Links for Keyword: Parkinsons

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By Dan Stark I used to tell people considering deep brain stimulation — which involves the surgical implantation of electrodes into the brain — that it gave the typical Parkinson’s sufferer perhaps 10 years of relief, during which the symptoms would be relatively minor. The bet — this is, after all, brain surgery that carries some risk of serious adverse results — would be that sometime during that decade, researchers would come up with a real solution. In other words, DBS was a way to buy time. Still, 10 years is no small period, particularly for those who have no other hope. My experience is typical. I had DBS just under 12 years ago. Things went so well that I became a huge fan of the procedure. But DBS works on only some Parkinson’s symptoms. (Drooling, for example, is not affected.) For slightly more than a decade, DBS performed wonders on me, eliminating the shakes that had accompanied my attempts to beat back Parkinson’s symptoms with medicine alone. But because DBS masks the symptoms while not affecting the underlying disease, in the end it will fail the Parkinson’s patient. For me, the failure was in the form of a one-two punch. The first blow was self-inflicted. In April, one of the batteries powering my neural implants died. That was my fault; one should monitor the batteries and replace them in advance. Because I hadn’t, I got a taste of what life would be like without the stimulators. © 1996-2017 The Washington Post

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: 24132 - Posted: 10.02.2017

Laura Sanders The brain chemical missing in Parkinson’s disease may have a hand in its own death. Dopamine, the neurotransmitter that helps keep body movements fluid, can kick off a toxic chain reaction that ultimately kills the nerve cells that make it, a new study suggests. By studying lab dishes of human nerve cells, or neurons, derived from Parkinson’s patients, researchers found that a harmful form of dopamine can inflict damage on cells in multiple ways. The result, published online September 7 in Science, “brings multiple pieces of the puzzle together,” says neuroscientist Teresa Hastings of the University of Pittsburgh School of Medicine. The finding also hints at a potential treatment for the estimated 10 million people worldwide with Parkinson’s: Less cellular damage occurred when some of the neurons were treated early on with antioxidants, molecules that can scoop up harmful chemicals inside cells. Study coauthor Dimitri Krainc, a neurologist and neuroscientist at Northwestern University Feinberg School of Medicine in Chicago, and colleagues took skin biopsies from healthy people and people with one of two types of Parkinson’s disease, inherited or spontaneously arising. The researchers then coaxed these skin cells into becoming dopamine-producing neurons. These cells were similar to those found in the substantia nigra, the movement-related region of the brain that degenerates in Parkinson’s. |© Society for Science & the Public 2000 - 2017.

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24049 - Posted: 09.08.2017

A test that involves drawing a spiral on a sheet of paper could be used to diagnose early Parkinson's disease. Australian researchers have trialled software that measures writing speed and pen pressure on the page. Both are useful for detecting the disease, which causes shaking and muscle rigidity. The Melbourne team said the test could be used by GPs to screen their patients after middle age and to monitor the effect of treatments. The study, published in Frontiers of Neurology, involved 55 people - 27 had Parkinson's and 28 did not. Speed of writing and pen pressure while sketching are lower among Parkinson's patients, particularly those with a severe form of the disease. Image copyright RMIT University Image caption Treatment options are effective only when the disease is diagnosed early In the trial, a tablet computer with special software took measurements during the drawing test and was able to distinguish those with the disease, and how severe it was. Poonam Zham, study researcher from RMIT University, said: "Our aim was to develop an affordable and automated electronic system for early-stage diagnosis of Parkinson's disease, which could be easily used by a community doctor or nursing staff." The system combines pen speed and pressure into one measurement, which can be used to tell how severe the disease is. David Dexter, deputy research director at Parkinson's UK, said current tests for the disease were not able to accurately measure how advanced someone's condition was. "This can impact on the ability to select the right people for clinical research, which is essential to develop new and better treatments for Parkinson's. "This new test could provide a more accurate assessment by measuring a wider range of features that may be affected by Parkinson's, such as co-ordination, pressure, speed and cognitive function." He added that the test could be a "stepping stone" to better clinical trials for Parkinson's. © 2017 BBC.

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24042 - Posted: 09.07.2017

By Mitch Leslie When people with asthma have trouble breathing, they may reach for an inhaler containing salbutamol, a drug that expands the airways. Salbutamol may have another beneficial effect—protecting against Parkinson’s disease. Individuals who inhaled the highest doses of salbutamol were about half as likely to develop the devastating neurological condition as those who didn’t take the drug, a study reveals. “I’m sure it’s going to be a landmark paper,” says neurologist Joseph Jankovic of Baylor College of Medicine in Houston, Texas, who wasn’t involved in the research. In Parkinson’s disease, gobs of the protein α-synuclein accumulate in certain brain cells and may kill them. Scientists have tried to craft drugs that speed the elimination of the protein or prevent it from clumping. Neurologist and genomicist Clemens Scherzer of Harvard Medical School in Boston and colleagues decided to try a different strategy. “We wanted to find a drug that could turn down the production of α-synuclein,” he says. To identify promising compounds, the team grew human nerve cells in the lab and tested whether more than 1100 medications, vitamins, dietary supplements, and other molecules altered their output of α-synuclein. Three of the drugs that cut the protein’s production, including salbutamol, work by stimulating the b2-adrenoreceptor—a molecule on some body cells that triggers a variety of effects, including relaxing the airways. The researchers found that these drugs appear to alter how tightly the DNA containing the α-synuclein gene coils, and thus whether the gene is active. © 2017 American Association for the Advancement of Science

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24023 - Posted: 09.01.2017

Ewen Callaway Japanese researchers report promising results from an experimental therapy for Parkinson’s disease that involves implanting neurons made from ‘reprogrammed’ stem cells into the brain. A trial conducted in monkeys with a version of the disease showed that the treatment improved their symptoms and seemed to be safe, according to a report published on 30 August in Nature1. The study’s key finding — that the implanted cells survived in the brain for at least two years without causing any dangerous effects in the body — provides a major boost to researchers’ hopes of testing stem-cell treatments for Parkinson’s in humans, say scientists. Jun Takahashi, a stem-cell scientist at Kyoto University in Japan who led the study, says that his team plans to begin transplanting neurons made from induced pluripotent stem (iPS) cells into people with Parkinson’s in clinical trials soon. The research is also likely to inform several other groups worldwide that are testing different approaches to treating Parkinson’s using stem cells, with trials also slated to begin soon. Parkinson’s is a neurodegenerative condition caused by the death of cells called dopaminergic neurons, which make a neurotransmitter called dopamine in certain areas of the brain. Because dopamine-producing brain cells are involved in movement, people with the condition experience characteristic tremors and stiff muscles. Current treatments address symptoms of the disease but not the underlying cause. © 2017 Macmillan Publishers 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: 24019 - Posted: 08.31.2017

By Mo Costandi Voluntary movements are one of the brain’s main “outputs,” yet science still knows very little about how networks of neurons plan, initiate and execute them. Now, researchers from Columbia University and the Champalimaud Center for the Unknown in Lisbon, Portugal, say they have discovered an “activity map” that the brain uses to guide animals’ movements. The findings, published Wednesday in Neuron, could advance our understanding of how the brain learns new movements—and of what goes wrong in related disorders such as Parkinson's disease. Movements are controlled and coordinated by multiple brain structures including the primary motor cortex. Located at the back of the frontal lobe, it contains cells whose long fibers extend down through the spinal cord, where they contact “secondary” motor neurons that signal the body muscles. A set of deep brain structures called the basal ganglia are also critical for movement, as evidenced by their degeneration in conditions such as Parkinson’s. One component of the basal ganglia, called the striatum, receives information about possible actions from the motor cortex and is thought to be involved in selecting, preparing and executing the appropriate commands before they are sent to the body. Earlier research had shown that signals leave the striatum along one of two distinct pathways: one that facilitates movement, and another that suppresses it. A number of more recent studies show that both pathways are active during motion, however, suggesting that they do not act by simply sending “stop” and “go” signals. And although it has long been suspected that different groups of neurons in the striatum represent distinct actions, exactly how they might do so has remained unclear. © 2017 Scientific American

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: 24016 - Posted: 08.31.2017

Nicola Davis A drug commonly used to treat diabetes could help those living with Parkinson’s disease, research has revealed. By 2020 it is predicted that 162,000 individuals in the UK will be living with the condition. While existing drugs help to control its symptoms, there are currently none available which slow or halt its progression. But now scientists say they have found that a drug commonly used to treat type 2 diabetes appears to improve movement-related issues. The benefit persisted even when the drug had not been taken for 12 weeks, suggesting it might be helping to slow the progression of the disease. “It is not ready for us to say ‘well, everyone needs to start this drug’,” said Thomas Foltynie, professor of neurology at University College London and co-author of the study. “[But] if we can replicate these findings in a multicentre trial, especially with longer follow-up, then this can change the face of our approach to treating Parkinson’s.” Writing in the Lancet, Foltynie and colleagues in the UK and US describe how they tested the impact of the drug, known as exenatide. With recent studies suggesting problems with insulin signalling in the brain could be linked to neurodegenerative disorders, hopes have been raised that diabetes drugs could also be used to tackle Parkinson’s, with previous research – including in cell cultures and animals, as well as a recent pilot study on humans by Foltynie and colleagues – backing up the notion.. But the latest study is the first robust clinical trial of the drug, randomly allocating 60 people with Parkinson’s to one of two treatments – either receiving injections of exenatide or a placebo once a week. © 2017 Guardian News and 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: 23918 - Posted: 08.05.2017

By Meredith Wadman The hallmark brain damage in Parkinson’s disease is thought to be the work of a misfolded, rogue protein that spreads from brain cell to brain cell like an infection. Now, researchers have found that the normal form of the protein—α-synuclein (αS)—may actually defend the intestines against invaders by marshaling key immune cells. But chronic intestinal infections could ultimately cause Parkinson’s, the scientists suggest, if αS migrates from overloaded nerves in the gut wall to the brain. “The gut-brain immune axis seems to be on a cusp of an explosion of new insights, and this work offers an exceptionally exciting new hypothesis,” says Charles Bevins, an expert in intestinal immunity at the University of California, Davis, who was not involved with the study. The normal function of αS has long been a mystery. Though the protein is known to accumulate in toxic clumps in the brain and the nerves of the gut wall in patients with Parkinson’s disease, no one was sure what it did in healthy people. Noting that a region of the αS molecule behaves similarly to small, microbe-targeting proteins that are part of the body’s immune defenses, Michael Zasloff, an immunologist at Georgetown University Medical Center in Washington, D.C., set out to find whether αS, too, might help fend off microbial invaders. © 2017 American Association for the Advancement of Science

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: 23784 - Posted: 06.28.2017

By Alice Klein EVIDENCE that Parkinson’s disease may be an autoimmune disorder could lead to new ways to treat the illness. Parkinson’s begins with abnormal clumping of a protein called synuclein in the brain. Neighbouring dopamine-producing neurons then die, causing tremors and difficulty moving. The prevailing wisdom has been that these neurons die from a toxic reaction to synuclein deposits. However, Parkinson’s has been linked to some gene variants that affect how the immune system works, leading to an alternative theory that synuclein causes Parkinson’s by triggering the immune system to attack the brain. An argument against this theory has been that brain cells are safe from immune system attack, because most neurons don’t have antigens – the markers immune cells use to recognise a target. But by studying postmortem brain tissue samples, David Sulzer at Columbia University and his team have discovered that dopamine-producing neurons do display antigens. The team has now conducted blood tests to reveal that people with Parkinson’s show an immune response to these antigens, while people who don’t have the condition do not (Nature, DOI: 10.1038/nature22815). These findings suggest Parkinson’s may be an autoimmune disorder, in which the immune system mistakenly attacks part of the body. There have been hints before that the immune system is involved in Parkinson’s, but this is the first evidence that it plays a major pathological role, says Roger Barker at the University of Cambridge. “It would be an attractive target for therapeutic intervention,” he says. However, it isn’t clear yet if the immune response directly causes neuron death, or if it is merely a side effect of the disease. Sulzer’s team plans to try blocking the autoimmune response in Parkinson’s, to see if this can stop the disease progressing. © Copyright New Scientist Ltd.

Related chapters from BN8e: 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: 23760 - Posted: 06.22.2017

Parkinson’s disease is commonly thought of as a movement disorder, but after years of living with the disease, approximately 25 percent of patients also experience deficits in cognition that impair function. A newly developed research tool may help predict a patient’s risk for developing dementia and could enable clinical trials aimed at finding treatments to prevent the cognitive effects of the disease. The research was published in Lancet Neurology and was partially funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “This study includes both genetic and clinical assessments from multiple groups of patients, and it represents a significant step forward in our ability to effectively model one of the most troublesome non-motor aspects of Parkinson’s disease,” said Margaret Sutherland, Ph.D., program director at the NINDS. For the study, a team of researchers led by Clemens Scherzer, M.D., combined data from 3,200 people with Parkinson’s disease, representing more than 25,000 individual clinical assessments and evaluated seven known clinical and genetic risk factors associated with developing dementia. From this information, they built a computer-based risk calculator that may predict the chance that an individual with Parkinson’s will develop cognitive deficits. Dr. Scherzer is head of the Neurogenomics Lab and Parkinson Personalized Medicine Program at Harvard Medical School and a member of the Ann Romney Center for Neurologic Diseases at Brigham and Women’s Hospital, Boston.

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 23759 - Posted: 06.22.2017

Jon Hamilton Researchers are working to revive a radical treatment for Parkinson's disease. The treatment involves transplanting healthy brain cells to replace cells killed off by the disease. It's an approach that was tried decades ago and then set aside after disappointing results. Now, groups in Europe, the U.S. and Asia are preparing to try again, using cells they believe are safer and more effective. "There have been massive advances," says Claire Henchcliffe, a neurologist at Weill Cornell Medicine in New York. "I'm optimistic." "We are very optimistic about ability of [the new] cells to improve patients' symptoms," says Viviane Tabar, a neurosurgeon and stem cell biologist at Memorial Sloan Kettering Cancer Center in New York. Henchcliffe and Tabar joined several other prominent scientists to describe plans to revive brain cell transplants during a session Tuesday at the International Society for Stem Cell Research meeting in Boston. Their upbeat message marks a dramatic turnaround for the approach. During the 1980s and 1990s, researchers used cells taken directly from the brains of aborted fetuses to treat hundreds of Parkinson's patients. The goal was to halt the disease. © 2017 npr

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: 23738 - Posted: 06.14.2017

By Clare Wilson Would you have pig cells implanted in your brain? Some people with Parkinson’s disease have, in the hope it will stop their disease progressing. The approach is still in the early stages of testing, but initial results from four people look promising, with all showing some improvement 18 months after surgery. People with Parkinson’s disease, which causes tremors and difficulty moving, usually get worse over time. The disease is caused by the gradual loss of brain cells that make dopamine, a compound that helps control our movements. Current medicines replace the missing dopamine, but their effectiveness wears off over the years. So Living Cell Technologies, based in Auckland, New Zealand, has been developing a treatment that uses cells from the choroid plexus in pigs. This brain structure makes a cocktail of growth factors and signalling molecules known to help keep nerve cells healthy. Last month, surgery was completed on a further 18 people in a placebo-controlled trial, using the choroid plexus cell implants. The hope is that compounds made by these cells will nourish the remaining dopamine-producing cells in the patients’ brains, slowing further loss. © Copyright New Scientist Ltd.

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: 23731 - Posted: 06.12.2017

Mo Costandi Since 1997, more than 100,000 Parkinson’s Disease patients have been treated with deep brain stimulation (DBS), a surgical technique that involves the implantation of ultra-thin wire electrodes. The implanted device, sometimes referred to as a ‘brain pacemaker’, delivers electrical pulses to a structure called the subthalamic nucleus, located near the centre of the brain, and effectively alleviates many of the physical symptoms of the disease, such as tremor, muscle rigidity, and slowed movements. DBS is generally safe but, like any surgical procedure, comes with some risks. First and foremost, it is highly invasive, requiring small holes to be drilled in the patient’s skull, through which the electrodes are inserted. Potential complications of this include infection, stroke, and bleeding on the brain. The electrodes, which are implanted for long periods of time, sometimes move out of place; they can also cause swelling at the implantation site; and the wire connecting them to the battery, typically placed under the skin of the chest, can erode, all of which require additional surgical procedures. Now, researchers at the Massachusetts Institute of Technology have a developed a new method that can stimulate cells deep inside the brain non-invasively, using multiple electric fields applied from outside the organ. In a study published today in the journal Neuron, they show that the method can selectively stimulate deep brain structures in live mice, without affecting the activity of cells in the overlying regions, and also that it can be easily adjusted to evoke movements by stimulation of the motor cortex. © 2017 Guardian News and Media Limited o

Related chapters from BN8e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 5: The Sensorimotor System
Link ID: 23700 - Posted: 06.02.2017

By: Ted Dinan, M.D., Ph.D, and John F. Cryan, Ph.D. O ver the past few years, the gut microbiota has been implicated in developmental disorders such as schizophrenia and autism, neurodegenerative disorders such as Alzheimer’s disease and Parkinson’s disease, mood disorders such as depression, and even addiction disorders. It now seems strange that for so many decades we viewed the gut microbiota as bacteria that did us no harm but were of little benefit. This erroneous view has been radically transformed into the belief that the gut microbiota is, in effect, a virtual organ of immense importance. What we’ve learned is that what is commonly referred to as “the brain-gut-microbiota axis” is a bidirectional system that enables gut microbes to communicate with the brain and the brain to communicate back to the gut. It may be hard to believe that the microbes in the gut collectively weigh around three pounds—the approximate weight of the adult human brain—and contain ten times the number of cells in our bodies and over 100 times as many genes as our genome. 1 If the essential microbial genes were to be incorporated into our genomes, it is likely that our cells would not be large enough for the extra DNA. Many of those genes in our microbiota are important for brain development and function; they enable gut bacteria to synthesize numerous neurotransmitters and neuromodulators such as γ-aminobutyric acid (GABA), serotonin, dopamine, and short-chain fatty acids. While some of these compounds act locally in the gut, many products of the microbiota are transported widely and are necessary for the proper functioning of diverse organs. This is a two-way interaction: gut microbes are dependent on us for their nourishment. Any pathological process that reduces or increases food intake has implications for our microbes. © 2017 The Dana Foundation. All Rights Reserved.

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: 23636 - Posted: 05.19.2017

By Andy Coghlan Using a virus to reprogram cells in the brain could be a radical way to treat Parkinson’s disease. People with Parkinson’s have difficulty controlling their movements due to the death of neurons that make dopamine, a brain signalling chemical. Transplants of fetal cells have shown promise for replacing these dead neurons in people with the disease, and a trial is currently under way. But the transplant tissue comes from aborted pregnancies, meaning it is in short supply, and some people may find this ethically difficult. Recipients of these cells have to take immunosuppressant drugs too. Ernest Arenas, at the Karolinska Institute in Stockholm, Sweden, and his team have found a new way to replace lost dopamine-making neurons. They injected a virus into the brains of mice whose dopamine neurons had been destroyed. This virus had been engineered to carry four genes for reprogramming astrocytes – the brain’s support cells – into dopamine neurons. Five weeks later, the team saw improvements in how the mice moved. “They walked better and their gait showed less asymmetry than controls,” says Arenas. This is the first study to show that reprogramming cells in the living brain can lead to such improvements, he says. © Copyright Reed Business Information Ltd.

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 23488 - Posted: 04.14.2017

By Knvul Sheikh For the past five decades pharmaceutical drugs like levodopa have been the gold standard for treating Parkinson’s disease. These medications alleviate motor symptoms of the disease, but none of them can cure it. Patients with Parkinson’s continue to lose dopamine neurons critical to the motor control centers of the brain. Eventually the drugs become ineffective and patients’ tremors get worse. They experience a loss of balance and a debilitating stiffness takes over their legs. To replace the lost dopamine neurons, scientists have begun investigating stem cell therapy as a potential treatment or even a cure. But embryonic cells and adult stem cells have proved difficult to harness and transplant into the brain. Now a study from the Karolinska Institute in Stockholm shows it is possible to coax the brain’s own astrocytes—cells that typically support and nurture neurons—into producing a new generation of dopamine neurons. The reprogrammed cells display several of the properties and functions of native dopamine neurons and could alter the course of Parkinson’s, according to the researchers. “You can directly reprogram a cell that is already inside the brain and change the function in such a way that you can improve neurological symptoms,” says senior author Ernest Arenas, a professor of medical biochemistry at Karolinska. Previously, scientists had to nudge specialized cells like neurons into becoming pluripotent cells before they could develop a different kind of specialized cell, he says. It was like having to erase all the written instructions for how a cell should develop and what job it should do and then rewriting them all over again. But Arenas and his team found a way to convert the instructions into a different set of commands without erasing them. © 2017 Scientific American

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: 23475 - Posted: 04.11.2017

By NICHOLAS BAKALAR Hepatitis infection may increase the risk for Parkinson’s disease, though the reasons for the link remain unknown. British investigators used records of 100,390 patients hospitalized with various forms of hepatitis or H.I.V. from 1999 to 2011. They compared Parkinson’s incidence in these patients with incidence in more than six million people admitted for medical or surgical conditions like cataracts, knee replacement or varicose veins. The study, in Neurology, found that people with hepatitis B had a 76 percent higher risk of having Parkinson’s, and people with hepatitis C a 51 percent higher risk, than the control group. Those with other forms of hepatitis or H.I.V. had no increased risk. The study was restricted to hospitalized patients, and the authors did not have detailed information about the severity and treatment of the diseases. “We can’t be sure what is underlying this association,” said the lead author, Dr. Julia Pakpoor, a researcher at the University of Oxford. “It could be the treatment for the hepatitis, or it could be that Parkinson’s and hepatitis have common risk factors we haven’t identified.” A different kind of study would be needed, she said, to determine possible mechanisms that might be involved. © 2017 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: 23430 - Posted: 03.31.2017

By Timothy Revell A smartphone app that uses deep learning lets people with Parkinson’s disease test their symptoms at home in just 4 minutes. The app could help people monitor the disease’s progression more closely, and uncover how lifestyle factors may affect their symptoms. “There’s very little understanding as to how Parkinson’s arises, and patients say that every day the condition is different,” says George Roussos at Birkbeck, University of London. People report symptom changes related to everything from exercise to socialising to diet, but it’s not yet possible to build a solid picture of how these factors interact. “To understand these differences, we need to monitor the condition regularly, in a quick and easy way, over a long period of time,” says Roussos. People with Parkinson’s usually only see a specialist once or twice a year. This makes it hard to track the disease progression in an individual in detail, and means that side effects of medication such as deterioration of mood can go unnoticed. With their Android app, called CloudUPDRS, Roussos and his colleagues want to make it easier to track symptoms and flag potential problems earlier. Similar to how a clinician would conduct a Parkinson’s severity test, the app includes both self-assessment questions and physical tests using a smartphone’s sensors. © Copyright Reed Business Information Ltd.

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 23313 - Posted: 03.04.2017

Swedish researchers say a simple blood test is effective at differentiating symptoms of Parkinson's disease from similar disorders, but it isn't ready for clinical use. In its early stages, neurologists say Parkinson's is difficult to distinguish from rarer disorders, called atypical parkinsonian disorders. They have overlapping symptoms that tend to worsen more quickly and are more likely to lead to death. Researchers are on the hunt for biomarkers to help diagnosis these disorders. One potential biomarker, a nerve protein that can be detected when nerve cells die, is found in higher concentrations in spinal fluid collected by lumbar puncture. Now medical scientists have also found the protein in less invasive blood tests. For the study published in Wednesday's online issue of the journal Neurology, Dr. Oskar Hansson of Sweden's Lund University and his team examined 504 people in three groups. Two of the groups, in England and Sweden, included healthy people and those who had been living with one of the disorders for an average of four to six years. The third group of 109 patients had the diseases for three years or less. "The results of the present study strongly indicate that NfL when measured in blood can be used to distinguish between patients with Parkinson's disease and patients with progressive supranuclear palsy multiple system atrophy and corticobasal degeneration with high diagnostic accuracy," the study's authors said. ©2017 CBC/Radio-Canada.

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 23206 - Posted: 02.09.2017

By JANE E. BRODY Susan Sills, a Brooklyn artist who until recently made life-size cutouts on plywood using a power saw, long suspected she might be at risk for developing Parkinson’s disease. Both her mother and grandfather had this neurological movement disorder, and she knew that it sometimes runs in families. So she was not surprised when at age 72 she first noticed hand tremors and a neurologist confirmed that she had the disease. But to watch her in action three years later, it would be hard for a layperson to tell. She stands straight, walks briskly, speaks in clarion tones and maintains a schedule that could tire someone half her age. Having wisely put the power saw aside, Ms. Sills now makes intricately designed art jewelry. She is also a docent at the Brooklyn Museum, participates in a cooperative art gallery and assists her husband’s business by entertaining customers. Ms. Sills attributes her energy and well-being partly to the medication she takes but primarily to the hours she spends working out with a physical therapist and personal trainer, who have helped her develop an exercise regimen that, while not a cure, can alleviate Parkinson’s symptoms and slow progression of the disease. “The exercises opened me up,” said Ms. Sills, allowing such symptoms as small steps, slow movements and tiny, cramped handwriting to subside. “The earlier people begin exercising after a Parkinson’s diagnosis, and the higher the intensity of exercise they achieve, the better they are,” Marilyn Moffat, a physical therapist on the faculty of New York University, said. “Many different activities have been shown to be beneficial, including cycling, boxing, dancing and walking forward and backward on a treadmill. If someone doesn’t like one activity, there are others that can have equally good results.” © 2017 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: 23132 - Posted: 01.23.2017