Links for Keyword: Parkinsons
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By Israel Robledo As has often been said, with great power comes great responsibility. As we saw in the recent election, social media is a great example of a powerful medium that can change minds and change lives but can also give credibility to false or misguiding information. As someone diagnosed with Parkinson’s disease (PD) nine years ago, I’ve thrilled at seeing social media’s growing power as an agent for good. As our advocacy community has grown, social media has allowed for more information to be circulated in the PD community than ever before, and has become a vital link through which we share experiences, raise awareness about quality of life issues, point people to clinical trials, spread knowledge about cutting-edge research—and importantly, raise critical dollars to fund it. Connecting our community more tightly together has underscored the important role each of us can play in finding an eventual cure. A downside to the awesome power of this platform comes from not knowing or perhaps not caring about the source of information shared on social media. Just as “fake news” has flourished in an environment where speed, rather than accuracy, is what counts, patients—who are understandably vulnerable to hopeful reports about their disease—must recognize that not everything they read is equally credible. In my years of advocating for PD-related causes, hundreds of so-called “miracles” have been announced, all of which have proven to have disappointing results. © 2016 Scientific American
By Clare Wilson WE HAVE been thinking about Parkinson’s disease all wrong. The condition may arise from damage to the gut, not the brain. If the idea is correct, it opens the door to new ways of treating the disease before symptoms occur. “That would be game-changing,” says David Burn at Newcastle University, UK. “There are lots of different mechanisms that could potentially stop the spread.” Parkinson’s disease involves the death of neurons deep within the brain, causing tremors, stiffness and difficulty moving. While there are drugs that ease these symptoms, they become less effective as the disease progresses. One of the hallmarks of the condition is deposits of insoluble fibres of a substance called synuclein. Normally found as small soluble molecules in healthy nerve cells, in people with Parkinson’s, something causes the synuclein molecules to warp into a different shape, making them clump together as fibres. The first clue that this transition may start outside the brain came about a decade ago, when pathologists reported seeing the distinctive synuclein fibres in nerves of the gut during autopsies – both in people with Parkinson’s and in those without symptoms but who had the fibres in their brain. They suggested the trigger was some unknown microbe or toxin. © Copyright Reed Business Information Ltd.
Laura Sanders SAN DIEGO — Over the course of months, clumps of a protein implicated in Parkinson’s disease can travel from the gut into the brains of mice, scientists have found. The results, reported November 14 at the annual meeting of the Society for Neuroscience, suggest that in some cases, Parkinson’s may get its start in the gut. That’s an intriguing concept, says neuroscientist John Cryan of the University College Cork in Ireland. The new study “shows how important gut health can be for brain health and behavior.” Collin Challis of Caltech and colleagues injected clumps of synthetic alpha-synuclein, a protein known to accumulate in the brains of people with Parkinson’s, into mice’s stomachs and intestines. The researchers then tracked alpha-synuclein with a technique called CLARITY, which makes parts of the mice’s bodies transparent. Seven days after the injections, researchers saw alpha-synuclein clumps in the gut. Levels there peaked 21 days after the injections. These weren’t the same alpha-synuclein aggregates that were injected, though. These were new clumps, formed from naturally occurring alpha-synuclein, that researchers believe were coaxed into forming by the synthetic versions in their midst. Also 21 days after the injections, alpha-synuclein clumps seemed to have spread to a part of the brain stem containing nerve cells that make up the vagus nerve, a neural highway that connects the gut to the brain. Sixty days after the injections, alpha-synuclein had accumulated in the midbrain, a region packed with nerve cells that make the chemical messenger dopamine. These are the nerve cells that die in people with Parkinson’s, a progressive brain disorder that affects movement. © Society for Science & the Public 2000 - 2016
Related chapters from BP7e: 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: 22881 - Posted: 11.17.2016
By Karen Weintraub Researchers have long believed that problems with mitochondria—the power plants of cells—underlie some cases of Parkinson’s disease. Now a new study details those problems, and suggests that they may form a common thread linking previously unexplained cases of the disease with those caused by different genetic anomalies or toxins. Finding a common mechanism behind different suspected causes of Parkinson’s suggests that there might also be a common means to measure, treat or cure it, says Marco Baptista, research director at the nonprofit Michael J. Fox Foundation, a leading center for study and advocacy in the fight against Parkinson’s. The study, published Thursday in Cell Stem Cell, did identify a possible way to reverse the damage of Parkinson’s—but only in individual cells and fruit flies. Finding a treatment that does the same thing in people will be challenging, Baptista says. Roughly one million Americans have Parkinson’s disease, which is characterized by motor problems and can cause other symptoms including cognitive and gastrointestinal difficulties. About 1 to 2 percent of cases are linked to mutations in the LRRK2 gene, with far fewer associated with genes known as PINK1 and Parkin. Exposure to environmental factors such as toxic chemicals can also lead to Parkinson’s, although most cases have no obvious cause. In the new paper Xinnan Wang, an assistant professor of neurosurgery at Stanford University, and her colleagues show that mitochondria are underpowered in several types of Parkinson’s and that these mitochondria also release toxic chemicals. Looking at fly models of the disease as well as cells taken from patients, the researchers found that they could correct these problems and reverse neurodegeneration if they reduced levels of a protein involved in mitochondrial activity. © 2016 Scientific American
Researchers may have discovered a method of detecting changes in the eye which could identify Parkinson's disease before its symptoms develop. Scientists at University College London (UCL) say their early animal tests could lead to a cheap and non-invasive way to spot the disease. Parkinson's affects 1 in 500 people and is the second most common neurodegenerative disease worldwide. The charity Parkinson's UK welcomed the research as a "significant step". The researchers examined rats and found that changes could be seen at the back of their eyes before visible symptoms occurred. Professor Francesca Cordeiro who led the research said it was a "potentially revolutionary breakthrough in the early diagnosis and treatment of one of the world's most debilitating diseases". "These tests mean we might be able to intervene much earlier and more effectively treat people with this devastating condition." Symptoms of Parkinson's include tremors and muscle stiffness, slowness of movement and a reduced quality of life. These symptoms usually only emerge after brain cells have been damaged. But there is currently no brain scan, or blood test, that can definitively diagnose Parkinson's disease. Parkinson's does not directly cause people to die, but symptoms do get worse over time. © 2016 BBC
Neuroscientists peered into the brains of patients with Parkinson’s disease and two similar conditions to see how their neural responses changed over time. The study, funded by the NIH’s Parkinson’s Disease Biomarkers Program and published in Neurology, may provide a new tool for testing experimental medications aimed at alleviating symptoms and slowing the rate at which the diseases damage the brain. “If you know that in Parkinson’s disease the activity in a specific brain region is decreasing over the course of a year, it opens the door to evaluating a therapeutic to see if it can slow that reduction,” said senior author David Vaillancourt, Ph.D., a professor in the University of Florida’s Department of Applied Physiology and Kinesiology. “It provides a marker for evaluating how treatments alter the chronic changes in brain physiology caused by Parkinson’s.” Parkinson’s disease is a neurodegenerative disorder that destroys neurons in the brain that are essential for controlling movement. While many medications exist that lessen the consequences of this neuronal loss, none can prevent the destruction of those cells. Clinical trials for Parkinson’s disease have long relied on observing whether a therapy improves patients’ symptoms, but such studies reveal little about how the treatment affects the underlying progressive neurodegeneration. As a result, while there are treatments that improve symptoms, they become less effective as the neurodegeneration advances. The new study could remedy this issue by providing researchers with measurable targets, called biomarkers, to assess whether a drug slows or even stops the progression of the disease in the brain. “For decades, the field has been searching for an effective biomarker for Parkinson’s disease,” said Debra Babcock, M.D., Ph.D., program director at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS).
Related chapters from BP7e: 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: 22562 - Posted: 08.16.2016
By ALAN COWELL LONDON — When Muhammad Ali died last week, the memories spooled back inevitably to the glory days of the man who called himself the Greatest, a champion whose life intertwined with America’s traumas of race, faith and war. It was a chronicle of valor asserted in the most public of arenas scrutinized by an audience that spanned the globe. But there was another narrative, just as striking to some admirers, of a private courage beyond his klieg-lit renown. For the minority afflicted by Parkinson’s disease, Ali’s 30-year struggle with the same illness magnified the broader status he built from his boxing prowess as a black man who embraced radical Islam, refused to fight in Vietnam, earned the opprobrium of the establishment and yet emerged as an icon. “It was his longest bout, and one that ultimately he could not win,” the reporter Patrick Sawer wrote in The Telegraph, referring to Ali’s illness. Yet the affliction “only served to increase the worldwide admiration he had gained before the disease robbed him of his powers.” As a global superstar, Ali touched many lands, and Britain felt a particular bond. Boxing fans recalled his far-flung bouts — the “Rumble in the Jungle” against George Foreman in Zaire, as the Democratic Republic of Congo was then called, in 1974; “The Thrilla in Manila” in the Philippines against Joe Frazier a year later. But in Britain, his two defeats in the 1960s of Henry Cooper, a much-loved British heavyweight who died in 2011, and his feisty appearances in prime-time television interviews left an indelible mark. © 2016 The New York Times Company
By Esther Landhuis About 100 times rarer than Parkinson’s, and often mistaken for it, progressive supranuclear palsy afflicts fewer than 20,000 people in the U.S.—and two thirds do not even know they have it. Yet this little-known brain disorder that killed comic actor Dudley Moore in 2002 is quietly becoming a gateway for research that could lead to powerful therapies for a range of intractable neurodegenerative conditions including Alzheimer’s and chronic traumatic encephalopathy, a disorder linked to concussions and head trauma. All these diseases share a common feature: abnormal buildup of a protein called tau in the brains of patients. Progressive supranuclear palsy has no cure and is hard to diagnose. Although doctors may have heard of the disease, many know little about it. It was not described in medical literature until 1964 but some experts believe one of the earliest accounts of the debilitating illness appeared in an 1857 short story by Charles Dickens and his friend Wilke Collins: “A cadaverous man of measured speech. A man who seemed as unable to wink, as if his eyelids had been nailed to his forehead. A man whose eyes—two spots of fire—had no more motion than if they had been connected with the back of his skull by screws driven through them, and riveted and bolted outside among his gray hair. He had come in and shut the door, and he now sat down. He did not bend himself to sit as other people do, but seemed to sink bolt upright, as if in water, until the chair stopped him.” © 2016 Scientific American
Related chapters from BP7e: 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: 22304 - Posted: 06.09.2016
By DENISE GRADY Muhammad Ali, who died on Friday after a long struggle with Parkinson’s disease, was given the diagnosis in 1984 when he was 42. The world witnessed his gradual decline over the decades as tremors and stiffness set in, replacing his athletic stride with a shuffle, silencing his exuberant voice and freezing his face into an expressionless mask. What is Parkinson’s disease? It is a progressive, incurable deterioration of the part of the brain that produces a chemical needed to carry signals to the regions that control movement. How common is Parkinson’s? About one million people in the United States, and between seven million and 10 million worldwide, are thought to have Parkinson’s, according to the Parkinson’s Disease Foundation. What causes it? Was boxing a factor for Ali? The exact cause is not known. As with many disorders, experts suspect a combination of genes and environment, meaning that people with a particular genetic makeup may be predisposed to the disease if they are exposed to certain environmental factors. Head injuries, such as those sustained repeatedly in boxing, are among the possible risk factors listed by the National Parkinson Foundation. So is exposure to certain pesticides. These factors have both been suggested as possible contributors in Muhammad Ali’s case. Can Parkinson’s disease be treated? Medication can ease the symptoms for a time, but the disease continues to progress. In some cases, implanted devices called deep-brain stimulators can also help with symptoms. But Parkinson’s is not curable. © 2016 The New York Times Company
By Dan Kiefer I’m on the heavy bag, throwing left jabs, ignoring the relentless blare of Kanye’s “Drive Slow, Homie” played at a volume that would raise the dead. I punch to a one-two count: left jab, right cross. I’m working as hard as I’ve ever worked, and even in this unheated gym I sweat as if it’s a sauna. Finally, the bell rings. It feels as if I’ve been at it for an hour; actually, three minutes have passed. The ensuing one-minute break seems to last four seconds. Let’s be clear: Boxing, even when the opponent is only a heavy bag, is a brutal sport. But brutality is needed, even welcome, when you’re facing a progressive, incurable neurological disease. I have Parkinson’s disease, and it causes my body to just freeze up. Weirdly enough, boxing helps me get unstuck. All 12 of us in this class bear the unmistakable signs of Parkinson’s disease. I spot a dapper, cheerful white-haired fellow shaking like a leaf (tremor). Next, a balding, heavyset guy stumbling forward awkwardly on his toes (dystonia, or muscle cramping). Then I see myself in a mirror: a man in a white T-shirt, khaki shorts and Nike running shoes, standing still, seemingly paralyzed. I’m in the midst of a Parkinson’s freeze (an extreme form of bradykinesia, or slow movement). Although Parkinson’s is generally thought of as an old-person’s disease, I was diagnosed with a young-onset version 18 years ago, at age 35. Since then, I’ve taken every sort of medication known to science. I’ve had brain surgery — two tiny electrodes were implanted deep in my brain to stimulate an area affected by Parkinson’s — which unquestionably have helped treat some of my symptoms. But medicine and surgery have not cured my freezing and falling, my gait and balance issues that worsen as my disease progresses: When walking across a busy street, I may suddenly, inexplicably come to a full stop as the light is about to change. Even the slightest downhill slope of a path causes me to fall forward.
Laura Sanders Iron, says aging expert Naftali Raz, is like the Force. It can be good or bad, depending on the context. When that context is the human brain, though, scientists wrangle over whether iron is a dark force for evil or a bright source of support. Some iron is absolutely essential for the brain. On that, scientists agree. But recent studies suggest to some researchers that too much iron, and the chemical reactions that ensue, can be dangerous or deadly, especially to nerve cells in the vulnerable brain area that deteriorates with Parkinson’s disease. Yet other work raises the possibility that those cells die because of lack of iron, rather than too much. “There are a lot of surprises in this field,” says iron biologist Nancy Andrews of Duke University. The idea that too much iron is dangerous captivates many researchers, including analytical neurochemist Dominic Hare of the University of Technology Sydney. “All of life is a chemical reaction,” he says, “so the start of disease is a chemical reaction as well.” And as Raz points out, reactions involving iron are both life-sustaining and dangerous. “Iron is absolutely necessary for conducting the very fundamental business in every cell,” says Raz, of Wayne State University in Detroit. It helps produce energy-storing ATP molecules. And that’s a dirty job, throwing off dangerous free radicals that can cause cellular mayhem as energy is made. But those free radicals are not the most worrisome aspect of iron, Hare believes. “The reaction that is much more dangerous is the reaction you get when iron and dopamine come together,” he says. © Society for Science & the Public 2000 - 2016.
Melissa Davey Researchers have developed the world’s first blood test that can detect the abnormal metabolism of blood cells in people with Parkinson’s disease, which means the blood test could be used to diagnose the disorder. At present the only way to diagnose Parkinson’s disease, a degenerative neurological condition, is through ordering a range of tests and scans to rule out other disorders, combined with examining symptoms. Patients are often diagnosed only after they have developed symptoms and brain cells have already been destroyed. While there is no cure for Parkinson’s, early detection allows treatment with medication and physiotherapy to begin, which may slow the deterioration of motor functions in patients. Because diagnosing the disease is a process of elimination, and the symptoms mimic those of other neurological disorders, patients are also at risk being diagnosed and treated for the wrong disease. The group of Australian researchers from La Trobe University believe their blood test will enable doctors to detect Parkinson’s disease with unprecedented reliability and lead to earlier treatment. Their findings are under review by an international medical journal. © 2016 Guardian News and Media Limited
By Amy Ellis Nutt Surgeons snaked the electrodes under the 65-year-old woman’s scalp. Thirty years of Parkinson’s disease had almost frozen her limbs. The wires, connected to a kind of pacemaker under the skin, were aimed at decreasing the woman’s rigidity and allowing for more fluid movement. But five seconds after the first electrical pulse was fired into her brain, something else happened. Although awake and fully alert, she seemed to plunge into sadness, bowing her head and sobbing. One of the doctors asked what was wrong. “I no longer wish to live, to see anything, to hear anything, feel anything,” she said. Was she in some kind of pain? “No, I’m fed up with life. I’ve had enough,” she replied. “Everything is useless.” The operating team turned off the current. Less than 90 seconds later, the woman was smiling and joking, even acting slightly manic. Another five minutes more, and her normal mood returned. The patient had no history of depression. Yet in those few minutes after the electrical pulse was fired, the despair she expressed met nine of the 11 criteria for severe major depressive disorder in the Diagnostic and Statistical Manual of Mental Disorders. Fascinated by the anomaly, the French physicians wrote up the episode for the New England Journal of Medicine. The year was 1999, and hers was one of the first documented cases of an electrically induced, instantaneous, yet reversible depression. © 1996-2016 The Washington Post
Related chapters from BP7e: Chapter 15: Emotions, Aggression, and Stress; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 5: The Sensorimotor System
Link ID: 21955 - Posted: 03.05.2016
Mo Costandi People who are prone to falling and injuring and injuring themselves in middle age are at significantly increased risk of developing Parkinson’s Disease decades later, according to a new study by researchers in Sweden. The findings, published earlier this month in the open access journal PLoS Medicine, suggest that frailty – and especially an increased risk of falling and fracturing one’s hip – could be a marker for degenerative brain changes, which may occur decades before disease symptoms appear, and possibly aid in early diagnosis. Parkinson’s Disease is a progressive neurodegenerative disease characterised by the death of dopamine-producing neurons in a region of the midbrain called the substantia nigra. This causes the three main symptoms of tremor, muscle rigidity, and slow movements, which typically appear at around 60 years of age, and progress at varying rates. Although widely considered to be a movement disorder, Parkinson’s is also associated with cognitive impairments, which in severe cases can develop into full-blown dementia. Last year, Peter Nordström of Umeå University and his colleagues published the results of a large population study, in which they examined the medical records of all the approximately 1.35 million Swedish men conscripted at age 18 for compulsory military service between the years of 1969 and 1996. Looking specifically at measures of muscle strength, they found that those who scored lowest on handgrip and elbow flexion strength at the time of conscription were significantly more likely to develop Parkinson’s 30 years later. © 2016 Guardian News and Media Limited
Jo Marchant The brain cells of people with Parkinson’s disease can be trained to reliably respond to placebo drugs, Italian neuroscientists report. The training wears off after 24 hours but the effect shows it may be possible to reduce the medication needed to treat Parkinson’s by interspersing real drugs with inert injections or pills, says placebo researcher Fabrizio Benedetti at the University of Turin, Italy, who led the work. A few people with Parkinson’s disease do respond dramatically to placebos, but most do not1. People with the condition suffer characteristic tremors and stiff muscles because their dopamine-producing brain cells are gradually dying off. They alleviate their symptoms by taking drugs such as apomorphine, which activate receptors for dopamine. For some conditions — such as pain and immune disorders — trials have shown2 that it is possible to train people to respond to placebos, although this practice hasn’t made its way into clinical care. Benedetti and his colleagues wondered whether the same effect might be possible for neurological disorders. They studied 42 people with advanced Parkinson’s disease who were having electrodes implanted into their brains for a therapy called deep brain stimulation, which eases symptoms by stimulating affected brain areas directly. That surgery gave Benedetti’s team a rare opportunity to measure the activity of individual neurons in the thalamus, a brain region known to be inhibited by lack of dopamine in people with Parkinson's. © 2016 Nature Publishing Grou
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 5: The Sensorimotor System
Link ID: 21884 - Posted: 02.10.2016
By Anne Pycha Future doctors may ask us to say more than “Ahhh.” Several groups of neuroscientists, psychiatrists and computer scientists are now investigating the extent to which patients' language use can provide diagnostic clues—before a single laboratory test is run. Increased computing power and new methods to measure the relation between behavior and brain activity have advanced such efforts. And although tests based on the spoken word may not be as accurate as gene sequencing or MRI scans, for diseases lacking clear biological indicators, language mining could help fill the gap. Psychiatrists at Columbia University interviewed 34 young adults at risk for psychosis, a common sign of schizophrenia that includes delusions and hallucinations. Two and a half years later five of the subjects had developed psychosis, and the remaining 29 remained free of the disorder. A specially designed algorithm combed the initial interviews collectively to look for language features that distinguished the two groups and found that psychosis correlated with shorter sentences, loss of flow in meaning from one sentence to the next and less frequent use of the words “that,” “what” and “which.” When later tested on each individual interview, the computer program predicted who did and who did not develop psychosis with 100 percent accuracy. The results were recently published in Schizophrenia, and a second round of testing with another group of at-risk subjects is now under way. Parkinson's Disease Twenty-seven subjects in a study at Favaloro University in Argentina listened to recorded sentences containing verbs associated with specific hand shapes (such as “applaud” or “punch”). As soon as they understood the sentence, participants pressed a button while keeping both hands in either a flat or clenched-fist position. © 2016 Scientific American
Related chapters from BP7e: 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: 21818 - Posted: 01.25.2016
Videos just discovered show the first people ever to be treated for the symptoms of Parkinson’s disease. The footage, hidden for half a century, shows Chilean miners with severe movement problems improving on daily doses of L-dopa. The videos were filmed by George Cotzias at Brookhaven National Laboratory in Upton, New York. In 1963, while studying the toxic effects of manganese in human tissues, Cotzias learned of four workers in the Corral del Quemado mine in Andacollo, Chile, who had developed a syndrome called manganism – which resembled Parkinson’s – through inhaling manganese dust. Cotzias travelled to Chile to include the miners in a trial of leva-dopa, a chemical building block that the body converts into dopamine, low levels of which cause uncontrolled movements in people with Parkinson’s. L-dopa was being tested in Parkinson’s patients around the same time but with little success – even small amounts caused adverse side-effects that prevented a high enough dose reaching the brain. The footage clearly shows the severe problems with walking and turning miners had before treatment. After several months of receiving a daily dose of L-dopa, they were able to feed themselves, shave, tie their shoelaces, and run. “It’s a very important part of the history of neurology,” says Marcelo Miranda, a researcher at Clinica Las Condes in Santiago, Chile, who found the footage, some of which was shown at a conference in the 1960s, but hasn’t been seen since. “It’s the only available document of that period that shows the first patients with Parkinson’s symptoms treated with L-dopa and their extraordinary response.” © Copyright Reed Business Information Ltd.
By Diana Kwon Six years before her husband was diagnosed with Parkinson’s disease, a progressive neurodegenerative disorder marked by tremors and movement difficulties, Joy Milne detected a change in his scent. She later linked the subtle, musky odor to the disease when she joined the charity Parkinson’s UK and met others with the same, distinct smell. Being one of the most common age-related disorders, Parkinson’s affects an estimated seven million to 10 million people worldwide. Although there is currently no definitive diagnostic test, researchers hope that this newly found olfactory signature will lead help create one. Milne, a super-smeller from Perth, Scotland, wanted to share her ability with researchers. So when Tilo Kunath, a neuroscientist at the University of Edinburgh, gave a talk during a Parkinson’s UK event in 2012, she raised her hand during the Q&A session and claimed she was able to smell the disease. “I didn’t take her seriously at first,” Kunath says. “I said, ‘No, I never heard of that, next question please.’” But months later Kunath shared this anecdote with a colleague and received a surprising response. “She told me that that lady wasn’t wrong and that I should find her,” Kunath says. Once the researchers found Milne, they tested her claim by having her sniff 12 T-shirts: six that belonged to people with Parkinson’s and six from healthy individuals. Milne correctly identified 11 out of 12, but miscategorized one of the non-Parkinson’s T-shirts in the disease category. It turned out, however, she was not wrong at all—that person would be diagnosed with Parkinson’s less than a year later. © 2015 Scientific American
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 21582 - Posted: 10.31.2015
Alan Hoffman says nilotinib has changed his life. Just weeks after he started taking the drug in a clinical trial, he began to feel himself recovering from his Parkinson’s disease. The retired professor of social science first started to show the signs of Parkinson’s in 1997. Over the years, his symptoms worsened. “I couldn’t get out of bed without my wife,” Hoffman says. Once a prolific reader, devouring four or five books a week, Hoffman found himself unable to keep his attention on even a short magazine article. His body became increasingly rigid, and he started to lose his sense of balance. “I fell a lot,” he says. And it affected his social life. The disorder was such a struggle, Hoffman says he considered taking his own life. He tried a range of medications, which eased his symptoms to varying degrees. In 2008, he had surgery to implant an electrode into his brain. The deep brain stimulation that followed helped with the rigidity, he says. But deep brain stimulation doesn’t offer a cure – the brain cells continue to die. So Hoffman agreed to join a six-month clinical trial of nilotinib – a drug typically used to treat leukaemia. Nilotinib blocks a protein that interferes with lysosomes – cell structures that destroy harmful proteins. Researchers behind the trial think that nilotinib can free up lysosomes to do a better job of clearing out proteins associated with Parkinson’s disease. (For a full report on the effect of the drug see “People with Parkinson’s walk again after promising drug trial”.) © Copyright Reed Business Information Ltd.
An expensive cancer drug may reverse late-stage Parkinson’s disease, enabling participants in a small clinical trial to speak and walk again for the first time in years. While there are several treatments for the symptoms of Parkinson’s, if confirmed this would be the first time a drug has worked on the causes of the disease. “We’ve seen patients at end stages of the disease coming back to life,” says Charbel Moussa of Georgetown University Medical Center in Washington DC, who led the trial. The drug, called nilotinib, works by boosting the brain’s own “garbage disposal system” to clear proteins that accumulate in the brains of people with Parkinson’s disease, says Moussa. These proteins are thought to trigger the death of brain cells that make molecules like dopamine that are needed for movement and other functions. Nilotinib is already approved to treat cancer – it blocks a protein that drives chronic myeloid leukaemia. It also blocks another protein that interferes with lysosomes – cell structures that destroy harmful proteins. Moussa thinks that nilotinib can free up lysosomes to do a better job of clearing out proteins associated with Parkinson’s disease. Tests in animals showed promise, so Moussa, his colleague Fernando Pagan and their team set up a small trial of 12 volunteers with Parkinson’s disease or a similar condition called dementia with Lewy bodies. The trial was designed to test only the safety of the oral drug, which was given as a daily dose for six months. © Copyright Reed Business Information Ltd.