Links for Keyword: Parkinsons

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By Phyllis Richman, With apologies to Michael J. Fox, I must say Parkinson’s disease is not the best thing that ever happened to me. Picture this: One Sunday evening I walked up the street for a “meet the neighbors” party, eager to make connections in my new neighborhood. My husband decided to stay home. No problem, the party was nearby. I didn’t even take my purse: 11 years into Parkinson’s, I’ve pared down what I carry. I was burdened enough with my walking stick, a house key and a covered tray of chocolate mousses I’d made for the potluck. I’d verified on MapQuest that the address was no more than a couple of blocks away, the outer limit of my walking ability nowadays. I was looking for house number 425. It didn’t exist. The house numbers jumped from 423 to 500. I grew anxious. With Parkinson’s, stress seems to instantly drain my brain of half of its dopamine. It makes my back ache, my legs weaken and my foot curl. I tried to relax as I rested my tray on the hood of a parked car. Surely some other partygoers would come by and direct me. This is who came by: A woman with a couple of children and an apple pie, on her way to a dinner. Two passersby who wished they knew where a party was. An energetic woman with a dog. Two men carrying fishing gear, who thought I might be looking for 525. * © 1996-2011 The Washington Post

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 15288 - Posted: 05.03.2011

By Nathan Seppa Using brain surgery to insert replacement genes, doctors can alleviate some movement problems in people with Parkinson’s disease. While not all of the gene therapy recipients in a new study improved, the group on average registered tangible gains after getting a gene that revs up production of a much-needed neurotransmitter, researchers report in an upcoming issue of Lancet Neurology. Notably, none of the patients had significant side effects attributable to the therapy. “The pendulum on gene therapy has really swung back and forth,” says study coauthor Matthew During, a physician and neuroscientist at Ohio State University in Columbus. “It was enormously hyped at first.” But the death of a patient in Philadelphia in 1999 and the appearance of leukemia in children in France getting gene therapy for an immune disorder — leading to a temporary suspension of trials in 2003 — stalled the research. “The field languished for a while,” During says. But he and his colleagues have continued to pursue the technology, using a disabled, nonpathogenic virus as the delivery vehicle for potentially useful genes. To treat Parkinson’s disease, the team has targeted a troublesome part of the brain where signaling gets obstructed in patients with the neurological disorder. In the new study, the researchers randomly assigned 16 patients with advanced Parkinson’s to undergo an operation to install gene replacements; 21 similar patients got sham surgery and received no genes. Neither group was told which operation they were getting. © Society for Science & the Public 2000 - 2011

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 15129 - Posted: 03.24.2011

by Ferris Jabr Gene therapy for Parkinson's disease has moved a step closer to acceptance in the wake of its first successful double-blind clinical trial. In 2007, Andrew Feigin of the Feinstein Institute for Medical Research in Manhasset, New York, and colleagues conducted an open-label trial – one in which both patients and researchers know which trial members are receiving the treatment and which are given a placebo – to assess a new gene therapy for Parkinson's, which is a neurodegenerative disorder. They demonstrated that a gene that codes for glutamic acid decarboxylase (GAD) can improve the condition of people with the disease when injected into their brains. GAD is an enzyme that catalyses production of an inhibitory neurotransmitter called gamma-aminobutyric acid (GABA). Typically, people with Parkinson's produce too little GABA, and consequently have overstimulation in an area of the brain called the subthalamic nucleus. This overactivity in turn puts strain on neurons that produce another neurotransmitter – dopamine – which is vital for movement control. This helps explain some of the symptoms of Parkinson's, which include tremors, sluggish movements, rigid muscles and impaired posture and balance. Now the team have put their therapy to the ultimate test: a double-blind clinical trial in which neither the patient nor the clinical staff – other than the surgeons performing the procedures – knew who was receiving the therapy and who was given a placebo. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 15112 - Posted: 03.17.2011

NEW YORK — People who regularly use ibuprofen to ease their aches and pains may be less likely to develop Parkinson's disease than those who do not use the painkiller, researchers reported Wednesday. In a study of more than 136,000 U.S. men and women, researchers found that the more ibuprofen tablets people took each week, the lower their odds of developing Parkinson's, a disorder in which movement-regulating brain cells degenerate over time. Ibuprofen, sold as name-brands like Advil and Motrin in the U.S., is a non-steroidal anti-inflammatory drug (NSAID). But the study found no connection between Parkinson's risk and other NSAIDS, like aspirin or naproxen (Aleve), or with acetaminophen (Tylenol). Experts caution, however, that the findings do not prove that ibuprofen itself can help ward off Parkinson's. "It's too early to recommend use of ibuprofen to prevent or treat Parkinson's disease," lead researcher Dr. Xiang Gao, of Harvard Medical School in Boston, told Reuters Health in an email. Instead, Gao said, the findings lay the groundwork for clinical trials to look at whether the painkiller, which costs only a few cents per pill, might help slow SOURCE: http://bit.ly/Q5TNl Neurology, online March 2, 2011. Copyright 2011 Thomson Reuters

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 15066 - Posted: 03.03.2011

New research shows a link between use of two pesticides, rotenone and paraquat, and Parkinson's disease. People who used either pesticide developed Parkinson’s disease approximately 2.5 times more often than non-users. "Rotenone directly inhibits the function of the mitochondria, the structure responsible for making energy in the cell," said Freya Kamel, Ph.D., a researcher in the intramural program at NIEHS and co-author of the paper appearing online in the journal Environmental Health Perspectives. "Paraquat increases production of certain oxygen derivatives that may harm cellular structures. People who used these pesticides or others with a similar mechanism of action were more likely to develop Parkinson's disease. The authors studied 110 people with Parkinson’s disease and 358 matched controls from the Farming and Movement Evaluation (FAME) Study (http://www.niehs.nih.gov/research/atniehs/labs/epi/studies/fame/index.cfm) to investigate the relationship between Parkinson’s disease and exposure to pesticides or other agents that are toxic to nervous tissue. FAME is a case-control study that is part of the larger Agricultural Health Study (http://www.niehs.nih.gov/research/atniehs/labs/epi/studies/ahs/index.cfm), a study of farming and health in approximately 90,000 licensed pesticide applicators and their spouses. The investigators diagnosed Parkinson's disease by agreement of movement disorder specialists and assessed the lifelong use of pesticides using detailed interviews.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 14992 - Posted: 02.12.2011

Scientists have identified five new genes linked to Parkinson's disease in a large genetic analysis of the illness, according to a new study. After reviewing nearly 8 million possible genetic mutations, researchers pinpointed five genes connected to Parkinson's disease. Previously, six other genes were identified, and experts say there is now increasing proof the degenerative disease is sparked by peoples' genes. The discovery doesn't mean there are any new treatments just yet, but experts are optimistic they are getting closer. "The major common genetic variants for Parkinson's have been found," said Nick Wood, a professor at the Institute of Neurology at University College London, one of the researchers who led the study. "We haven't put together all the pieces of the puzzle yet, but we're not that far off," he said. He predicted a diagnostic test might be ready within a few years. Until recently, scientists hadn't been sure what caused Parkinson's disease, but assumed environmental factors such as exposure to chemicals or past head injuries were largely to blame. Scientists analyzed genetic samples from more than 12,000 people with Parkinson's disease and more than 21,000 from the general population in Europe and the U.S. They found people with the highest number of mutations in the 11 genes linked to Parkinson's were two-and-a-half times more likely to develop the disease than people who had the least amount of mutations. © CBC 2011

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 14948 - Posted: 02.03.2011

by Catherine de Lange Calcium activity in the brain plays an important role in the onset of Parkinson's disease, according to a study in mice. The finding helps explain why common calcium-blocking drugs, such as those used to control blood pressure, appear to protect against the disease. Damage to dopamine-releasing cells in a brain area called the substantia nigra (SN) is known to be involved in the onset of Parkinson's disease. "Pacemaking" cells in this area release pulses of dopamine, a hormone crucial for movement and balance. So damage to these cells leads to the symptoms of Parkinson's – such as tremors and stiffness. A key question is why cells of the SN are so much more susceptible to damage than those in surrounding areas. Now it seems that calcium, which enters these cells to regulate their activity, is the culprit. Jaime Guzman from Northwestern University in Chicago and colleagues compared the effect of calcium activity in two brain areas in mice – the pacemaking SN and a neighbouring area where there was no pacemaking activity. They found that the calcium influx in the SN caused much higher levels of oxidative stress – pressure on cells to counteract the effects of molecules such as free radicals, that can damage proteins and DNA. Oxidative stress is thought to be the source of the cell damage that leads to Parkinson's disease. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 14652 - Posted: 11.11.2010

By Ferris Jabr In the past researchers have observed an association between poor mitochondrial function and Parkinson's disease, a neurodegenerative disorder of the central nervous system that impairs speech and motor functions and affects five million people worldwide. A new meta-analysis suggests that low expression levels of 10 related gene sets responsible for mitochondrial machinery play an important role in this disorder—all previously unlinked to Parkinson's. The study, published online today in Science Translational Medicine, further points to a master switch for these gene sets as a potential target of future therapies. Mitochondria, specialized organelles found in nearly every cell of the body, use cellular respiration to generate one of the most important sources of chemical energy—adenosine triphosphate (ATP), a versatile nucleotide that powers everything from cell division to cell signaling to transportation of large molecules across the cell membrane. Because mitochondria are so vital to a cell's normal functions, damaged and dysfunctional mitochondria have been implicated in a wide array of diseases and disorders, such as diabetes and schizophrenia. Brain tissue is particularly susceptible to mitochondrial deficits because neurons generally have high-energy requirements. Charleen Chu, a neuropathologist at the University of Pittsburgh School of Medicine who has studied the link between mitochondrial function and Parkinson's, but was not involved in the new study, called it " a very interesting paper," adding that the massive study "indicates that mitochondrial dysfunction occurs early and for whatever reason mitochondrial biogenesis is either impaired or not stepping up to the demand of the neurons." © 2010 Scientific American

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 14530 - Posted: 10.07.2010

The immune system may have a key role in the development of Parkinson's disease, say US researchers. In a 20-year study of 4,000 people, half with Parkinson's disease, the team found an association between genes controlling immunity and the condition. The results raise the possibility of new targets for drug development, Nature Genetics reports. Parkinson's UK said the study strengthened the idea that immunity is an important driver of the disease. The team were not just looking for a genetic cause of the disease, but also considered clinical and environmental factors. During their search, they discovered that groups of genes collectively known as HLA genes are associated with the condition. These genes are key for the immune system to differentiate between foreign invaders and the body's own tissues. In theory, that enables the immune system to attack infectious organisms without turning on itself - but it is not always an infallible system. The genes vary considerably between individuals. Some versions of the genes are associated with increased risk or protection against infectious disease, while others can induce autoimmune disorders in which the immune system attacks the body's own tissues. Inflammation Multiple sclerosis has already been shown to be associated with the same HLA genetic variant seen in the latest study in Parkinson's disease, the researchers said. (C)BBC

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 11: Emotions, Aggression, and Stress
Link ID: 14362 - Posted: 08.16.2010

Having low vitamin D levels may increase a person's risk of developing Parkinson's disease later in life, say Finnish researchers. Their study of 3,000 people, published in Archives of Neurology, found people with the lowest levels of the sunshine vitamin had a three-fold higher risk. Vitamin D could be helping to protect the nerve cells gradually lost by people with the disease, experts say. The charity Parkinson's UK said further research was required. Parkinson's disease affects several parts of the brain, leading to symptoms like tremor and slow movements. The researchers from Finland's National Institute for Health and Welfare measured vitamin D levels from the study group between 1978 and 1980, using blood samples. They then followed these people over 30 years to see whether they developed Parkinson's disease. They found that people with the lowest levels of vitamin D were three times more likely to develop Parkinson's, compared with the group with the highest levels of vitamin D. Most vitamin D is made by the body when the skin is exposed to sunlight, although some comes from foods like oily fish, milk or cereals. As people age, however, their skin becomes less able to produce vitamin D. Doctors have known for many years that vitamin D helps calcium uptake and bone formation. But research is now showing that it also plays a role in regulating the immune system, as well as in the development of the nervous system. (C)BBC

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 14260 - Posted: 07.13.2010

By GINA KOLATA Dr. Bastiaan R. Bloem of the Radboud University Nijmegen Medical Center in the Netherlands thought he had seen it all in his years of caring for patients with Parkinson’s disease. But the 58-year-old man who came to see him recently was a total surprise. A video from the Netherlands of a 58-year-old man with a 10-year history of Parkinson’s disease showed him freezing in his movements after a few steps. Yet he was able to ride a bicycle. The man had had Parkinson’s disease for 10 years, and it had progressed until he was severely affected. Parkinson’s, a neurological disorder in which some of the brain cells that control movement die, had made him unable to walk. He trembled and could walk only a few steps before falling. He froze in place, his feet feeling as if they were bolted to the floor. But the man told Dr. Bloem something amazing: he said he was a regular exerciser — a cyclist, in fact — something that should not be possible for patients at his stage of the disease, Dr. Bloem thought. “He said, ‘Just yesterday I rode my bicycle for 10 kilometers’ — six miles,” Dr. Bloem said. “He said he rides his bicycle for miles and miles every day.” “I said, ‘This cannot be,’ ” Dr. Bloem, a professor of neurology and medical director of the hospital’s Parkinson’s Center, recalled in a telephone interview. “This man has end-stage Parkinson’s disease. He is unable to walk.” Copyright 2010 The New York Times Company

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 13931 - Posted: 06.24.2010

HONG KONG - People of Japanese and European descent who have mutant versions of five genes may be at higher risk of developing Parkinson's disease, two large teams of researchers have found. The two independent studies, published in the latest issue of Nature Genetics, involved more than 25,000 participants in total and are the largest studies to date to try to uncover genetic associations behind Parkinson's disease. A study in Japan looked only at ethnic Japanese while a second study, in the United States, focused only on people of European heritage. In the first study, Tatsushi Toda of Japan's Kobe University and colleagues sequenced the genes of 2,011 participants with the disease and 18,381 others without the disease. They found that those with the disease had variants of the genes PARK16, BST1, SNCA and LRRK2. In the second study, researchers led by Andrew Singleton at the National Institutes of Health's (NIH) laboratory of neurogenetics in the United States analyzed the genes of more than 5,000 patients of European ancestry who suffer from the disease and detected strong links between Parkinson's and variants of the genes SNCA and MAPT. The two teams later compared their data and found that variants of PARK16, SNCA and LRRK2 carry risk of Parkinson's in both Japanese and European populations, while variants of BST1 and MAPT were population-specific. Copyright 2009 Reuters.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 13470 - Posted: 06.24.2010

Researchers funded by the National Institutes of Health have turned simple baker’s yeast into a virtual army of medicinal chemists capable of rapidly searching for drugs to treat Parkinson’s disease. In a study published online today in Nature Chemical Biology, the researchers showed that they can rescue yeast cells from toxic levels of a protein implicated in Parkinson’s disease by stimulating the cells to make very small proteins called cyclic peptides. Two of the cyclic peptides had a protective effect on the yeast cells and on neurons in an animal model of Parkinson’s disease. "This biological approach to compound development opens up an entirely new direction for drug discovery, not only for Parkinson’s disease, but theoretically for any disease where key aspects of the pathology can be reproduced in yeast," says Margaret Sutherland, Ph.D., a program director at NIH’s National Institute of Neurological Disorders and Stroke (NINDS). "A key step for the future will be to identify the cellular pathways that are affected by these cyclic peptides." The research emerged from the lab of Susan Lindquist, Ph.D., a professor of biology at the Massachusetts Institute of Technology (MIT). Parkinson’s disease attacks cells in a part of the brain responsible for motor control and coordination. As those neurons degenerate, the disease leads to progressive deterioration of motor function including involuntary shaking, slowed movement, stiffened muscles, and impaired balance. The neurons normally produce a chemical called dopamine. A synthetic precursor of dopamine called L-DOPA or drugs that mimic dopamine’s action can provide symptomatic relief from Parkinson’s disease. Unfortunately, these drugs lose much of their effectiveness in later stages of the disease, and there is currently no means to slow the disease’s progressive course.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 13051 - Posted: 06.24.2010

By SANDRA BLAKESLEE By electrically stimulating the spinal cords of rodents, scientists have reversed some of the worst symptoms of Parkinson’s disease. As long as a mild current flows up their spines and into their brains, the animals regain the ability to scamper around their cages, as if they were normal. The therapy, described in Friday’s issue of the journal Science, is a potential alternative to direct stimulation, which requires risky and invasive surgery to implant electrodes deep in the brain, researchers said. Only 30 percent of severely impaired Parkinson’s patients qualify for the operation. Spinal cord stimulation would be less invasive and inherently safer, and it would reduce the amount of drugs needed to treat the disease, said the report’s lead author, Dr. Miguel A. L. Nicolelis, a neuroscientist at Duke. Dr. Nicolelis added that the procedure was now being tested on monkeys, and “if it succeeds, human clinical trials could begin in the next few years.” An expert on stimulation theories who was not involved in the research, Dr. Rodolfo Llins, said the treatment “makes good sense,” but he added: “How successfully it will translate to humans is an important issue. The human spinal cord is much more complex than the rodent counterpart, and long-term stimulation might result in nasty secondary effects.” Copyright 2009 The New York Times Company

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 12668 - Posted: 06.24.2010

By Nathan Seppa Brain surgeon Kenneth Follett had never received thank-you cards from his patients after performing an operation — until he started putting electrodes in their brains. Follett, who holds positions at the University of Nebraska Medical Center and the Veterans Affairs Medical Center in Omaha, is among a select group of surgeons who over the past decade have been treating Parkinson’s disease by installing two tiny electrodes in a patient’s brain. The change these devices induce can be astonishing, he says. Parkinson’s is characterized by brain degeneration, marked by a shortage of the neurotransmitter dopamine. That shortage results in movement problems. After surgery, many patients are suddenly able to get around, do household chores and even go shopping, Follett says. “It has the potential to change people’s lives.” Follett’s firsthand observations are now supported by clinical research. He and a team of fellow surgeons and scientists report in the Jan. 7 Journal of the American Medical Association that Parkinson’s patients randomly assigned to get medication plus the surgery show dramatic improvements, whereas patients getting just the best available medication do not. The surgery, called deep-brain stimulation, isn’t new, having been first approved by regulators in 1997. But only one other study — reported by German scientists in 2006 — has tested the surgery against medication in a large, randomized trial. That study also showed benefits in patients who received both surgery and medication (SN: 9/2/06, p. 149). © Society for Science & the Public 2000 - 2009

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 12418 - Posted: 06.24.2010

For many people, our only experience with Parkinson’s disease is that of watching actor Michael J. Fox struggle publicly with the illness as he has campaigned for more research and funding. But as my colleague Karen Barrow notes in the latest “Patient Voices” feature, there are many less-famous faces of Parkinson’s. Parkinson’s disease is a neurologic disorder that occurs as a result of the death of nerve cells in the brain that produce dopamine. The loss of dopamine production in the brain can lead to tremors, balance problems, stiff facial expressions and muffled speech, among other things. In the United States, an estimated 1 million people have the disease, and another 60,000 are diagnosed each year. Although the condition usually develops after the age of 60, 15 percent of those diagnosed are under 50. One of those is runner Alyssa Johnson, 43, who was training for the Boston Marathon in 2003 when she started dragging her leg and developed a shin cramp. After searching for answers, she was finally diagnosed with Parkinson’s. “It’s not something you’d expect with someone my age,'’ she said. “I used to run with my husband all the time. We don’t run together anymore because it’s still too hard for me emotionally. He’s still competitive, and I’m still trying to get from point A to point B.'’ Copyright 2008 The New York Times Company

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 11910 - Posted: 06.24.2010

"I couldn't live the way I was living. It was just too intense," says Nathan Klein. The married freelance television producer and father of two was 45 years old when he found out that that his tremors and loss of motor control were symptoms of Parkinson's disease. He tried various treatments and medications, including dopamine drugs. Explains Klein, "The symptoms don't get better. They get worse. And the pills you take eventually don't help out. So, you know, what's there to look forward to? Nothing." So Klein researched experimental therapies and four years ago decided to enroll in a clinical trial to assess the safety of an experimental gene therapy for Parkinson's. He became the first person in the world to undergo the procedure. Neurosurgeon Michael Kaplitt of Weill Cornell Medical Center operated on Klein. He injected viruses carrying the therapeutic genes directly into the overactive area of his brain, the subthalamic nucleus, that controls movement. Because of the experimental nature of the study, the twelve participants were only treated on one side of the brain. The study was a joint endeavor with The Feinstein Institute for Medical Research in Long Island. © ScienCentral, 2000-2007

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 11151 - Posted: 06.24.2010

In 2003, ScienCentral interviewed researcher Michael Kaplitt, assistant professor of neurological surgery at New York-Presbyterian/Weill Cornell Medical Center, and co-founder of Neurologix, Inc. Kaplitt and his team had gotten approval for a Phase 1 study to determine the safety of gene therapy in patients with Parkinson's disease and had performed the world's first gene therapy surgery on a patient with the disease. The findings of the completed study are published in the June 23 issue of the British medical journal The Lancet. The video to the right includes excerpts from our 2003 interview with Kaplitt. For more information on the newly published study, read on. The study reported positive results from the first ever gene therapy trial for Parkinson's disease. The clinical trial studied 12 patients, 11 men and one woman, ranging in age from 50 to 67, who had advanced Parkinson's disease. It was a "Phase 1" study, meaning it was designed primarily to test and prove that the therapy is safe. Kaplitt and his team used a harmless virus called an adeno-associated virus (AAV) as a sort of cargo ship for the corrective gene they wanted to deliver to the patient's brains. The virus carrying the gene called "GAD" (glutamic acid decarboxylase) was injected into a part of the brain called the subthalamic nucleus (STN), which usually has abnormally high activity in Parkinson's patients. This heightened activity leads to the loss of muscle control that is a hallmark of Parkinson's. © ScienCentral, 2000-2007

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 10419 - Posted: 06.24.2010

By CLAUDIA DREIFUS CAMBRIDGE, Mass. — Short of a Nobel Prize, there are few scientific honors that the biologist Susan L. Lindquist has not won. In The Lab Susan Lindquist and her team tested 5,000 genes to find a few that express a protein capable of saving a yeast cell from the Parkinson’s gene. Among other accolades, she is a Howard Hughes Medical Investigator, a member of the National Academies of Science and the American Academy of Arts and Sciences, and the 2006 recipient of the Sigma Xi William Procter Prize for Scientific Achievement. It has all come her way because of her imaginative research into how proteins function. Dr. Lindquist, the former director of the Whitehead Institute for Biomedical Research at the Massachusetts Institute of Technology, studies how molecular proteins change shape in cell division. The process, called protein folding, can— when it goes wrong — lead to diseases like Alzheimer’s and Parkinson’s. Last June, Dr. Lindquist and a group of colleagues published a paper in the journal Science reporting new clues about how Parkinson’s develops and how it might be treated. Copyright 2007 The New York Times Company

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 10210 - Posted: 06.24.2010

In humans, a dearth of the neurotransmitter dopamine has long been known to play a role in Parkinson's disease. It is also known that mutations in a protein called parkin cause a form of Parkinson's that is inherited. Now, UCLA scientists, reporting in the Jan. 31 issue of The Journal of Neuroscience, have put the two together. Using a new model of Parkinson's disease they developed in the simple Drosophila (fruit fly), the researchers show for the first time that a mutated form of the human parkin gene inserted into Drosophila specifically results in the death of dopaminergic cells, ultimately resulting in Parkinson's-like motor dysfunction in the fly. Thus, the interaction of mutant parkin with dopamine may be key to understanding the cause of familial Parkinson's disease — Parkinson's that runs in families. Conventional wisdom has held that parkin is recessive, meaning that two copies of the mutated gene were required in order to see the clinical signs of Parkinson's disease. But the researchers, led by George Jackson, M.D., Ph.D., UCLA associate professor of neurology and senior scientist at the Semel Institute for Neuroscience and Human Behavior at UCLA, wanted to see if they could get the protein to act in a dominant fashion, so they put only one copy of the mutation into their fly model. The result was the death of the neurons that use dopamine, the neurotransmitter long implicated in Parkinson's disease. "We put the mutant parkin in all different kinds of tissues and in different kinds of neurons, and it was toxic only to the ones that used dopamine," Jackson said. "No one's shown this degree of specificity for dopaminergic neurons."

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 9916 - Posted: 06.24.2010