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by Catherine de Lange Why wait for the doctor to see you? A smart patch attached to your skin could diagnose health problems automatically – and even administer drugs. Monitoring movement disorders such as Parkinson's disease or epilepsy relies on video recordings of symptoms and personal surveys, says Dae-Hyeong Kim at the Seoul National University in South Korea. And although using wearable devices to monitor the vital signs of patients is theoretically possible, the wearable pads, straps and wrist bands that can do this are often cumbersome and inflexible. To track the progression of symptoms and the response to medication more accurately would require devices that monitor cues from the body, store recorded data for pattern analysis and deliver therapeutic agents through the human skin in a controlled way, Kim says. So Kim and his team have developed an adhesive patch that is flexible and can be worn on the wrist like a second skin. The patch is 1 millimetre thick and made of a hydrocolloid dressing – a type of thin flexible bandage. Into it they embedded a layer of silicon nanoparticles. These silicon nanomembranes are often used for flexible electronics, and can pick up the bend and stretch of human skin and convert these into small electronic signals. The signals are stored as data in separate memory cells made from layers of gold nanoparticles. The device could be used to detect and treat tremors in people who have Parkinson's disease, or epileptic seizures, says Kim. If these movements are detected, small heaters in the patch trigger the release of drugs from silicon nanoparticles. The patch also contains temperature sensors to make sure the skin doesn't burn during the process. © Copyright Reed Business Information Ltd.
Helen Shen For Frank Donobedian, sitting still is a challenge. But on this day in early January, he has been asked to do just that for three minutes. Perched on a chair in a laboratory at Stanford University in California, he presses his hands to his sides, plants his feet on the floor and tries with limited success to lock down the trembling in his limbs — a symptom of his Parkinson's disease. Only after the full 180 seconds does he relax. Other requests follow: stand still, lie still on the floor, walk across the room. Each poses a similar struggle, and all are watched closely by Helen Bronte-Stewart, the neuroscientist who runs the lab. “You're making history,” she reassures her patient. “Everybody keeps saying that,” replies the 73-year-old Donobedian, a retired schoolteacher, with a laugh. “But I'm not doing anything.” “Well, your brain is,” says Bronte-Stewart. Like thousands of people with Parkinson's before him, Donobedian is being treated with deep brain stimulation (DBS), in which an implant quiets his tremors by sending pulses of electricity into motor areas of his brain. Last October, a team of surgeons at Stanford threaded the device's two thin wires, each with four electrode contacts, through his cortex into a deep-seated brain region known as the subthalamic nucleus (STN). But Donobedian's particular device is something new. Released to researchers in August 2013 by Medtronic, a health-technology firm in Minneapolis, Minnesota, it is among the first of an advanced generation of neurostimulators that not only send electricity into the brain, but can also read out neural signals generated by it. On this day, Bronte-Stewart and her team have temporarily turned off the stimulating current and are using some of the device's eight electrical contacts to record abnormal neural patterns that might correlate with the tremors, slowness of movement and freezing that are hallmarks of Parkinson's disease. © 2014 Nature Publishing Group,
by Ashley Yeager With a little help from implanted electrodes, Parkinson's patients make fewer driving errors, at least on a computer. When steering a simulator, patients with active brain stimulators averaged 3.8 driving errors, compared with 7.5 for healthy people and 11.4 for those with Parkinson's disease who did not have implants. The Parkinson’s patients’ driving skills were also more accurate when receiving deep brain stimulation than when taking levodopa, a common treatment for the disease, researchers report December 18 in Neurology. © Society for Science & the Public 2000 - 2013
Scientists at the National Institutes of Health have used RNA interference (RNAi) technology to reveal dozens of genes which may represent new therapeutic targets for treating Parkinson’s disease. The findings also may be relevant to several diseases caused by damage to mitochondria, the biological power plants found in cells throughout the body. “We discovered a network of genes that may regulate the disposal of dysfunctional mitochondria, opening the door to new drug targets for Parkinson’s disease and other disorders,” said Richard Youle, Ph.D., an investigator at the National Institute of Neurological Disorders and Stroke (NINDS) and a leader of the study. The findings were published online in Nature. Dr. Youle collaborated with researchers from the National Center for Advancing Translational Sciences (NCATS). Mitochondria are tubular structures with rounded ends that use oxygen to convert many chemical fuels into adenosine triphosphate, the main energy source that powers cells. Multiple neurological disorders are linked to genes that help regulate the health of mitochondria, including Parkinson’s, and movement diseases such as Charcot-Marie Tooth Syndrome and the ataxias. Some cases of Parkinson’s disease have been linked to mutations in the gene that codes for parkin, a protein that normally roams inside cells, and tags damaged mitochondria as waste. The damaged mitochondria are then degraded by cells’ lysosomes, which serve as a biological trash disposal system. Known mutations in parkin prevent tagging, resulting in accumulation of unhealthy mitochondria in the body.
Helen Shen Long used to treat movement disorders, deep-brain stimulation (DBS) is rapidly emerging as an experimental therapy for neuropsychiatric conditions including depression, Tourette’s syndrome, obsessive–compulsive disorder and even Alzheimer’s disease. But despite some encouraging results in patients, it remains largely unknown how the electrical pulses delivered by implants deep within the brain affect neural circuits and change behaviour. Now there is a prototype DBS device that could provide some answers, researchers reported on 10 November at the Society for Neuroscience’s annual meeting in San Diego, California. Called Harmoni, the device is the first DBS implant to monitor electrical and chemical responses in the brain while delivering electrical stimulation. “That’s new data that we haven’t really had access to in humans before,” says Cameron McIntyre, a biomedical engineer at Case Western Reserve University in Cleveland, Ohio, who is not involved in the work. Researchers hope that the device will identify the electrical and chemical signals in the brain that correlate in real time with the presence and severity of symptoms, including the tremors experienced by people with Parkinson’s disease. This information could help to uncover where and how DBS exerts its therapeutic effects on the brain, and why it sometimes fails, says Kendall Lee, a neurosurgeon at the Mayo Clinic in Rochester, Minnesota, who is leading the project. The results come at a time of great excitement in the DBS field. Last month, the US government's Defense Advanced Research Projects Agency (DARPA) announced a 5-year, US$70-million initiative to support development of the next generation of therapeutic brain-stimulating technologies. © 2013 Nature Publishing Group,
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 18922 - Posted: 11.13.2013
By PAM BELLUCK It is probably no accident that the pivotal object in Martin Cruz Smith’s newest detective thriller, “Tatiana,” is a notebook nobody can read. Early on, Mr. Smith worried that his novel, being published Tuesday by Simon & Schuster, would be unreadable too — or wouldn’t be written at all. Author of the 1981 blockbuster “Gorky Park” and many acclaimed books since, Mr. Smith writes about people who uncover and keep secrets. But for 18 years, he has had a secret of his own. In 1995, he received a diagnosis of Parkinson’s disease. But he kept it hidden, not only from the public, but from his publisher and editors. He concealed it, although for years, tremors and stiffness have kept him from taking detailed notes and sketching people, places and objects for his research — and even as he became unable to type the words he needed to finish his 2010 best seller “Three Stations.” “I didn’t want to be judged by that,” Mr. Smith, 71, explained recently in his light-filled Victorian home north of San Francisco. “Either I’m a good writer or I’m not. ‘He’s our pre-eminent Parkinson’s writer.’ Who needs that?” In talking about his Parkinson’s odyssey, including a relatively new but promising treatment, Mr. Smith is opening a window on the still incurable disorder affecting four million people worldwide, a disease that is becoming increasingly prevalent as baby boomers age. His experience reflects a common desire to conceal often-stigmatizing symptoms, like shaking, slowness, and rigidity. (He mostly didn’t mind his Parkinsonian hallucinations: a black cat in his lap, whirlwinds spiraling from computer keys, a butler, a British military officer in full regalia. “Having hallucinations for a fiction writer is redundant,” he said.) Copyright 2013 The New York Times Company
Roughly a year ago, I found myself at an elegant dinner party filled with celebrities and the very wealthy. I am a young professor at a major research university, and my wife and I were invited to mingle and chat with donors to the institution. To any outside observer, my career was ascendant. Having worked intensely and passionately at science for my entire adult life, I had secured my dream job directing an independent neuroscience research laboratory. I was talking to a businessman who had family members affected by a serious medical condition. He turned to me and said: “You're a neuroscientist. What do you know about Parkinson's disease?” My gaze darted to catch the eyes of my wife, but she was involved in another conversation. I was on my own, and I paused to gather my thoughts before responding. Because I had a secret. It was a secret that I hadn't yet told any of my colleagues: I have Parkinson's. I am still at the beginning of my fascinating, frightening and ultimately life-affirming journey as a brain scientist with a disabling disease of the brain. Already it has given me a new perspective on my work, it has made me appreciate life and it has allowed me to see myself as someone who can make a difference in ways that I never expected. But it took a bit of time to get here. The first signs I remember the first time I noticed that something was wrong. Four years ago, I was filling out a mountain of order forms for new lab equipment. After a few pages, my hand became a quaking lump of flesh and bone, locked uselessly in a tense rigor. A few days later, I noticed my walk was changing: rather than swinging my arm at my side, I held it in front of me rigidly, even grabbing the bottom edge of my shirt. I also had an occasional twitch in the last two fingers of my hand. © 2013 Nature Publishing Group
People with Parkinson's disease are dancing at the National Ballet School as part of a study into how learning dance moves can change the brain. Anecdotally, learning to dance seems to improve motor skills in the short-term among people with Parkinson's disease, a neurological disorder that interferes with gait and balance. As part of a 12-week program, 20 people with Parkinson's disease are taking weekly dance classes at the National Ballet School in Toronto. The classes began in September. The research team is led by neuroscientist Prof. Joseph DeSouza of York University's Faculty of Health and National Ballet School instructor Rachel Bar. The volunteers are also getting a series of functional MRI scans to help researchers understand how the brain reacts and learns. "We know that balance can improve and gait can improve and even there's social benefits but we want to see why that's happening, how is it happening? To do that, we're looking inside the brain," Bar said. People aren't able to dance in scanner but they are asked to visualize the dance while listening to the accompanying music. "If you visualize a dance, theoretically you're using almost all the same neural circuitry as if you were doing it," DeDouza said. The hypothesis is that the brain of someone with Parkinson's may develop new paths around damaged areas if stimulated by the movement of dance. © CBC 2013
Kashmira Gander A team in Bristol have created an implant that encourages cells damaged by the disease to grow again. It does this through a system of tubes and catheters that pump proteins into patients’ brain once a month, potentially stopping the disease from progressing by encouraging the damaged cells to grow again. The port located behind a patient’s ear releases a protein called glial cell line-derived neurotrophic factor (GDNF). Six patients at Frenchay Hospital, Bristol, have trialled the system, and doctors are now looking for another 36 to help them continue their research. Dr Kieran Breen, director of research and innovation at Parkinson's UK, said: “For years, the potential of GDNF as a treatment for Parkinson's has remained one of the great unanswered research questions. ”This new study will take us one step closer to finally answering this question once and for all. “We believe GDNF could have the potential to unlock a new approach for treating Parkinson's that may be able to slow down and ultimately stop the progression of the condition all together. ”Currently there are very few treatments available for people with Parkinson's and none capable of stopping the condition from advancing.“ More than 127,000 people in the UK currently have the disease, which is caused when nerve cells in the brain die due to a lack of the chemical dopamine. Symptoms include slowness of movement, stiffness and tremors. © independent.co.uk
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: 18783 - Posted: 10.14.2013
By Todd Sherer Parkinson’s disease is coming to prime time. Tomorrow night Michael J. Fox returns to television as the star of his own sitcom nearly 15 years after retiring from Spin City to focus on finding a cure for his disease. Michael has been careful to emphasize that the show isn’t really about Parkinson’s. Based loosely on his real life, The Michael J. Fox Show mines laughs from the everyday trials and tribulations of family man Mike Henry as he resumes his TV news job following a Parkinson’s diagnosis. Yet simply by featuring a main character living with the disease, the show puts Parkinson’s into the national conversation. This is a good moment to consider how much work remains to be done in the realm of neurodegeneration research. The question we’ve heard most often at The Michael J. Fox Foundation is: After more than 20 years with Parkinson’s, how is Michael doing well enough to go back to work? There’s no simple answer. He acknowledges the good fortune he has in a loving, supportive family and financial independence, which have provided advantages in dealing with his disease. He says, “Everybody gets their own version of Parkinson’s. Different meds work for different people, and you’re always trying to find the perfect combination. I think I found what works for me right now. And I’m so lucky.” But the reality is that for the estimated five million Parkinson’s patients worldwide, the status quo is still not good enough. They are living with Parkinson’s movement difficulties and nonmotor symptoms such as mood and sleep disorders as well as cognitive impairment. Medication and therapies alleviate some symptoms, but create their own problems and fail to address all the effects of Parkinson’s. We have some disease-modifying treatments in clinical trials, but nothing on the market yet. The grim truth is that those diagnosed with Parkinson’s will get worse. And for every patient, a community is affected, as the impact of the disease ripples to loved ones and caregivers. This is a global problem, but one that we can solve. © 2013 Scientific American
By John von Radowitz TARGETING poor housekeeping in cells could lead to new treatments for Parkinson's disease, scientists believe. Research has linked the disease to a genetic defect that stops cells clearing out defective mitochondria, tiny metabolic generators that supply energy. Dysfunctional mitochondria are potentially very harmful. Cells normally dispose of them through a "hazardous waste" management system called mitophagy that causes the bean-like bodies to be digested and broken down. Scientists have now discovered a biological pathway that allows mutations in a gene called FBxo7 to interfere with mitophagy. In people with Parkinson's, this leads to a build-up of defective mitochondria that may result in the death of brain cells. The study, published in the journal Nature Neuroscience, indicates that mitophagy might be the key to new treatment options for the disease. Dr Helene Plun-Favreau, one of the researchers from the University College London Institute of Neurology, said: "These findings suggest that treatment strategies that target mitophagy might be developed to benefit patients with Parkinson's disease in the future. "What makes the study so robust is the confirmation of defective mitophagy in a number of different Parkinson's models, including cells of patients who carry a mutation in the Fbxo7 gene." News Ltd 2013 Copyright
By Dina Fine Maron All eyes were on Perry Cohen when he froze at the microphone. His voice failed him. He couldn’t read his notes. Eventually, the once-powerful Parkinson’s disease speaker had to be helped off the stage halfway through his speech. That was in February 2012, but the memory of that day is emblazoned in his mind. “It was the adrenaline and the pressure of speaking — it drained all the dopamine out,” Cohen says, referring to the brain chemical that is found lacking in the neurodegenerative disorder. “That’s why my symptoms got worse.” When Cohen learned he had Parkinson’s disease 17 years ago his symptoms were subtle. In the past couple years, however, the deterioration of his nervous system has become increasingly obvious, ultimately threatening to silence one of the most prominent voices in the Parkinson’s patient community. Cohen is now first in line to try a novel treatment he hopes will halt or even reverse the symptoms of his Parkinson’s disease. Two months ago he became the inaugural patient to undergo a gene therapy treatment led by the National Institutes of Health. The trial attempts to devise an intervention for Parkinson’s disease at the root of the problem: protecting dopamine in the brain. Researchers in this trial are attempting to surgically deliver a gene into the body that will make a natural protein to protect dopaminergic neurons, the brain cells attacked by the disease. To date no Parkinson’s treatment is geared toward reversing the progression of Parkinson’s disease. © 2013 Scientific American
By Melinda Wenner Moyer Many studies over the past decade have pointed to pesticides as a potential cause of Parkinson's disease, a neurodegenerative condition that impairs motor function and afflicts a million Americans. Yet scientists have not had a good idea of how these chemicals harm the brain. A recent study suggests a possible answer: pesticides may inhibit a biochemical pathway that normally protects dopaminergic neurons, the brain cells selectively attacked by the disease. Preliminary research also indicates that this pathway plays a role in Parkinson's even when pesticides are not involved, providing an exciting new target for drug development. Past studies have shown that a pesticide called benomyl, which lingers in the environment despite having been banned in the U.S. in 2001 because of health concerns, inhibits the chemical activity of aldehyde dehydrogenase (ALDH) in the liver. Researchers at the University of California, Los Angeles, U.C. Berkeley, the California Institute of Technology and the Greater Los Angeles Veterans Affairs Medical Center wondered whether the pesticide might also affect levels of ALDH in the brain. ALDH's job is to break down DOPAL, a naturally forming toxic chemical, rendering it harmless. To find out, the researchers exposed different types of human brain cells—and, later, whole zebra fish—to benomyl. They found that it “killed almost half of the dopamine neurons while leaving all other neurons tested intact,” according to lead author and U.C.L.A. neurologist Jeff Bronstein. When they zeroed in on the affected cells, they confirmed that the benomyl was indeed inhibiting the activity of ALDH, which in turn spurred the toxic accumulation of DOPAL. Interestingly, when the scientists lowered DOPAL levels using a different technique, benomyl did not harm the dopamine neurons, a finding that suggests that the pesticide kills these neurons specifically because it allows DOPAL to build up. © 2013 Scientific American,
It only takes one bad apple to spoil the bunch, and the same may be true of certain proteins in the brain. Studies have suggested that just one rogue protein (in this case, a protein that is misfolded or shaped the wrong way) can act as a seed, leading to the misfolding of nearby proteins. According to an NIH-funded study, various forms of these seeds — originating from the same protein — may lead to different patterns of misfolding that result in neurological disorders with unique sets of symptoms. “This study has important implications for Parkinson’s disease and other neurodegenerative disorders,” said National Institute of Neurological Disorders and Stroke (NINDS) Director Story Landis, Ph.D. “We know that among patients with Parkinson’s disease, there are variations in the way that the disorder affects the brains. This exciting new research provides a potential explanation for why those differences occur.” An example of such a protein is alpha-synuclein, which can accumulate in brain cells, causing synucleinopathies, multiple system atrophy, Parkinson’s disease, Parkinson’s disease with dementia (PDD), and dementia with Lewy bodies (DLB). In addition, misfolded proteins other than alpha-synuclein sometimes aggregate, or accumulate, in the same brains. For example, tau protein collects into aggregates called tangles, which are the hallmark of Alzheimer’s disease and are often found in PDD and DLB brains. Findings from this study raise the possibility that different structural shapes, or strains, of alpha-synuclein may contribute to the co-occurrence of synuclein and tau accumulations in PDD or DLB.
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: 18346 - Posted: 07.04.2013
By PAULA SPAN It was supposed to be a short stay. In 2006, Roger Anderson was to undergo surgery to relieve a painfully compressed spinal disk. His wife, Karen, figured the staff at the hospital, in Portland, Ore., would understand how to care for someone with Parkinson’s disease. It can be difficult. Parkinson’s patients like Mr. Anderson, for example, must take medications at precise intervals to replace the brain chemical dopamine, which is diminished by the disease. “You don’t have much of a window,” Mrs. Anderson said. “If you have to wait an hour, you have tremendous problems.” Without these medications, people may “freeze” and be unable to move, or develop uncontrolled movements called dyskinesia, and are prone to falls. But the nurses at the Portland hospital didn’t seem to grasp those imperatives. “You’d have to wait half an hour or an hour, and that’s not how it works for Parkinson’s patients,” Mrs. Anderson said. Nor did hospital rules, at the time, permit her to simply give her husband the Sinemet pills on her own. Surgery and anesthesia, the disrupted medications, an incision that subsequently became infected — all contributed to a tailspin that lasted nearly three months. Mr. Anderson developed delirium, rotated between rehab centers and hospitals, took a fall, lost 60 pounds. “People were telling me, ‘He’s never going to come home,’” Mrs. Anderson said. He did recover, and at 69 is doing well, his wife said, though his disease has progressed. But his wasn’t an unusual story, neurologists say. © 2013 The New York Times Company
Nearly half of those with Parkinson's face regular discrimination, such as having their symptoms mistaken for drunkenness, a survey suggests. The survey of more than 2,000 people was commissioned by charity Parkinson's UK. One person in 500 people is affected by the condition in Britain. Parkinson's sufferer Mark Worsfold was arrested during last year's Olympics because police thought he looked suspicious. He was detained during the cycling road race in Leatherhead, Surrey, reportedly because he was not smiling - the condition means his face can appear expressionless. Parkinson's is a progressive neurological condition that attacks the part of the brain that controls movement. The main symptoms of Parkinson's are tremors or shaking that cannot be controlled, and rigidity of the muscles, which can make movement difficult and painful. Speech, language and facial expressions can also be affected. Most people who get it are aged 50 or over but younger people can have it too. The survey found that one in five people living with Parkinson's had been mistaken for being drunk, while one in 10 had been verbally abused or experienced hostility in public because of their condition. Around 62% said they thought the public had a poor understanding of how the condition affects people. BBC © 2013
Fran Lowry Salivary gland biopsy appears to be a diagnostic test for Parkinson's disease, a new study suggests. A biopsy of the submandibular gland that shows the presence of the abnormal protein alpha-synuclein is highly indicative of Parkinson's, as distinct from other neurodegenerative disorders that can mimic the disease, said lead study author, Charles Adler, MD, PhD, from the Mayo Clinic Arizona, Scottsdale, Arizona. "There is currently no diagnostic test for Parkinson's disease in living patients. The only way to make the diagnosis is at autopsy, when you can see an abnormal protein, alpha-synuclein, in certain brain regions," Dr. Adler, a fellow of the American Academy of Neurology, told Medscape Medical News. Their preliminary findings were released January 10; full results will be presented at the American Academy of Neurology's 65th Annual Meeting in San Diego. Dr. Adler and his team have been working on determining whether there is evidence of alpha-synuclein in other organs of the body so that they could develop a diagnostic test in living patients. "We previously published the fact that the submandibular gland has one of the densest concentrations of alpha-synuclein in an organ outside the brain. When we tested this in an autopsy study of 28 Parkinson's disease patients, we found that all 28 of them had alpha-synuclein in the submandibular gland," he said. The discovery led the researchers to biopsy the submandibular gland in living patients with Parkinson's disease to see whether this protein was present. If it was, then the biopsy could potentially be used as a diagnostic test, they reasoned. © 1994-2013 by WebMD LLC
By JAMES GORMAN For the first time, researchers at the Massachusetts Institute of Technology report, brain imaging has been able to show in living patients the progressive damage Parkinson’s disease causes to two small structures deep in the brain. The new technique confirms some ideas about the overall progress of the disease in the brain. But the effects of Parkinson’s vary in patients, the researchers said, and in the future, the refinement in imaging may help doctors monitor how the disease is affecting different people and adjust treatment accordingly. The outward symptoms and progress of Parkinson’s disease — tremors, stiffness, weakness — have been well known since James Parkinson first described them in 1817. But its progress in the brain has been harder to document. Some of the structures affected by the disease have been buried too deep to see clearly even with advances in brain imaging. An important recent hypothesis about how the disease progresses was based on the examinations of brains of patients who had died. Now, a group of scientists at M.I.T. and Massachusetts General Hospital report that they have worked out a way to combine four different sorts of M.R.I. to get clear pictures of damage to two brain structures in people living with Parkinson’s. In doing so, they have added support to one part of the recent hypothesis, which is that the disease first strikes an area involved in movement and later progresses to a higher part of the brain more involved in memory and attention. Suzanne Corkin, a professor emerita of behavioral neuroscience at M.I.T. and the senior author on the paper published online Monday in The Archives of Neurology, said that this progression was part of the hypothesis put forward in 2003 by Heiko Braak, a German neuroscientist, based on autopsies. © 2012 The New York Times Company
By Laura Sanders The insidious spread of an abnormal protein may be behind Parkinson’s disease, a study in mice suggests. A harmful version of the protein crawls through the brains of healthy mice, killing brain cells and damaging the animals’ balance and coordination, researchers report in the Nov. 16 Science. If a similar process happens in humans, the results could eventually point to ways to stop Parkinson’s destruction in the brain. “I really think that this model will increase our ability to come up with Parkinson’s disease therapies,” says study coauthor Virginia Lee of the University of Pennsylvania Perelman School of Medicine in Philadelphia. The new study targets a hallmark of Parkinson’s disease — clumps of a protein called alpha-synuclein. The clumps, called Lewy bodies, pile up inside nerve cells in the brain and cause trouble, particularly in cells that make dopamine, a chemical messenger that helps control movement. Death of these dopamine-producing cells leads to the characteristic tremors and muscle rigidity seen in people with Parkinson’s. Lee and her team injected alpha-synuclein into the brains of healthy mice. After 30 days, the protein had spread to connected brain regions, suggesting that rouge alpha-synuclein moves from cell to cell, the scientists found. Months later, the spreading was even more extensive. © Society for Science & the Public 2000 - 2012
By Dan Cossins There’s a new suspect in the search for the causes of Parkinson’s disease—deformities in the nuclear membrane of neural stem cells. Scientists observed the same defects, caused by a single gene mutation, in brain tissue samples from deceased Parkinson’s patients, suggesting that nuclear deterioration—and the mutation that drives it—could play a role in the pathology of the disease. The study, published today (October 17) in Nature, also shows that correcting the mutation reverses this phenotype, pointing to new ways to treat this cause of neurodegeneration. “I don’t recall anyone ever suggesting this as a major phenotype [for Parkinson’s], so that’s really quite a big new direction for the field,” said Mark Cookson, a neuroscientist at the National Institutes of Health in Bethesda, Maryland, who did not participate in the study. Parkinson’s disease has traditionally been attributed to a loss of dopamine-generating neurons, which leads to the degenerative muscle control that is characteristic of the disease. But Parkinson’s also causes many other sensory problems, which cannot be explained by a dopaminergic mechanism. Over the past 5 years, several groups have shown that disruption of the structure of the nuclear envelope—the lipid bilayer that separates nucleus from cytoplasm—is correlated with aging and certain age-related pathologies in the human brain, though the precise role of nuclear defects in the diseases remained unclear. Meanwhile, since 2004 scientists including Cookson have demonstrated that a mutation in the luceine-rich repeat kinase 2 (LRRK2) gene is correlated with Parkinson’s. However, the molecular and cellular mechanisms by which the LRRK2 mutation might drive disease progression remained a mystery. © 1986-2012 The Scientist