Links for Keyword: Parkinsons

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 1 - 20 of 404

Ashley Yeager During her time as a postdoc at the University of Basel in Switzerland, Sarah Shahmoradian decided to study the abnormal aggregates of protein that develop inside nerve cells and contribute to Parkinson’s disease. The protein clumps develop over time in the brains of Parkinson’s patients, leading some scientists to think they wreak havoc on nerve cells, causing severe damage and hastening their death. A fresh look at the clumps, called Lewy bodies, with cutting-edge microscopy tools could reveal insights that might lead to new treatments for Parkinson’s, Shahmoradian recalls thinking. “The original goal was to really find out what the building blocks of Lewy bodies are, what they are made of, and what they actually look like.” The clumps were first identified in the early 1900s, appearing as abnormal material in nerve cells viewed under a microscope. Additional studies using antibodies that bound to various proteins revealed that the clumps contained a protein called α-synuclein, and after more work probing Lewy bodies, scientists developed a rough sketch of their structure—essentially, a dense mass surrounded by a halo of twisted filaments of α-synuclein. It’s these filaments, known as fibrils, that Shahmoradian and her colleagues were most interested to analyze in postmortem human brains. Fibrils had been repeatedly produced in cultured cells and in animal models, but no one had ever gotten a clear view of them in human brain tissue. “We were originally looking for fibrils,” Shahmoradian says, “but unexpectedly, we found an abundance of . . . mitochondria, other organelles, and lipid membranes [in the Lewy bodies].” The researchers also found evidence of lysosomes, organelles that facilitate cellular waste removal. They did see α-synuclein in the Lewy bodies, as well, but the cores of the structures weren’t composed of twisted and tangled fibrils as researchers had thought. Instead, the protein was intermingled with other cellular material. © 1986–2019 The Scientist

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 26669 - Posted: 10.03.2019

By Dean McLaughlin BBC News NI A Londonderry man who was diagnosed with Parkinson's at the age of 30 says more young people need to be aware of the disease. Ronan Coyle first noticed the symptoms at 24 but only found out what the problem was six years later. "People think I'm drunk when I walk down the street," he told BBC Radio Foyle. Now 37, Ronan plays golf and squash and likes to swim to take his mind off the disease. A spokesperson for Parkinson's UK said playing sport "helps ease the mind". Parkinson's is thought to be linked to a chemical called dopamine, which is lacking in the brains of people with the condition. There are more than 40 symptoms and these can include vomiting as the body struggles to process food in the gut. Parkinson's can also affect people's mood. Often a person will feel they have got to grips with their condition and then a new symptom will emerge. It was while studying for his Irish history and politics degree that Ronan first noticed the symptoms. "I was writing notes for an essay and I couldn't write properly," he said. "Come exam time, I was under a lot of stress. It got really bad. "Then I noticed my walking was funny. I went to a couple of neurologists and they more or less said you have a tremor and that it was nothing to worry about." When Ronan turned 30 he was referred to a neurologist in Belfast. After a number of scans it was confirmed that he had the disease. © 2019 BBC

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 26658 - Posted: 10.01.2019

By Michelle Roberts Health editor, BBC News online A drug used to treat enlarged prostates may be a powerful medicine against Parkinson's disease, according to an international team of scientists. Terazosin helps ease benign prostatic hyperplasia (BPH) by relaxing the muscles of the bladder and prostate. But researchers believe it has another beneficial action, on brain cells damaged by Parkinson's. They say the drug might slow Parkinson's progression - something that is not possible currently. Cell death They studied thousands of patients with both BPH and Parkinson's. Their findings, published in the Journal of Clinical Investigation, suggest the alpha-blocker drug protects brain cells from destruction. Parkinson's is a progressive condition affecting the brain, for which there is currently no cure. Existing Parkinson's treatments can help with some of the symptoms but can't slow or reverse the loss of neurons that occurs with the disease. Terazosin may help by activating an enzyme called PGK1 to prevent this brain cell death, the researchers, from the University of Iowa, in the US and the Beijing Institute for Brain Disorders, China, say. When they tested the drug in rodents it appeared to slow or stop the loss of nerve cells. To begin assessing if the drug might have the same effect in people, they searched the medical records of millions of US patients to identify men with BPH and Parkinson's. They studied 2,880 Parkinson's patients taking terazosin or similar drugs that target PGK1 and a comparison group of 15,409 Parkinson's patients taking a different treatment for BPH that had no action on PGK1. Patients on the drugs targeting PGK1 appeared to fare better in terms of Parkinson's disease symptoms and progression, which the researchers say warrants more study in clinical trials, which they plan to begin this year. Lead researcher Dr Michael Welsh says while it is premature to talk about a cure, the findings have the potential to change the lives of people with Parkinson's. © 2019 BBC

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 26619 - Posted: 09.17.2019

Sarah Horn, M.D., and Howard Hurtig, M.D. While people usually regard Parkinson’s disease (PD) as a disorder characterized by abnormalities of the brain’s motorfunctions (movement), such as tremor, stiffness, and difficulties with balance and walking, there is less public awareness that non-motor features, such as cognitive impairment, are equally important. At some point during the long course of this progressive disorder, most patients will be confronted with one or more non-motor symptoms, some of which develop during the premotor or prodromalstage of the illness, when a loss of neurons is accumulating throughout the nervous system before the onset of the classic motor symptoms. Understanding the full range of motor and non-motor features of PD can alert people to recognize the earliest phases of PD and thereby proactively begin a partnership with a health care provider (usually a neurologist) to develop a comprehensive plan of management. In 1817, the British neurologist James Parkinson, in his essay The Shaking Palsy, accurately described through casual observation the same motor signs and symptoms of PD that we see today. He would never learn about the disease’s non-motor abnormalities, nor would he believe that intellect was affected. Much has changed in 200 years, but only in the last two decades has it become clear that non-motor features are an integral to the pathophysiology of PD. Such features have in fact become defining markers of the disease process, particularly during the prodromal stage of the disease. The recognition of PD as a common neurological disorder—caused by a lack of the chemical dopamine in the brain—has been bolstered by its prevalence among celebrities, including Muhammad Ali, Michael J. Fox, Linda Ronstadt, Pope John Paul II, and more recently Jesse Jackson and Alan Alda. The average age at diagnosis is 62.5 years, and an estimated 10 percent of patients are diagnosed at age 50 or younger .

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 26545 - Posted: 08.27.2019

Nicola Davis Evidence that Parkinson’s disease may start off in the gut is mounting, according to new research showing proteins thought to play a key role in the disease can spread from the gastrointestinal tract to the brain. The human body naturally forms a protein called alpha-synuclein which is found, among other places, in the brain in the endings of nerve cells. However, misfolded forms of this protein that clump together are linked to damage to nerve cells, a deterioration of the dopamine system and the development of problems with movement and speech – hallmarks of Parkinson’s disease. The latest findings, which are based on studies in mice, back up a long-held theory that abnormally folded alpha-synuclein may start off in the gut and then spread to the brain via the vagus nerve – a bundle of fibres that starts in the brainstem and transports signals to and from many of the body’s organs, including the gut. “It supports and really provides the first experimental evidence that Parkinson’s disease can start in the gut and go up the vagus nerve,” said Ted Dawson, professor of neurology at the Johns Hopkins University school of medicine and co-author of the research. The researchers say the way the misfolded alpha-synuclein spreads in the brains of the mice, and the animals’ symptoms, closely mirrors the disease in humans. Parkinson's disease 'could be detected early on by brain changes' © 2019 Guardian News & Media Limited

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: 26360 - Posted: 06.26.2019

Nicola Davis Changes in the brain that can be spotted years before physical symptoms of Parkinson’s disease occur might act as an early warning sign for the condition, researchers say. It is thought that about 145,000 people in the UK are living with Parkinson’s disease, a neurological condition that can lead to mobility problems, including slowness and tremors, as well as other symptoms such as memory difficulties. There are treatments to help manage symptoms but as yet the disease cannot be slowed or cured. The researchers, based at King’s College London, say the latest findings could eventually lead to new ways to identify people who might go on to develop Parkinson’s; the discoveries could also confirm diagnoses, monitor the disease progression, and aid the development and testing of drugs. Those developments could be some way off though, some scientists have said. Most of the time Parkinson’s appears to have no known cause, so people affected by the disease are not studied before their symptoms appear. But the King’s College studies concerned with genetic mutations making the development of Parkinson’s disease more likely, could point to the warning signs. Marios Politis, a professor and lead author of the research, said: “If you carry the gene [SNCA] it means it is almost certain you are going to develop Parkinson’s in the course of your life.” © 2019 Guardian News & Media Limited

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 26344 - Posted: 06.20.2019

By Anna Groves | Bipolar patients are seven times more likely to develop Parkinson’s disease, according to a new study. Though the news may be disheartening to those suffering from the already-trying condition, the link might also lead to clues about the causes behind the two conditions. Parkinson’s is a complex disease associated with a gradual decline in dopamine levels produced by neurons, or brain cells. It eventually leads to impaired movements and other bodily functions. The causes are unknown, and there is no cure. Bipolar disorder, also known as manic-depressive illness, is characterized by episodic fluctuations in mood, concentration or energy levels. Its causes are also unknown, though some bipolar-associated genes have been identified. Researchers are still figuring out how brain structure and function changes under the disease. Previous research has linked Parkinson’s with depression. So when the authors of the new study, most of whom are practicing physicians, noticed some of their bipolar patients developing Parkinson’s, they wondered if there was a connection. The study, out today in Neurology, was led by Huang Mao-Hsuan, who practices in the department of psychiatry at Taipei Veterans General Hospital. The researchers compared data from two groups of adults in the Taiwan National Health Insurance Research Database. Members of one group — over 56,000 individuals — were diagnosed with bipolar disorder between 2001 and 2009. The other — 225,000 individuals — had never been diagnosed with the disorder. No one in either cohort had received a Parkinson’s diagnosis and all the patients were over 20. And researchers ensured the two groups had similar ages, socioeconomic status, and other traits that might influence health.

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 5: The Sensorimotor System
Link ID: 26264 - Posted: 05.23.2019

By Pallab Ghosh Science correspondent, BBC News A treatment that has restored the movement of patients with chronic Parkinson's disease has been developed by Canadian researchers. Previously housebound patients are now able to walk more freely as a result of electrical stimulation to their spines. A quarter of patients have difficulty walking as the disease wears on, often freezing on the spot and falling. Parkinson's UK hailed its potential impact on an aspect of the disease where there is currently no treatment. Prof Mandar Jog, of Western University in London, Ontario, told BBC News the scale of benefit to patients of his new treatment was "beyond his wildest dreams". "Most of our patients have had the disease for 15 years and have not walked with any confidence for several years," he said. "For them to go from being home-bound, with the risk of falling, to being able to go on trips to the mall and have vacations is remarkable for me to see." Normal walking involves the brain sending instructions to the legs to move. It then receives signals back when the movement has been completed before sending instructions for the next step. Prof Jog believes Parkinson's disease reduces the signals coming back to the brain - breaking the loop and causing the patient to freeze. The implant his team has developed boosts that signal, enabling the patient to walk normally. However, Prof Jog was surprised that the treatment was long-lasting and worked even when the implant was turned off. He believes the electrical stimulus reawakens the feedback mechanism from legs to brain that is damaged by the disease. "This is a completely different rehabilitation therapy," he said. "We had thought that the movement problems occurred in Parkinson's patients because signals from the brain to the legs were not getting through. "But it seems that it's the signals getting back to the brain that are degraded." © 2019 BBC

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 26166 - Posted: 04.23.2019

Ian Sample Science editor Scientists have developed a test for Parkinson’s disease based on its signature odour after teaming up with a woman who can smell the condition before tremors and other clinical symptoms appear. The test could help doctors diagnose patients sooner and identify those in the earliest stages of the disease, who could benefit from experimental drugs that aim to protect brain cells from being killed off. Perdita Barran, of the University of Manchester, said the test had the potential to decrease the time it took to distinguish people with normal brain ageing from those with the first signs of the disorder. “Being able to say categorically, and early on, that a person has Parkinson’s disease would be very useful,” she said. Get Society Weekly: our newsletter for public service professionals Read more Most people cannot detect the scent of Parkinson’s, but some who have a heightened sense of smell report a distinctive, musky odour on patients. One such “super smeller” is Joy Milne, a former nurse, who first noticed the smell on her husband, Les, 12 years before he was diagnosed. Milne only realised she could sniff out Parkinson’s when she attended a patient support group with her husband and found everyone in the room smelled the same. She thought little more about it until she mentioned the odour to Tilo Kunath, a neurobiologist who studies Parkinson’s at Edinburgh University. © 2019 Guardian News & Media Limited

Related chapters from BN8e: Chapter 9: Hearing, Vestibular Perception, Taste, and Smell; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 6: Hearing, Balance, Taste, and Smell; Chapter 5: The Sensorimotor System
Link ID: 26056 - Posted: 03.20.2019

By Alex Therrien Health reporter, BBC News A radical Parkinson's treatment that delivers a drug directly to the brain has been tested in people. Patients in the trial were either given the drug, which is administered via a "port" in the side of the head, or a dummy treatment (placebo). Both groups showed improved symptoms, meaning it was not clear if the drug was responsible for the benefits. However, scans did find visual evidence of improvements to affected areas of the brain in those given the drug. The study's authors say it hints at the possibility of "reawakening" brain cells damaged by the condition. Other experts, though, say it is too early to know whether this finding might result in improvements in Parkinson's symptoms. Researchers believe the port implant could also be used to administer chemotherapy to those with brain tumours or to test new drugs for Alzheimer's and stroke patients. Parkinson's causes parts of the brain to become progressively damaged, resulting in a range of symptoms, such as involuntary shaking and stiff, inflexible muscles. About 145,000 people a year in the UK are diagnosed with the degenerative condition, which cannot be slowed down or reversed. For this new study, scientists gave patients an experimental treatment called glial cell line-derived neurotrophic factor (GDNF), in the hope it could regenerate dying brain cells and even reverse the condition. © 2019 BBC.

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: 25989 - Posted: 02.27.2019

By David Blum Many of us have personally experienced or witnessed the impact of Parkinson’s disease (PD), a movement disorder that affects nearly 10 million people worldwide. This chronic, progressive neurodegenerative disorder leads to disability from motor impairments, such as tremors, rigidity, absence or slowness of movement and impaired balance, as well as from non-motor symptoms including sleep disruption, gastrointestinal issues, sexual dysfunction or loss of sense of smell or taste, to name a few. The ideal outcome of PD clinical research would be to find a cure. But researchers are also looking at novel ways to administer proven Parkinson’s medicines in order to help people living with the disease better control their symptoms and maintain their regular, daily activities. The brain cells that die from PD are responsible for producing dopamine, a neurotransmitter involved in complex behaviors including motor coordination, addiction and motivation. As a result, treatment typically includes the use of levodopa—a medication that is converted into dopamine in the brain and relieves PD symptoms. For the first few years after diagnosis, many individuals’ symptoms are well controlled by levodopa. The average age of onset is 60, but some people are diagnosed at 40 or even younger, potentially requiring treatment for decades. Over time, a patient’s response to levodopa changes, and the therapeutic window, or period when levodopa is effective, narrows, often leading to the prescription of additional levodopa or more frequent dosing of levodopa to manage symptoms. © 2019 Scientific American

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 25883 - Posted: 01.19.2019

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