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 BN: 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 BN: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 4: Development of the Brain
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 BN: 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 BN: Chapter 11: Motor Control and Plasticity; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 2: 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 BN: 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 BN: 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 BN: 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 BN: 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 BN: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 4: Development of the Brain
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 BN: 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 BN: Chapter 11: Motor Control and Plasticity; Chapter 9: Hearing, Balance, Taste, and Smell
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 24438 - Posted: 12.19.2017

By GRETCHEN REYNOLDS Intense treadmill exercise can be safe for people who have recently been given diagnoses of Parkinson’s disease and may substantially slow the progression of their condition, according to an important new study of adults in the early stages of the disease. But the same study’s results also indicate that gentler exercise, while safe for people with Parkinson’s, does not seem to delay the disease’s advance. As most of us know, Parkinson’s disease is a progressive neurological disorder that involves problems with motor control. Symptoms like weakness, stiffness, loss of balance and falls can make exercise difficult and potentially hazardous. Though Parkinson’s is currently incurable, its symptoms can be eased for a time with various drugs. But most of those drugs lose their effectiveness in people over time. So some researchers have begun searching for other treatment options, particularly for use in the beginning stages of the disease. If people with early Parkinson’s could brake the disease’s advance and delay their need to start medications, the researchers have reasoned, they might change the arc of their disease, delaying its most severe effects. That possibility recently led a consortium of researchers from Northwestern University, the University of Colorado’s Anschutz Medical Campus in Aurora and other institutions to look at exercise as a treatment. There were precedents. Animal studies already had shown that exercise reduced symptoms and slowed physical decline in a rodent version of Parkinson’s. But rodents are not people. © 2017 The New York Times Company

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24423 - Posted: 12.14.2017

By Lydia Denworth A macaque monkey sat in front of a computer. A yellow square—the target—appeared in the periphery on the left side of the screen. After a few seconds delay, a second target appeared on the right. The question was: Which target would the monkey look at first? So far so routine as neuroscience experiments go, but the next step was unusual. By non-invasively directing bursts of inaudible acoustic energy at a specific visual area of the brain, a team of scientists steered the animal’s responses. If they focused on the left side of the brain, the monkey looked to the right more often. If they focused on the right side, the monkey looked to the left more often. The results of the experiment, which were presented last week at the annual Society for Neuroscience meeting, marked the first time that focused ultrasound was safely and effectively used in a nonhuman primate to alter brain activity rather than destroy tissue. A second study, in sheep, had similar results. “The finding paves the way to noninvasive stimulation of specific brain regions in humans,” says Jan Kubanek, a neural engineer at Stanford University School of Medicine and lead author of the macaque study. The technology might ultimately be used to diagnose or treat neurological diseases and disorders like Parkinson’s disease, epilepsy, addiction and depression. Other scientists are optimistic. “The idea that, with a very carefully designed dose, you could actually deliver [focused ultrasound] and stimulate the brain in the place you want and modulate a circuit rather than damage it, is a really important proof of principle,” said Helen Mayberg, MD, of Emory University School of Medicine, who was not involved with the study. © 2017 Scientific American

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 24384 - Posted: 12.01.2017

By NIRAJ CHOKSHI The Rev. Jesse L. Jackson, the longtime civil rights leader and former Democratic presidential candidate, said Friday he has Parkinson’s disease. In a letter posted on Twitter on Friday afternoon, Mr. Jackson, 76, shared the news and his struggle to accept it. “Recognition of the effects of this disease on me has been painful, and I have been slow to grasp the gravity of it,” he wrote. “For me, a Parkinson’s diagnosis is not a stop sign but rather a signal that I must make lifestyle changes and dedicate myself to physical therapy in hopes of slowing the disease’s progression.” Parkinson’s is a movement disorder. Its symptoms include muscle tremors and stiffness and poor balance and coordination. It typically begins after age 50 and can cause difficulty sleeping, chewing, swallowing or speaking. Mr. Jackson has been a civil rights advocate for 50 years and sought the Democratic presidential nominations in 1984 and 1988. He was also a close associate of the Rev. Dr. Martin Luther King Jr. Mr. Jackson wrote that he and his family about three years ago began to notice he was having increasing difficulty performing routine tasks and was initially reluctant to see doctors. He said he saw the diagnosis as “an opportunity” to use his platform to advocate a cure and said that he would not let it disrupt his other advocacy. “I will continue to try to instill hope in the hopeless, expand our democracy to the disenfranchised and free innocent prisoners around the world,” he wrote. © 2017 The New York Times Company

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24338 - Posted: 11.20.2017

By RONI CARYN RABIN A. Parkinsonism refers to a group of movement abnormalities — such as stiffness, slowness, shuffling of the feet and often tremor — that are classic features of Parkinson’s disease but that can also be caused by medications and other disorders with overlapping symptoms, said Dr. Michael S. Okun, a neurologist and the national medical director of the Parkinson’s Foundation. He said that he makes no assumptions about the cause of parkinsonism “until I see the patient and pinpoint the diagnosis.” Determining the cause of parkinsonism involves asking a series of questions, starting with, “Do we think this is regular Parkinson’s disease?” said Dr. Okun, who is also co-director of the Center for Movement Disorders and Neurorestoration at the University of Florida College of Medicine in Gainesville. Though a diagnosis of Parkinson’s disease strikes fear in patients, Dr. Okun said that the illness, a neurodegenerative brain disorder caused by the loss of dopamine-containing neurons and other cells, progresses slowly in many people and generally responds well to drugs that replenish dopamine in the brain. Some patients whose parkinsonism is not caused by Parkinson’s disease also respond to these drugs, but the medications are most effective for people with Parkinson’s disease, Dr. Okun said. It’s important to rule out other potential causes of parkinsonism, he said. The condition can be triggered by antipsychotic medications that affect dopamine levels in the brain, as well as by other drugs, including stimulants like amphetamines and cocaine. Discontinuing the drugs may stop the symptoms over time, though not always. Parkinsonism may also be caused by repeated injuries to the head, exposure to various toxins or brain lesions. Once doctors rule out Parkinson’s disease, they must consider several other serious neurological disorders. The three most common ones are multiple system atrophy, a degenerative disorder also referred to as Shy-Drager syndrome, which may or may not respond well to Parkinson’s medications; progressive supranuclear palsy, or PSP, which also may respond to high doses of drugs that replace dopamine in the brain; and corticobasal degeneration (CBD). Patients with a form of dementia called Lewy body dementia may also exhibit symptoms of parkinsonism, which may or may not respond to dopamine. Various other movement disorders, called ataxias or dystonias, also may display features of parkinsonism. © 2017 The New York Times Company

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24335 - Posted: 11.17.2017

A new study published in the journal Neuron sheds light on the normal function of LRRK2, the most common genetic cause for late-onset Parkinson’s disease. The study was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. For more than 10 years, scientists have known that mutations in the LRRK2 gene can lead to Parkinson’s disease, yet both its role in the disease and its normal function in the brain remain unclear. In a study in mice, researchers have now found that LRRK is necessary for the survival of dopamine-containing neurons in the brain, the cells most affected by Parkinson’s. Importantly, this finding could alter the design of treatments against the disease. “Since its discovery, researchers have been trying to define LRRK2 function and how mutations may lead to Parkinson’s disease,” said Beth-Anne Sieber, Ph.D., program director at NINDS. “The findings in this paper emphasize the importance of understanding the normal role for genes associated with neurodegenerative disorders.” LRRK2 is found along with a closely related protein, LRRK1, in the brain. A mutation in LRRK2 alone can eventually produce Parkinson’s disease symptoms and brain pathology in humans as they age. In mice, however, LRRK2 loss or mutation does not lead to the death of dopamine-producing neurons, possibly because LRRK1 plays a complementary or compensatory role during the relatively short, two-year mouse lifespan.

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24254 - Posted: 10.28.2017

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 BN: Chapter 11: Motor Control and Plasticity; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 2: 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 BN: 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 BN: 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 BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24023 - Posted: 09.01.2017