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Posted by Rachel Dolhun, MD, The ability to quit smoking, especially “cold turkey” or on the first attempt, has been heralded as a marker of strong willpower and determination. But could the ease with which one eschews cigarettes also serve as an early sign of Parkinson’s disease (PD)? This is the conclusion drawn by Beate Ritz, MD, PhD, and colleagues from the University of California, Los Angeles in a recent study published in Neurology. Researchers compared lifelong tobacco use, use of nicotine substitutes, and individual’s rating of their difficulty in trying to quit tobacco among 1,808 Danish people with PD and 1,876 control volunteers. They found that those with PD were less inclined to ever pick up the smoking habit, but, even if they did, they were less likely to need nicotine replacement therapies and able to more effortlessly stop smoking cigarettes. Therefore, ease of quitting smoking may be a sign of early PD. This joins a short list of other symptoms — smell loss, constipation and REM sleep behavior disorder — that usually predate diagnosis and are strongly associated with PD. Physicians rely heavily on such information to help confirm the diagnosis of Parkinson’s, given that biomarkers, objective measurements of disease, are currently lacking. Research led by The Michael J. Fox Foundation is ongoing to identify biological markers of PD, which could help diagnose and treat people earlier. In the meantime, doctors must look for symptoms and behaviors to help identify Parkinson’s. Researchers have long known that tobacco use was linked to a lower risk of PD. An ongoing Foundation-funded study is investigating whether nicotine might guard against or slow the progression of PD.
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20189 - Posted: 10.11.2014
By Lenny Bernstein Comedian Robin Williams was grappling with severe depression when he committed suicide Monday, and on Thursday we learned that he also was in the early stages of Parkinson's disease. Sadly, the two conditions are often found together. In a 2012 study conducted by the National Parkinson Foundation, 61 percent of 5,557 Parkinson's patients surveyed reported that they also suffered from depression, with symptoms that ranged from mild to severe. Both conditions are associated with a shortage of dopamine, a neurotransmitter that helps regulate movement and control the brain's pleasure center. "Dopamine is a feel-good chemical. If you are low in dopamine, you are not going to feel so good," said Joyce Oberdorf, president and CEO of the National Parkinson Foundation. "There are [also] other neurotransmitters that can be low." A separate study published Friday found that newly-diagnosed Parkinson's patients have higher rates of depression, anxiety, fatigue, and apathy than a control group of people without Parkinson's. Researchers from the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania found that 13.9 percent of patients had symptoms of depression when they were diagnosed with Parkinson's, a proportion that rose to 18.7 percent after 24 months. Just 6.6 percent of people without the disease had depression, and that dropped to just 2.4 percent after 24 months. Despite their depressive symptoms, most of the Parkinson's patients who also had that condition were not treated with anti-depressants at any point in the two-year study. The findings were published in the journal Neurology.
Related chapters from BP7e: 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: 19961 - Posted: 08.16.2014
Using data from over 18,000 patients, scientists have identified more than two dozen genetic risk factors involved in Parkinson’s disease, including six that had not been previously reported. The study, published in Nature Genetics, was partially funded by the National Institutes of Health (NIH) and led by scientists working in NIH laboratories. A gene chip. Scientists used gene chips to help discover new genes that may be involved with Parkinson's disease “Unraveling the genetic underpinnings of Parkinson’s is vital to understanding the multiple mechanisms involved in this complex disease, and hopefully, may one day lead to effective therapies,” said Andrew Singleton, Ph.D., a scientist at the NIH’s National Institute on Aging (NIA) and senior author of the study. Dr. Singleton and his colleagues collected and combined data from existing genome-wide association studies (GWAS), which allow scientists to find common variants, or subtle differences, in the genetic codes of large groups of individuals. The combined data included approximately 13,708 Parkinson’s disease cases and 95,282 controls, all of European ancestry. The investigators identified potential genetic risk variants, which increase the chances that a person may develop Parkinson’s disease. Their results suggested that the more variants a person has, the greater the risk, up to three times higher, for developing the disorder in some cases.
Maggie Fox NBC News Walking is an almost magic elixir, doctors like to say. It can reverse diabetes, lower blood pressure, and help people keep the fat off. Now a study shows it can also help people with Parkinson’s disease. Parkinson’s patients who walked just three times a week felt less tired, less depressed and they found their Parkinson’s symptoms improved, also. “The results of our study suggest that walking may provide a safe and easily accessible way of improving the symptoms of Parkinson’s disease and improve quality of life,” Dr. Ergun Uc of the University of Iowa and the Veterans Affairs Medical Center of Iowa City, who led the study. The findings would only apply to Parkinson’s patients who can still walk easily. Parkinson’s is caused by the loss of brain cells that produce a message carrying-chemical, or neurotransmitter, that is important for movement. Symptoms can start with a barely noticeable trembling but worsen to difficulty walking and talking, depression and other disability. There’s no cure and the drugs used to treat the condition usually stop helping over time. Some people have trouble walking. But for those who don’t, the study found, walking can help their symptoms. And other research suggests that regular exercise can help slow down the progression of Parkinson’s. Various programs show that dancing,cycling, Pilates and even boxing can help. But walking has a big advantage – people can do it anywhere, without special equipment, and on their own schedules.
by Laura Sanders Transplanted cells can flourish for over a decade in the brain of a person with Parkinson’s disease, scientists write in the June 26 Cell Reports. Finding that these cells have staying power may encourage clinicians to pursue stem cell transplants, a still-experimental way to counter the brain deterioration that comes with Parkinson’s. Penelope Hallett of Harvard University and McLean Hospital in Belmont, Mass., and colleagues studied postmortem brain tissue from five people with advanced Parkinson’s. The five had received stem cell transplants between four and 14 years earlier. In all five people’s samples, neurons that originated from the transplanted cells showed signs of good health and appeared capable of sending messages with the brain chemical dopamine, a neurotransmitter that Parkinson’s depletes. Results are mixed about whether these transplanted cells are a good way to ease Parkinson’s symptoms. Some patients have shown improvements after the new cells stitched themselves into the brain, while others didn’t benefit from them. The cells can also cause unwanted side effects such as involuntary movements. P. J. Hallett et al. Long-term health of dopaminergic neuron transplants in Parkinson’s disease patients. Cell Reports. Vol. 7, June 26, 2014. doi: 10.1016/j.celrep.2014.05.027. © Society for Science & the Public 2000 - 2013
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: 19707 - Posted: 06.07.2014
Scientists may have discovered how the most common genetic cause of Parkinson’s disease destroys brain cells and devastates many patients worldwide. The study was partially funded by the National Institutes of Health’s National Institute of Neurological Disorders and Stroke (NINDS); the results may help scientists develop new therapies. The investigators found that mutations in a gene called leucine-rich repeat kinase 2 (LRRK2; pronounced “lark two” or “lurk two”) may increase the rate at which LRRK2 tags ribosomal proteins, which are key components of protein-making machinery inside cells. This could cause the machinery to manufacture too many proteins, leading to cell death. “For nearly a decade, scientists have been trying to figure out how mutations in LRRK2 cause Parkinson’s disease,” said Margaret Sutherland, Ph.D., a program director at NINDS. “This study represents a clear link between LRRK2 and a pathogenic mechanism linked to Parkinson’s disease.” Affecting more than half a million people in the United States, Parkinson’s disease is a degenerative disorder that attacks nerve cells in many parts of the nervous system, most notably in a brain region called the substantia nigra, which releases dopamine, a chemical messenger important for movement. Initially, Parkinson’s disease causes uncontrolled movements; including trembling of the hands, arms, or legs. As the disease gradually worsens, patients lose ability to walk, talk or complete simple tasks.
|By Bret Stetka The data confirm it: farmers are more prone to Parkinson’s than the general population. And pesticides could be to blame. Over a decade of evidence shows a clear association between pesticide exposure and a higher risk for the second most common neurodegenerative disease, after Alzheimer's. A new study published in Neurology proposes a potential mechanism by which at least some pesticides might contribute to Parkinson’s. Regardless of inciting factors — and there appear to be many — Parkinson’s ultimately claims dopamine-releasing neurons in a small, central arc of brain called the “substantia nigra pars compacta.” The nigra normally supplies dopamine to the neighboring striatum to help coordinate movement. Through a series of complex connections, striatal signals then find their way to the motor cortex and voila, we move. But when nigral neurons die, motor function goes haywire and the classic symptoms set in, including namely tremors, slowed movements, and rigidity. Pesticides first came under suspicion as potentially lethal to the nigra in the early 1980s following a tragic designer drug debacle straight out of Breaking Bad. Patients started showing up at Northern California ERs nearly unresponsive, rigid, and tremoring — in other words, severely Parkinsonian. Savvy detective work by neurologist Dr. William Langston and his colleagues, along with the Santa Clara County police, traced the mysterious outbreak to a rogue chemist and a bad batch. He’d been trying to synthesize a “synthetic heroin” — not the snow cone flavorings he claimed — however a powder sample from his garage lab contained traces of an impurity called MPTP. MPTP, it turned out, ravages dopaminergic neurons in the nigra and causes what looks like advanced Parkinson’s. All of the newly Parkinsonian patients were heroin users who had injected the tainted product. And MPTP, it also turned out, is awfully similar in structure to the widely used herbicide paraquat, leading some neurologists to turn their attention to farms and fields. © 2014 Scientific American
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,