Links for Keyword: Parkinsons

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Laura Beil Martha Carlin married the love of her life in 1995. She and John Carlin had dated briefly in college in Kentucky, then lost touch until a chance meeting years later at a Dallas pub. They wed soon after and had two children. John worked as an entrepreneur and stay-at-home dad. In his free time, he ran marathons. Almost eight years into their marriage, the pinky finger on John’s right hand began to quiver. So did his tongue. Most disturbing for Martha was how he looked at her. For as long as she’d known him, he’d had a joy in his eyes. But then, she says, he had a stony stare, “like he was looking through me.” In November 2002, a doctor diagnosed John with Parkinson’s disease. He was 44 years old. Carlin made it her mission to understand how her seemingly fit husband had developed such a debilitating disease. “The minute we got home from the neurologist, I was on the internet looking for answers,” she recalls. She began consuming all of the medical literature she could find. With her training in accounting and corporate consulting, Carlin was used to thinking about how the many parts of large companies came together as a whole. That kind of wide-angle perspective made her skeptical that Parkinson’s, which affects half a million people in the United States, was just a malfunction in the brain. “I had an initial hunch that food and food quality was part of the issue,” she says. If something in the environment triggered Parkinson’s, as some theories suggest, it made sense to her that the disease would involve the digestive system. Every time we eat and drink, our insides encounter the outside world. |© Society for Science & the Public 2000 - 2018.

Related chapters from BN8e: 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: 25765 - Posted: 12.08.2018

David Cyranoski Japanese neurosurgeons have implanted ‘reprogrammed’ stem cells into the brain of a patient with Parkinson’s disease for the first time. The condition is only the second for which a therapy has been trialled using induced pluripotent stem (iPS) cells, which are developed by reprogramming the cells of body tissues such as skin so that they revert to an embryonic-like state, from which they can morph into other cell types. Scientists at Kyoto University use the technique to transform iPS cells into precursors to the neurons that produce the neurotransmitter dopamine. A shortage of neurons producing dopamine in people with Parkinson’s disease can lead to tremors and difficulty walking. In October, neurosurgeon Takayuki Kikuchi at Kyoto University Hospital implanted 2.4 million dopamine precursor cells into the brain of a patient in his 50s. In the three-hour procedure, Kikuchi’s team deposited the cells into 12 sites, known to be centres of dopamine activity. Dopamine precursor cells have been shown to improve symptoms of Parkinson’s disease in monkeys. Stem-cell scientist Jun Takahashi and colleagues at Kyoto University derived the dopamine precursor cells from a stock of IPS cells stored at the university. These were developed by reprogramming skin cells taken from an anonymous donor. “The patient is doing well and there have been no major adverse reactions so far,” says Takahashi. The team will observe him for six months and, if no complications arise, will implant another 2.4 million dopamine precursor cells into his brain. © 2018 Springer Nature Limited

Related chapters from BN8e: 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, Learning, and Development
Link ID: 25682 - Posted: 11.14.2018

Aimee Cunningham The appendix, a once-dismissed organ now known to play a role in the immune system, may contribute to a person’s chances of developing Parkinson’s disease. An analysis of data from nearly 1.7 million Swedes found that those who’d had their appendix removed had a lower overall risk of Parkinson’s disease. Also, samples of appendix tissue from healthy individuals revealed protein clumps similar to those found in the brains of Parkinson’s patients, researchers report online October 31 in Science Translational Medicine. Together, the findings suggest that the appendix may play a role in the early events of Parkinson’s disease, Viviane Labrie, a neuroscientist at the Van Andel Research Institute in Grand Rapids, Mich., said at a news conference on October 30. Parkinson’s, which affects more than 10 million people worldwide, is a neurodegenerative disease that leads to difficulty with movement, coordination and balance. It’s unknown what causes Parkinson’s, but one hallmark of the disease is the death of nerve cells, or neurons, in a brain region called the substantia nigra that helps control movement. Lewy bodies, which are mostly made of clumped bits of the protein alpha-synuclein (SN: 1/12/2013, p. 13), also build up in those neurons but the connection between the cells’ death and the Lewy bodies isn’t clear yet. Symptoms related to Parkinson’s can show up in the gut earlier than they do in the brain (SN: 12/10/2016, p. 12). So Labrie and her colleagues turned their attention to the appendix, a thin tube around 10 centimeters long that protrudes from the large intestine on the lower right side of the abdomen. Often considered a “useless organ,” Labrie said, “the appendix is actually an immune tissue that’s responsible for sampling and monitoring pathogens.” |© Society for Science & the Public 2000 - 2018.

Related chapters from BN8e: 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: 25632 - Posted: 11.01.2018

Rory Cellan-Jones Technology correspondent Chinese tech giant Tencent and London medical firm Medopad have teamed up to use artificial intelligence in the diagnosis of Parkinson's Disease. A camera captures the way patients move their hands to determine the severity of their symptoms. The research team has trained the system with existing videos of patients who have been assessed by doctors, working with King's College Hospital in London. "We use the AI to measure the deterioration of Parkinson's disease patients without the patient wearing any sensors or devices," explains Dr Wei Fan, head of the Tencent Medical AI lab. The aim is to speed up a motor function assessment process, which usually takes more than half an hour. Using smartphone technology developed by Medopad, the hope is that patients could be assessed within three minutes - and might not even have to attend a hospital. Medopad is a London-based firm that has been developing apps and wearable devices to monitor patients with various medical conditions. It has been growing fast - but is a minnow compared with Tencent, which is spearheading China's huge investment in AI. Medopad's chief executive Dan Vahdat sais that there was no British company that could match what Tencent offered as a partner. "Our ambition is to impact a billion patients around the world - and to be able to get to that kind of scale we need to work with partners that have international reach," he told me. © 2018 BBC

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 25539 - Posted: 10.08.2018

By Nicholas Bakalar Symptoms of poor cardiovascular health may be linked to an increased risk for Parkinson’s disease, a new study has found. Researchers used data on 17,163,560 South Koreans over 40 years old and found 44,205 cases of Parkinson’s over the course of a five-year follow-up. They looked for five cardiovascular risk factors that define the metabolic syndrome: abdominal obesity, high triglycerides, high cholesterol, high blood pressure and high glucose readings. The study is in PLOS Medicine. After controlling for age, sex, smoking, alcohol consumption, physical activity, income, body mass index and history of stroke, they found that each component of the metabolic syndrome significantly increased the risk for Parkinson’s disease. The more risk factors a person had, the greater the risk. Compared with having none of the risk factors, having all five was associated with a 66 percent increased risk for Parkinson’s disease. The association was particularly strong for people over 65. There are about 60,000 new diagnoses of Parkinson’s each year in the United States, and about a million Americans are living with the disease. “The metabolic syndrome and its components are independent risk factors for Parkinson’s,” the authors wrote. “Future studies are warranted to examine whether control of metabolic syndrome and its components can decrease the risk of Parkinson’s disease development.” © 2018 The New York Times Company

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 25376 - Posted: 08.25.2018

David Cyranoski Doctors in Japan are poised to implant neural cells made from ‘reprogrammed’ stem cells into the brains of people with Parkinson’s disease. It is only the third clinical application of induced pluripotent stem (iPS) cells, which are developed by reprogramming the cells of body tissues such as skin to revert to an embryonic-like state, from which they can morph into other cell types. Researchers have used the technique to generate precursors to the neurons that make the neurotransmitter dopamine, which degenerate and die in people with Parkinson’s disease. Physicians at Kyoto University Hospital will inject 5 million of these precursor cells into the brains of seven people with the condition. Because dopamine-producing neurons are involved in motor skills, people with the condition typically experience tremors and stiff muscles. Participants will be observed for two years after the transplantation. One of the trial’s leaders, stem-cell scientist Jun Takahashi at the Center for iPS Cell Research and Application in Kyoto, demonstrated in 2017 that the precursor cells differentiated into dopamine-producing neurons in monkeys that had a version of the disease. They also had improved symptoms1. In 2014, ophthalmologist Masayo Takahashi — Takahashi’s wife — at the RIKEN Center for Developmental Biology in Kobe developed an iPS-cell-based therapy to treat retinal disease. And in May, a team at Osaka University received approval to use cells created from iPS cells to treat heart disease. © 2018 Springer Nature Limited

Related chapters from BN8e: 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, Learning, and Development
Link ID: 25363 - Posted: 08.22.2018

By Emily Willingham Celebrity plays a role in increasing public awareness of Parkinson’s disease—and drums up funding. A foundation named after actor Michael J. Fox is the largest nonprofit funder of Parkinson’s research. Another actor, Alan Alda, generated global news coverage with his recent announcement that he received a diagnosis more than three years ago. Tech titan Sergey Brin carries a version of a gene that greatly increases risk for Parkinson’s (PD), but the gene has an unwieldy name that few would otherwise recognize. These high-profile associations call attention to PD and its causes, including mutations like the one Brin carries. A handful of gene mutations are linked to inherited PD, but they account for less than 15 percent of the one million U.S. cases and the five million worldwide. The most common of these is a mutated version of leucine-rich repeat kinase 2 (LRRK2), the one Brin carries. It is responsible for one to two percent of PD cases, but the percentage is much higher in certain groups, including those with Ashkenazi Jewish or Basque ancestry. LRRK2 has drawn the interest of pharmaceutical companies because it is an accessible drug target. The gene encodes a namesake protein that functions as a a type of enzyme called a kinase. The LRRK2 protein attaches chemical tags called phosphates to other proteins. Like a molecular switch, these phosphate tags activate or silence LRRK2’s targets. Dozens of drugs that inhibit the activity of kinases have been approved in the last 30 years, primarily for cancer. © 2018 Scientific American

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 25301 - Posted: 08.07.2018

By Alex Marshall Alan Alda has been living with Parkinson’s disease for over three years, the actor revealed Tuesday in an appearance on CBS’s “This Morning.” “The reason I want to talk about it in public is that I was diagnosed three-and-a-half years ago, and I’ve had a full life since,” he said. “I thought it’s probably only a matter of time before somebody does a story about this from a sad point of view,” he added, pointing out that one of his thumbs had been twitching in recent TV appearances. “But that’s not where I am.” Parkinson’s is a movement disorder with symptoms that include muscle tremors and stiffness, poor balance and coordination. It affects over a million Americans, according to the American Parkinson Disease Association, including Michael J. Fox and the Rev. Jesse L. Jackson, the longtime civil rights leader. Mr. Alda, who made his name in the TV series “M*A*S*H,” said he went to the doctors after reading an article in The New York Times, by Jane E. Brody, which said that acting out one’s dreams could be an early warning sign of the disorder. “By acting out your dreams, I mean I was having a dream that somebody was attacking me and I threw a sack of potatoes at them,” Mr. Alda, 82, said in the interview. “But what I was really doing is throwing a pillow at my wife.” He said he had no other symptoms, but a few months later noticed a thumb twitch. Mr. Alda said he was also speaking out to reassure people that they do not have to be fearful after a diagnosis. “You still have things you can do,” he said. Mr. Alda goes boxing three times a week, plays tennis and marches to John Philip Sousa music. “Marching to march music is good for Parkinson’s,” he explained. Mr. Alda was not trying to belittle people who have severe symptoms, he added. “That’s difficult,” he said. © 2018 The New York Times Company

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 10: Biological Rhythms and Sleep
Link ID: 25277 - Posted: 08.01.2018

By Dennis Normile Researchers in Japan today announced the launch of a clinical trial to treat Parkinson’s disease with neurological material derived from induced pluripotent stem (iPS) cells, mature cells chemically manipulated to return to an early stage of development from which they can theoretically differentiate into any of the body’s specialized cells. The study team will inject dopaminergic progenitors, a cell type that develops into neurons that produce dopamine, directly into a region of the brain known to play a key role in the neural degeneration associated with Parkinson’s disease. The effort is being led by Jun Takahashi, a neurosurgeon at Kyoto University's Center for iPS Cell Research and Application (CiRA), in cooperation with Kyoto University Hospital. Parkinson’s disease results from the death of specialized cells in the brain that produce the neurotransmitter dopamine. A lack of dopamine leads to a decline in motor skills, resulting in difficulty walking and involuntary trembling. As the disease progresses it can lead to dementia. The trial strategy is to derive dopaminergic progenitors from iPS cells and inject them into the putamen, a round structure located at the base of the forebrain. Surgeons will drill two small holes through a patient’s skull and use a specialized device to inject roughly 5 million cells. © 2018 American Association for the Advancement of Science.

Related chapters from BN8e: 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, Learning, and Development
Link ID: 25275 - Posted: 07.31.2018

Mutations in the gene LRRK2 have been linked to about three percent of Parkinson’s disease cases. Researchers have now found evidence that the activity of LRRK2 protein might be affected in many more patients with Parkinson’s disease, even when the LRRK2 gene itself is not mutated. The study was published in Science Translational Medicine and was supported in part by the National Institute of Neurological Disorders and Stroke (NINDS), a part of the National Institutes of Health (NIH). “This is a striking finding that shows how normal LRRK2 may contribute to the development of Parkinson’s disease,” said Beth-Anne Sieber, Ph.D., program director at NINDS. “This study also identifies LRRK2 as an integral protein in the neurobiological pathways affected by the disease.” More than 10 years ago, researchers linked mutations in the LRRK2 gene with an increased risk for developing Parkinson’s disease. Those mutations produce a version of LRRK2 protein that behaves abnormally and is much more active than it would be normally. Despite its importance in Parkinson’s disease, the very small amount of normal LRRK2 protein in nerve cells has made it difficult to study. In the current study, the authors developed a new method for observing LRRK2 cells that makes them glow fluorescently only when LRRK2 is in its activated state. They have also used detection of fluorescent signals to demonstrate loss of binding of an inhibitor protein to LRRK2 when LRRK2 is activated.

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 25259 - Posted: 07.27.2018

By Sukanya Charuchandra Researchers in China have taken cell therapy for Parkinson’s disease one step further. In research published in Stem Cell Reports on June 14, scientists report improvements in the motor abilities of monkeys with Parkinsonian symptoms after grafting dopamine neurons derived from embryonic stem cells (ESCs) into their brains. The findings will serve as preclinical data for China’s first ESC-based clinical study for the neurological disease. “Since there are a number of therapies being developed, there is no overwhelming theoretical support for a particular cell type, and actually studying them in advanced animal models and then even in patients makes sense to determine what works best,” D. Eugene Redmond Jr., a psychiatrist and neurosurgeon at Yale Stem Cell Center who was not involved in the study, writes in an email to The Scientist. See “Parkinson’s Disease Cell Therapy Relieves Symptoms in Monkeys” Parkinson’s disease is a neurological condition that originates from the death of dopamine-producing cells in the brain. Since the early 1990s, groups around the world have been developing cell-replacement therapies to counteract this depletion, with recent efforts focusing on stem cells. Scientists have conducted rodent and primate research using dopamine-producing neurons derived from adult stem cells, ESCs, and induced pluripotent stem cells to treat Parkinson’s disease. © 1986-2018 The Scientist

Related chapters from BN8e: 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, Learning, and Development
Link ID: 25117 - Posted: 06.22.2018

Deep brain stimulation has been used to treat Parkinson’s disease symptoms for 25 years, but limitations have led researchers to look for ways to improve the technique. This study describes the first fully implanted DBS system that uses feedback from the brain itself to fine-tune its signaling. The study was supported by the National Institutes of Health’s Brain Research through Advancing Innovative Technologies (BRAIN) Initiative and the National Institute of Neurological Disorders and Stroke (NINDS). “The novel approach taken in this small-scale feasibility study may be an important first step in developing a more refined or personalized way for doctors to reduce the problems patients with Parkinson’s disease face every day,” said Nick B. Langhals, Ph.D., program director at NINDS and team lead for the BRAIN Initiative. Deep brain stimulation is a method of managing Parkinson’s disease symptoms by surgically implanting an electrode, a thin wire, into the brain. Traditional deep brain stimulation delivers constant stimulation to a part of the brain called the basal ganglia to help treat the symptoms of Parkinson’s. However, this approach can lead to unwanted side effects, requiring reprogramming by a trained clinician. The new method described in this study is adaptive, so that the stimulation delivered is responsive in real time to signals received from the patient’s brain. “This is the first time a fully implanted device has been used for closed-loop, adaptive deep brain stimulation in human Parkinson’s disease patients,” said Philip Starr, M.D., Ph.D., professor of neurological surgery, University of California, San Francisco, and senior author of the study, which was published in the Journal of Neural Engineering.

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 25034 - Posted: 05.30.2018

By Shawna Williams Even as patients with Parkinson’s disease, obsessive-compulsive disorder, and other conditions turn to deep brain stimulation (DBS) to keep their symptoms in check, it’s been unclear to scientists why the therapy works. Now, researchers in Texas report that in mice, the treatment dials the activity of hundreds of genes up or down in brain cells. Their results, published in eLife March 23, hint that DBS’s use could be expanded to include improving learning and memory in people with intellectual disabilities. “The paper is very well done. . . . It’s really a rigorous study,” says Zhaolan “Joe” Zhou, a neuroscientist at the University of Pennsylvania’s Perelman School of Medicine who reviewed the paper for eLife. Now that the genes and pathways DBS affects are known, researchers can home in on ways to improve the treatment, or perhaps combine the therapy with pharmacological approaches to boost its effect, he says. In DBS, two electrodes are surgically implanted in a patient’s brain (the area depends on the disorder being treated), and connected to generators that are placed in the chest. Gentle pulses of electricity are then passed continuously through the electrodes. The treatment reduces motor symptoms in many people with Parkinson’s, and allows some patients to reduce their use of medications, but it does not eliminate symptoms or slow the disease’s progression. In addition to its use in movement disorders, DBS is being explored as a potential therapy for a range of other brain-related disorders. For instance, as a way to boost learning and memory in people with Alzheimer’s disease, researchers are looking into stimulating the fimbria-fornix, a brain region thought to regulate the activity of the memory-storing hippocampus. © 1986-2018 The Scientist

Related chapters from BN8e: 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: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 24982 - Posted: 05.16.2018

A new tool developed by researchers at the National Institutes of Health has determined, for the first time, how two distinct sets of neurons in the mouse brain work together to control movement. The method, called spectrally resolved fiber photometry (SRFP), can be used to measure the activity of these neuron groups in both healthy mice and those with brain disease. The scientists plan to use the technique to better understand what goes wrong in neurological disorders, such as Parkinson’s disease. The study appeared online in the journal Neuron. According to Guohong Cui, M.D., Ph.D., head of the In Vivo Neurobiology Group at the National Institute of Environmental Health Sciences (NIEHS), part of NIH, the project began because he wanted to find out why patients with Parkinson’s disease have problems with movement. Typically, the disease motor symptoms include tremor, muscle stiffness, slowness of movement, and impaired balance. Cui explained that an animal’s ability to move was controlled by two groups of neurons in the brain called the direct pathway (D1) and indirect pathway (D2). Based on clinical studies of patients with Parkinson’s and primate models, some researchers hypothesized that the loss of the neurotransmitter dopamine in the midbrain resulted in an imbalance of neural activities between D1 and D2. Since previous methods could not effectively distinguish different cell types in the brain, the hypothesis remained under debate. However, using SRFP, Cui’s team was able to label D1 and D2 neurons with green and red fluorescent sensors to report their neural activity.

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24976 - Posted: 05.15.2018

By CEYLAN YEGINSU LONDON — Two decades after creating the clone Dolly the sheep and paving the way for new research into Parkinson’s, Dr. Ian Wilmut revealed on Wednesday that he has the disease himself. The 73-year-old professor, who lives in Scotland, announced on World Parkinson’s Day that he learned four months ago that he had the disease, and that he would participate in a major research program to test new types of treatments intended to slow the disease’s progression. “Initiatives of this kind are very effective not only because they bring more people together, but because they will include people with different experience and expertise,” Dr. Wilmut said in a statement. He was referring to the new Dundee-Edinburgh Parkinson’s Research Initiative, which aims to investigate the causes of the disease and to translate scientific discoveries into new therapies. “It was from such a rich seedbed that Dolly developed, and we can hope for similar benefits in this project,” he added. In 1996, Dr. Wilmut and a team of scientists at the Roslin Institute in Edinburgh cloned an adult sheep, resulting in the birth of Dolly. The achievement shocked researchers who had said it could not be done. But Dolly’s birth proved that cells from anywhere in the body could behave like a newly fertilized egg, an idea that transformed scientific thinking and encouraged researchers to find techniques to reprogram adult cells. The new research led to the discovery of induced pluripotent stem cells, or iPSCs, which hold great promise as a therapy for Parkinson’s because of their potential to repair damaged tissues, according to the Dundee-Edinburgh Parkinson’s Research Initiative. © 2018 The New York Times Company

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24863 - Posted: 04.13.2018

by Erin Blakemore April is Parkinson’s Disease Awareness Month, a time to think about how much you know about the disease. You may know about the tremors and stiffness that gradually take over patients’ bodies. You may know about famous people with the disease, including Michael J. Fox. For what you may not know, there’s the PD Library. If you have Parkinson’s disease or care for someone who does, you need information. And you might just find answers in the PD Library. The free online resource — maintained by the Parkinson’s Foundation — is a gold mine for anyone with an interest in the disease. About 60,000 Americans get a Parkinson’s diagnosis every year. The movement disorder happens when brain cells can’t produce enough dopamine. There is no cure for Parkinson’s disease, but there is help for those experiencing symptoms. The library includes PSAs, podcasts and pamphlets about such things as hallucinations, medication adherence and nutrition. Medical providers might want to take a look: There are videos of webcasts for nurses who care for patients with Parkinson’s disease and for caregivers who need help with such things as engaging patients in their own care and administering medication. One helpful tool on the site is a series of slides from expert briefings. There are free booklets, too, including one on psychosis and one on sleep. © 1996-2018 The Washington Post

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24807 - Posted: 04.02.2018

/ By Venkat Srinivasan It started as a tremor in his left hand and arm. It seemed harmless, but it surprised him. He was a gardener in his 50s and had no history of rheumatism or seizures or any other significant pain. He brushed it off at first, chalking it up to the exhausting daily work. But it wouldn’t go away. Writing and reading became difficult. He could not direct his fork to his mouth, and had to be fed. “It’s like a Russian doll. Within each molecule, there are so many functions.” It was the early 1800s, and a surgeon in London had started to collect notes — not just on the gardener but on a number of patients with similar symptoms. Their hands simply failed “to answer with exactness to the dictates of the will.” The years dragged on; the disease spread to the gardener’s legs, and his trunk started to bow significantly. People couldn’t understand him when he spoke. He passed urine without knowing. The tremors became more and more violent, waking him at night. Nobody understood what he was suffering from. Finally, in 1817, Dr. James Parkinson published an essay on this shaking palsy. He apologized for his speculative approach, writing that “analogy is the substitute for anatomical examination, the only sure foundation for pathological knowledge.” Two centuries later, the disease named for Parkinson is still a puzzle. It is now known that the telltale external symptoms — rigidity, slow movement, a resting tremor — result from a loss of dopamine-rich neurons in a region of the brain called the substantia nigra. But the complete network of steps leading to this cell death is still vague, and the underlying causes remain one of medicine’s great mysteries. Copyright 2018 Undark

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24763 - Posted: 03.16.2018

By Katarina Zimmer | Cellular senescence, the process by which cells cease to divide in response to stress, may be a double-edged sword. In addition to being an important anti-cancer mechanism, recent studies show it may also contribute to age-related tissue damage and inflammation. A study published in Cell Reports yesterday (January 23) suggests that cellular senescence could be a factor underlying neurodegeneration in sporadic forms of Parkinson’s disease. “I think the proposition that cellular senescence drives neurodegeneration in Parkinson’s disease and other ageing-related neurodegenerative diseases . . . has a great deal of merit,” writes D James Surmeier, a physiologist at Northwestern University, to The Scientist in an email. “To my knowledge, [this study] is the first strong piece of evidence for this model.” Cellular senescence may be the basis by which the herbicide and neurotoxin paraquat, which has been previously linked to Parkinson’s disease, can contribute to the disease, the researchers propose. The vast majority of Parkinson’s disease cases are sporadic, rather than inherited, and caused by a combination of environmental and genetic factors. Julie Andersen, a neuroscientist at the Buck Institute for Research on Aging, says her laboratory decided to focus on paraquat based on epidemiological evidence linking it to the condition in humans and on lab work showing that mice treated with the chemical suffer a loss of dopaminergic neurons in the same region that is affected in humans. It is an acutely toxic chemical—capable of causing death—and was banned in the E.U. in 2007 over safety concerns, but is still used extensively by American farmworkers. © 1986-2018 The Scientist

Related chapters from BN8e: 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, Learning, and Development
Link ID: 24574 - Posted: 01.26.2018

Ian Sample Science editor In work that could open a new front in the war on Parkinson’s disease, and even ageing itself, scientists have shown that they can stave off some of the effects of the neurodegenerative disease by flushing “zombie cells” from the brain. The research in mice raises hopes for a fresh approach to treating the most common forms of Parkinson’s disease, which typically arise through a complex interplay of genetics, lifestyle and potentially toxic substances in the environment. But the approach may have benefits far beyond Parkinson’s, with other neurodegenerative diseases – and the ageing process more broadly – all being linked to the ill effects of these “senescent” cells, which linger in tissues after entering a state of suspended animation in the body. “It’s a completely new way of looking at neurodegenerative disease and finding potential drugs,” said Marco Demaria, a molecular biologist on the team at the University of Groningen in the Netherlands. “For most of these conditions, we don’t have any way to counteract them.” Parkinson’s disease affects about 10 million people worldwide, and usually takes hold when certain types of neurons in the brain become impaired or die off completely. The neurons in question produce a substance called dopamine, which is crucial for enabling the brain to produce smooth and coordinated physical movements. © 2018 Guardian News and Media Limited

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24562 - Posted: 01.24.2018

By Elizabeth Quigley BBC Scotland news Scientists are close to establishing what causes a smell associated with sufferers of Parkinson's disease. They hope it could lead to the first diagnostic test for the disease. The breakthrough came after Joy Milne astonished doctors with her ability to detect the disease through smell under scientific conditions. A team from Manchester has found distinctive molecules that seem to be concentrated on the skin of Parkinson's patients. One in 500 people in the UK has Parkinson's - that is 127,000 across Britain. Musky smell It can leave them struggling to walk, speak and sleep. Currently there is no definitive test for the disease, with clinicians diagnosing patients by observing symptoms. This is how the disease has been diagnosed since 1817, when James Parkinson first established it as a recognised medical condition. However, that could change because of Joy Milne from Perth, whose husband Les was told he had Parkinson's at the age of 45. About a decade before her consultant anaesthetist husband was diagnosed, Joy noticed she could detect an unusual musky smell. Joy said: "We had a very tumultuous period, when he was about 34 or 35, where I kept saying to him, 'you've not showered. You've not brushed your teeth properly'. "It was a new smell - I didn't know what it was. I kept on saying to him, and he became quite upset about it. So I just had to be quiet." The retired nurse only linked the odour to the disease after meeting people with the same distinctive smell at a Parkinson's UK support group. © 2017 BBC.

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 24438 - Posted: 12.19.2017