and Aliya Uteuova For decades, Swiss chemical giant Syngenta has manufactured and marketed a widely used weed-killing chemical called paraquat, and for much of that time the company has been dealing with external concerns that long-term exposure to the chemical may be a cause of the incurable brain ailment known as Parkinson’s disease. Syngenta has repeatedly told customers and regulators that scientific research does not prove a connection between its weedkiller and the disease, insisting that the chemical does not readily cross the blood-brain barrier, and does not affect brain cells in ways that cause Parkinson’s. But a cache of internal corporate documents dating back to the 1950s reviewed by the Guardian suggests that the public narrative put forward by Syngenta and the corporate entities that preceded it has at times contradicted the company’s own research and knowledge. And though the documents reviewed do not show that Syngenta’s scientists and executives accepted and believed that paraquat can cause Parkinson’s, they do show a corporate focus on strategies to protect product sales, refute external scientific research and influence regulators. In one defensive tactic, the documents indicate that the company worked behind the scenes to try to keep a highly regarded scientist from sitting on an advisory panel for the US Environmental Protection Agency (EPA). The agency is the chief US regulator for paraquat and other pesticides. Company officials wanted to make sure the efforts could not be traced back to Syngenta, the documents show. And the documents show that insiders feared they could face legal liability for long-term, chronic effects of paraquat as long ago as 1975. One company scientist called the situation “a quite terrible problem” for which “some plan could be made … ”

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 4: Development of the Brain
Link ID: 28522 - Posted: 10.22.2022

Ian Sample Science editor It was while watching University Challenge that the doctor first suspected something wrong with Jeremy Paxman. Normally highly animated, the TV presenter was less effusive and exuberant than usual. He had acquired what specialists in the field call the “Parkinson’s mask”. Paxman was formally diagnosed with Parkinson’s disease in hospital after he collapsed while walking his dog and found himself in hospital. There, Paxman recalled in an ITV documentary, the doctor walked in and said: “I think you’ve got Parkinson’s”. For Paxman, at least, the news came out of the blue. Parkinson’s was first described in medical texts more than 200 years ago, yet there is still no cure. It’s a common condition, particularly in the over-50s. About 1 in 37 people in the UK will be diagnosed at some point in their life. Existing drugs aim to manage patients’ symptoms, rather than slow down or stop the condition’s progression. But scientists have made progress in understanding the neurodegenerative disorder. The hope now is that gamechanging therapies are finally on the horizon. Advertisement “Parkinson’s is a hugely complex condition and there’s probably no single cure,” says Katherine Fletcher, a research communications manager at Parkinson’s UK. “It’s the progressive loss of dopamine-producing cells in the brain. If you want to slow or stop the condition, you somehow need to protect those cells or maybe even regrow those cells in the brain. That is the ultimate goal.” Why brain cells die off in Parkinson’s is still unknown. The condition strikes a brain region called the substantia nigra, where neurons make a chemical called dopamine. The loss of these brain cells causes dopamine to plunge, and this drives most of the problems patient’s experience. It is not a fast decline: typically, patients only become aware of symptoms when about 80% of nerve cells in the substantia nigra have failed. © 2022 Guardian News & Media Limited or its affiliated companies.

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 28507 - Posted: 10.08.2022

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