Links for Keyword: Parkinsons

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By Gunjan Sinha Light therapy can help lift moods, heal wounds, and boost the immune system. Can it improve symptoms of Parkinson’s disease, too? A first-of-its-kind trial scheduled to launch this fall in France aims to find out. In seven patients, a fiber optic cable implanted in their brain will deliver pulses of near-infrared (NIR) light directly to the substantia nigra, a region deep in the brain that degenerates in Parkinson’s disease. The team, led by neurosurgeon Alim- Louis Benabid of the Clinatec Institute—a partnership between several government-funded research institutes and industry—hopes the light will protect cells there from dying. The study is one of several set to explore how Parkinson’s patients might benefit from light. “I am so excited,” says neuropsychologist Dawn Bowers of the University of Florida College of Medicine, who is recruiting patients for a trial in which NIR will be beamed into the skull instead of delivered with an implant. Small tests in people with Parkinson’s and animal models of the disease have already suggested benefits, but some mainstream Parkinson’s researchers are skeptical. No one has shown exactly how light might protect the key neurons—or why it should have any effect at all on cells buried deep in the brain that never see the light of day. Much or all of the encouraging hints seen so far in people may be the result of the placebo effect, skeptics say. Because there are no biomarkers that correlate well with changes in Parkinson’s symptoms, “we are reliant on observing behavior,” says neurobiologist David Sulzer of Columbia University Irving Medical Center, an editor of the journal npj Parkinson’s Disease. “It’s not easy to guard against placebo effects.” © 2020 American Association for the Advancement of Science

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 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27482 - Posted: 09.19.2020

By Laura J. Snyder I’m an inveterate storyteller,” confesses the celebrated neurologist and writer Oliver Sacks at the start of Oliver Sacks: His Own Life. “I tell many stories, some comic, some tragic.” Tales of both types abound in this elegiac yet lighthearted film based on director Ric Burns’s interviews with Sacks and his friends, colleagues, family members, and patients in the months before and after the physician’s death in 2015 at the age of 82. The result is a vivid portrait of an ebullient, provocative, brilliant man who transformed the practice of medicine and spearheaded the neurodiversity movement. Born into an upper-middle-class Jewish family in northwest London in 1933, Sacks was the youngest of four sons. He was an outsider: one of only three Jews at his elite prep school; a gay adolescent at a time when gay sex was illegal; an introverted, dreamy, chemistry-obsessed boy in a family of accomplished physicians. His father was a general practitioner who made house calls, and his mother was one of the first female surgeons in England. His two eldest brothers were already studying medicine when he was in high school. Sacks dutifully followed his expected career path and was drawn to neurology when his third brother, Michael, developed schizophrenia. But after completing medical training, Sacks fled the homophobic confines of his nation and family—his mother had called him “an abomination.” Paul Theroux tells Burns that Sacks’s “great luck” was ending up in Los Angeles in 1960, where he found ample “guys, weights, drugs, and hospitals.” © 2020 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: 27477 - Posted: 09.19.2020

By Jane E. Brody Michael Richard Clifford, a 66-year-old retired astronaut living in Cary, N.C., learned before his third spaceflight that he had Parkinson’s disease. He was only 44 and in excellent health at the time, and had no family history of this disabling neurological disorder. What he did have was years of exposure to numerous toxic chemicals, several of which have since been shown in animal studies to cause the kind of brain damage and symptoms that afflict people with Parkinson’s. As a youngster, Mr. Clifford said, he worked in a gas station using degreasers to clean car engines. He also worked on a farm where he used pesticides and in fields where DDT was sprayed. Then, as an aviator, he cleaned engines readying them for test flights. But at none of these jobs was he protected from exposure to hazardous chemicals that are readily inhaled or absorbed through the skin. Now Mr. Clifford, a lifelong nonsmoker, believes that his close contact with these various substances explains why he developed Parkinson’s disease at such a young age. Several of the chemicals have strong links to Parkinson’s, and a growing body of evidence suggests that exposure to them may very well account for the dramatic rise in the diagnosis of Parkinson’s in recent decades. To be sure, the medical literature is replete with associations between people’s habits and exposures and their subsequent risk of developing various ailments, from allergies to heart disease and cancer. Such linkages do not — and cannot by themselves — prove cause and effect. Sometimes, though, the links are so strong and the evidence so compelling that there can be little doubt that one causes the other. The link of cigarette smoking to lung cancer is a classic example. Despite tobacco industry claims that there was no definitive proof, the accumulation of evidence, both experimental and epidemiological, eventually made it impossible to deny that years of smoking can cause cancer even long after a person has quit. © 2020 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: 27378 - Posted: 07.21.2020

Ruth Williams Turning off just one factor in the brain’s astrocyte cells is sufficient to convert them into neurons in live mice, according to a paper published in Nature today (June 24) and one this spring by another research team in Cell. By flipping this cellular identity switch, researchers have, to some extent, been able to reverse the neuron loss and motor deficits caused by a Parkinson’s-like illness. Not everyone is entirely convinced by the claims. “I think this is very exciting work,” says Pennsylvania State University’s Gong Chen of the Nature paper. It reaffirms that “using the brain’s internal glial cells to regenerate new neurons is a really new avenue for the treatment of brain disorders,” he continues. Chen, who is also based at Jinan University and is the chief scientific officer for NeuExcell—a company developing astrocyte-to-neuron conversion therapies—has performed such conversions in the living mouse brain by a different method but was not involved in the new study. In Parkinson’s disease, dopaminergic neurons within the brain’s substantia nigra—a region in the midbrain involved in movement and reward—gradually die. This results in a deterioration of motor control, characterized by tremors and other types of dyskinesia, with other faculties such as cognition and mood sometimes affected too, especially at later stages of the disease. While treatments to boost diminishing dopamine levels, such as the drug levodopa, can ameliorate symptoms, none can stop the underlying disease process that relentlessly eats away at the patient’s neurological functions and quality of life. © 1986–2020 The Scientist.

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 1: Cells and Structures: The Anatomy of the Nervous System
Link ID: 27324 - Posted: 06.26.2020

By Sam Roberts Oleh Hornykiewicz, a Polish-born pharmacologist whose breakthrough research on Parkinson’s disease has spared millions of patients the tremors and other physical impairments it can cause, died on May 27 in Vienna. He was 93. His death was confirmed by his longtime colleague, Professor Stephen J. Kish of the University of Toronto, where Professor Hornykiewicz (pronounced whor-nee-KEE-eh-vitch) taught from 1967 until his retirement in 1992. Professor Hornykiewicz was among several scientists who were considered instrumental in first identifying a deficiency of the neurotransmitter dopamine as a cause of Parkinson’s disease, and then in perfecting its treatment with L-dopa, an amino acid found in fava beans. The Nobel laureate Dr. Arvid Carlsson and his colleagues had earlier shown that dopamine played a role in motor function. Drawing on that research, Professor Hornykiewicz and his assistant, Herbert Ehringer, discovered in 1960 that the brains of patients who had died of Parkinson’s had very low levels of dopamine. He persuaded another one of his collaborators, the neurologist Walther Birkmayer, to inject Parkinson’s patients with L-dopa, the precursor of dopamine, which could cross the barrier between blood vessels and the brain and be converted into dopamine by enzymes in the body, thus replenishing those depleted levels. The treatment alleviated symptoms of the disease, and patients who had been bedridden started walking. The initial results of this research were published in 1961 and presented at a meeting of the Medical Society of Vienna. The “L-dopa Miracle,” as it was called, inspired Dr. Oliver Sacks’s memoir “Awakenings” (1973) and the fictionalized movie of the same name in 1990. © 2020 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: 27299 - Posted: 06.13.2020

Sandra G. Boodman First she toppled off a ladder. Then Carol Hardy-Fanta tripped on a step outside her western Massachusetts home while gazing at her cellphone. Next she fell three times during a five-mile hike after catching her left foot on a rock or tree root. At first, Hardy-Fanta thought her repeated stumbles had a simple cause: She was distracted. But when she racked up more than 30 falls in a three-year period — some for no apparent reason — she repeatedly asked her doctors whether an undiagnosed medical problem might be causing her to “drop like a log.” The 10 doctors she consulted between 2016 and 2019 — four orthopedists, three neurologists, a rheumatologist, a podiatrist and her internist — reached disparate conclusions. One suggested she was clumsy. Others suspected her problem was primarily orthopedic or could find no clear explanation. It wasn't until September 2019 that a scan revealed what Hardy-Fanta had come to suspect — a diagnosis she said several of her doctors had brushed off. “These are the smartest people,” said Hardy-Fanta, now 71, whose husband is a Boston physician. “They really wanted to help” but appeared to be misled by her symptoms. “If someone’s falling that much, they should really pay attention.” The falls started in 2016, shortly after Hardy-Fanta and her husband sold their house in a Boston suburb and began splitting their time between a condo in the city and what she described as their “dream home” in the Berkshires. Hardy-Fanta had retired as director of a university think tank. Her fourth book on women and politics had just been published. She was in excellent health, which she regarded as a legacy from her mother, who remained mentally sharp and physically able until shortly before her death at age 100. Hardy-Fanta said she was looking forward to traveling with her husband and taking long bike rides along the scenic rural roads that snake through the Berkshires.

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: 27216 - Posted: 04.27.2020

By E. Ray Dorsey, Todd Sherer, Michael S. Okun, Bastiaan R. Bloem The number of people with Parkinson’s disease more than doubled from 1990 to 2015 and could double again by 2040. An aging population alone does not account for this rise. Air pollution, metal production, certain industrial chemicals, and some synthetic pesticides are linked to Parkinson’s. Yet we are doing little to manage known risk factors. Neither our increased awareness of the disease nor our lengthening life spans can fully account for the upsurge in diagnoses that we now face. Our knowledge of another neurological disorder, multiple sclerosis, has increased too, and we have improved diagnostic tools for it. Rates for multiple sclerosis have indeed gone up, but that increase is nothing like the exponential rise of Parkinson’s (see figure below). As for aging, more people are, of course, living longer. For example, from 1900 to 2014, the number of individuals over age 65 in the United Kingdom increased about sixfold. However, over that same period, the number of deaths due to Parkinson’s disease increased almost three times faster. Parkinson’s disease is characterized by tremors, slowness in movement, stiffness, and difficulties with balance and walking. It can also cause a wide range of symptoms that are not visible—loss of smell, constipation, sleep disorders, and depression. Most people with Parkinson’s are diagnosed in their fifties or later. But it is not just a disease of the elderly. Up to 10 percent of those with the condition develop the disease in their forties or younger. © 2020 Sigma Xi, The Scientific Research Honor Society

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 27213 - Posted: 04.24.2020

By Denise Grady A lifelong swimmer leapt into deep water near his lakeside home, and was horrified to find himself completely unable to swim. Had his wife not rescued him, he might have drowned. He had recently received an electronic brain implant to control tremors and other symptoms of Parkinson’s disease, and somehow the signals from the device had knocked out his ability to coordinate his arms and legs for swimming. He was one of nine patients, all good swimmers despite having Parkinson’s, who had the same strange, dangerous side effect from deep brain stimulators. Three of them tried turning off the stimulators, and immediately could swim again, according to an article in the journal Neurology by a medical team from the University of Zurich. At first, doctors thought the case of the man in the lake was an isolated event, Dr. Christian R. Baumann, an author of the paper, said in an interview. But when the same thing happened to another patient, one who had been a competitive swimmer, Dr. Baumann and his colleagues began to ask other patients about swimming. They found seven more cases among about 250 patients. About 150,000 people worldwide have brain implants made by Medtronic, the leading manufacturer, the company said. Most had the implants for relief of Parkinson’s symptoms. The swimming problem is not that common Dr. Baumann said, adding: “I think it’s a minority of patients. We find many who are still wonderfully able to swim and we don’t know why. We have no clue. They are treated in the same region of the brain. But this is life-threatening, and we need to pay more attention in the future.” Now, Dr. Baumann warns all patients with stimulators never to go into deep water alone. © 2019 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: 26860 - Posted: 11.29.2019

Maheen Mausoof Adamson, Ph.D. The 1982 science fiction film classic Blade Runner is a gritty detective story set in the dystopian future that raises questions about what it means to be human. In the film, Harrison Ford plays Rick Deckard, a police officer turned bounty hunter searching the streets of Los Angeles for a replicant (human-like androids) rebellion leader Roy Batty. Batty is presented as a technologically perfected being fitted with a human-template brain completely rewired to create an enemy to be deathly feared. Fear of the perfect altered brain is prominent in science fiction—and may be particularly prevalent today, amid growing concerns about genetic editing and artificial intelligence. The prospect of a fully artificial human brain remains very distant. However, we are in the midst of a neuromodulation revolution that will increase our ability to treat disease and optimize human performance. We must, however, carefully consider the benefits and risks of these techniques in fully evaluating their potential for society as well as the individual. A large number of patients suffering from neurological or psychiatric disorders—depression, pain, and post-traumatic stress disorder among them—are resistant to or can develop resistance to standard medication and psychotherapy, suggesting the need for new approaches. Neuromodulation may possibly be such an approach. The term (aka neurostimulation) refers to direct stimulation and modification of the nervous system through the use of electrical, chemical, or mechanical signals. Neuromodulation therapy is already used to treat many brain disorders, most commonly movement disorders, chronic pain, and depression. © 2019 The Dana Foundation.

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: 26797 - Posted: 11.07.2019

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 BN: 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 BN: 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 BN: 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 BN: 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 BN: Chapter 11: Motor Control and Plasticity; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 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 BN: Chapter 11: Motor Control and Plasticity; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 1: 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 BN: 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 BN: 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 BN: Chapter 9: Hearing, Balance, 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 BN: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 13: Memory and Learning
Link ID: 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 BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 25883 - Posted: 01.19.2019