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by Jessica Hamzelou How well can you control your thoughts? Mind-control training could improve symptoms of Parkinson's disease. Deep brain stimulation, which involves implanting electrodes in the brain, helps to alleviate problems with movement experienced by people with Parkinson's disease. "If putting in an electrode works, we thought training brains to self-regulate might work as well," says David Linden at Cardiff University, UK. To find out, Linden's team asked 10 people with Parkinson's to think about moving while having their brains scanned by fMRI for 45 minutes. Five were given real-time neurofeedback showing how well they activated a brain region that controls movement. Each participant was then told to practice such thoughts at home. Two months later, movement problems including rigidity and tremor had improved by 37 per cent in the group that received feedback compared with no change in the rest. "Sending signals to brain areas normally deprived of input could be reshaping neural networks," says Linden. Roger Barker, a neuroscientist at the University of Cambridge, points out that the treatment would not work for everyone with Parkinson's disease. "If the person has a bad tremor then it would be difficult to get an image, while others don't like being inside the scanners," he says. © Copyright Reed Business Information Ltd.
By GRETCHEN REYNOLDS Scientific discoveries can be serendipitous, and so it was when Jay L. Alberts, then a Parkinson’s disease researcher at Emory University in Atlanta, mounted a tandem bike with Cathy Frazier, a Parkinson’s patient. The two were riding the 2003 RAGBRAI bicycle tour across Iowa, hoping to raise awareness of the neurodegenerative disease and “show people with Parkinson’s that you don’t have to sit back and let the disease take over your life,” Dr. Alberts says. But something unexpected happened after the first day’s riding. One of Ms. Frazier’s symptoms was myographia, a condition in which her handwriting, legible at first, would quickly become smaller, more spidery and unreadable as she continued to write. After a day of pedaling, though, she signed a birthday card with no difficulty, her signature “beautifully written,” Dr. Alberts says. She also told him that she felt as if she didn’t have Parkinson’s. Impressed, Dr. Alberts, who now holds an endowed research chair at the Cleveland Clinic in Ohio, embarked on a series of experiments in which he had people with Parkinson’s disease ride tandem bicycles. The preliminary results are raising fascinating questions not only about whether exercise can help to combat the disease but also — and of broader import — whether intense, essentially forced workouts affect brains differently than gentler activity, even in those of us who are healthy. Scientists have known for some time that, in lab animals, forced and voluntary exercise can lead to different outcomes. Generally, mice and rats enjoy running, so if you put a running wheel in a rodent’s cage, it will hop aboard and run. © 2011 The New York Times Company
National Institutes of Health researchers have found that Parkin, an important protein linked with some cases of early-onset Parkinson’s disease, regulates how cells in our bodies take up and process dietary fats. Parkinson’s disease is a complex, progressive, and currently incurable neurological disorder characterized by shaking, stiffness, slowed movement, and impaired balance. Parkinson’s primarily affects people over 50, but in about 5 to10 percent of cases it occurs in people as young as their 20s. This form of the disease, which affects actor, author, and Parkinson’s activist Michael J. Fox, is known as early-onset Parkinson’s. Parkin mutations are present in as many as 37 percent of early-onset Parkinson’s cases. However, laboratory mice with defective Parkin do not display obvious signs of the disease. This preliminary study, which will appear online in the Journal of Clinical Investigation on Aug. 25, suggests defective Parkin may indirectly contribute to the development of some early-onset Parkinson's by changing the amount and types of fat in people’s bodies. The research team, composed of scientists from the NHLBI and the NIH’s National Institute of Neurological Disorders and Stroke, observed that mice with defective Parkin did not gain weight in response to a high-fat laboratory diet, as regular mice typically do. When the researchers examined several organs of the Parkin-defective mice, they noticed that the cells contained low levels of certain proteins that transport fat in the body. In contrast, normal mice that were fed the same high-fat diet had high levels of these fat-carrying proteins, as well as high levels of Parkin, suggesting that Parkin is involved in fat transportation.
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 15724 - Posted: 08.27.2011
By Tina Hesman Saey Stabilizing the ties that bind a protein important in Parkinson’s disease to its buddies might help fend off the disease, a new study of the protein’s structure suggests. Alpha-synuclein builds up in tough aggregates in the brains of patients with Parkinson’s disease. Researchers thought that this protein was normally a floppy, snakelike molecule. But now, neuroscientist and neurologist Dennis Selkoe of Brigham and Women’s Hospital and Harvard Medical School and his colleagues show that alpha-synuclein normally forms bands of four molecules in living cells. These quartets (scientists call them tetramers) of alpha-synuclein molecules resist the clumping that leads single molecules of the protein down the path to brain cell destruction, Selkoe and colleagues report online August 14 in Nature. Discovering that alpha-synuclein works in groups of four could be important in treating or preventing Parkinson’s disease, says Patrik Brundin, a neuroscientist at Lund University in Sweden. The findings suggest that loner alpha-synuclein molecules could be “part of the ‘bad guy’ pathway, and stabilizing it as a tetramer might help avoid the disease,” he says. No one yet knows whether quartets of alpha-synuclein disintegrate into single molecules in the brains of people with Parkinson’s disease, leading to big brain-cell-killing plaques. Studies comparing normally aging brains with those of people with the disease may help answer those and other questions raised by the study, Brundin says. © Society for Science & the Public 2000 - 2011
Alla Katsnelson Peggy Willocks was 44 when she was diagnosed with Parkinson's disease. It progressed quickly, forcing her to retire four years later from her job as a primary-school principal in Elizabethton, Tennessee. Soon, her condition had deteriorated so much that she was often unable to dress and feed herself, take care of basic hygiene or walk unaided across a room. Willocks enrolled in a trial for an experimental therapy called Spheramine, developed by Titan Pharmaceuticals, a biotechnology company in South San Francisco, California. Spheramine consists of cultured human retinal epithelial cells bound to specialized man-made carrier molecules. The cells are implanted into the brain, where it is hoped that they will produce the dopamine precursor levodopa, which can reduce the symptoms of Parkinson's disease. In August 2000, Willocks became the second person ever to receive the treatment. After having a steel halo — a stereotactic frame — bolted to her skull, she was put under general anaesthesia. Surgeons then used the frame and coordinates obtained from numerous magnetic resonance imaging (MRI) scans to pinpoint the location at which to drill. They then snaked a catheter through her brain's white matter to deliver the cells into the striatum. At first there was no effect, but Willocks says that after 6–8 months she began to feel better. The changes were always moderate and gradual, except for once, about nine months after her surgery, when she showed what her doctor called a "radical" improvement in balance. By a year after the treatment, she and the five other patients in the phase I trial showed an improvement in motor ability of 48%, and those gains largely held 4 years later1. © 2011 Nature Publishing Group,
by Andy Coghlan People with Parkinson's disease might one day be treated with brain cells made from their own skin. Two teams of researchers have independently worked out how to turn skin cells into specialised neurons that make dopamine. This neurotransmitter, which is vital for mobility, is depleted in the brains of people with Parkinson's. The studies raise the possibility of improving mobility in people with Parkinson's by restoring dopamine production to normal. At present, most patients take a drug called L-dopa to readjust levels, but with varying levels of success. Both techniques avoid the initial step of converting skin cells into embryo-like pluripotent cells – a technique which poses a possible cancer risk. Vania Broccoli of the San Raffaele Scientific Institute in Milan, and colleagues, first reprogrammed mouse skin cells using three transcription factors – proteins previously linked with the development of the neurons. The same trio of factors transformed skin cells taken from human embryos, healthy adults and people with Parkinson's. The only drawback is that Broccoli's team first had to infect the skin cells with viruses carrying genes to make the transcription factors, although the viruses used are not ones that might disrupt DNA and cause cancer. © Copyright Reed Business Information Ltd.
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: 15536 - Posted: 07.07.2011
By Nathan Seppa A nutritional supplement that is free of charge, offers a wide range of health benefits and poses little risk sounds like fodder for a late-night TV commercial. But proponents of vitamin D are increasingly convinced that the sunshine vitamin delivers the goods, no strings attached. It offers a safe route to better health, these advocates say, by promoting proper function of the bones, heart, brain, immune system, you name it. Yet, the proponents claim, most people don’t get enough. Whereas humans’ prehistoric ancestors lived outdoors and made oodles of vitamin D in their sun-exposed skin, people today have become shut-ins by comparison — and scant sun exposure means low vitamin D. Of course, not everyone sees such a grand reach for the vitamin. While scientists concur that it is essential for bone maintenance, some stop right there. The skeptics note that vitamin D’s other promising qualities have shown up largely in studies that fall short of the gold standard of medicine — the randomized controlled trial, in which groups of people get either a placebo or the real thing. While a handful of randomized trials have shown additional benefits, others have not, leaving a gap in the vitamin’s otherwise sterling reputation. This debate came to a head last November, when an Institute of Medicine panel of scientists announced new vitamin D recommendations. The old intake levels were barely high enough to prevent rickets, a bone condition associated with the Industrial Revolution. The IOM panel boosted the recommended daily intake of the vitamin from 200 to 600 international units per day for most of the population. The new dose is about 15 micrograms, in the range of vitamin D found in most multivitamins. © Society for Science & the Public 2000 - 2011
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 8: Hormones and Sex
Link ID: 15531 - Posted: 07.05.2011
By Stephen Adams, Medical Correspondent The research, which follows studies indicating that it slows the progress of Alzheimer's, suggests lithium could be a cheap therapy to combat a range of brain disorders common in the elderly. Scientists at the Buck Institute for Ageing in San Francisco made the finding in a study of mice. They hope to conduct their first trials in humans soon. Compounds of lithium - itself a soft alkali metal - have been used for over 50 years to treat mania and mood swings. But its effect on a range of neuro-degenerative diseases is only starting to be appreciated. Earlier this year a small-scale study of people with mild cognitive impairment -trouble with memory and thinking - found it delayed the onset of full-blown Alzheimer's. Psychiatrists believe it slows the formation of amyloid plaques and brain cell tangles thought to cause the disease. The American researchers think lithium works in a similar way to prevent Parkinson's, which is caused because specific brain nerve cells die. They said their study - the first in animals - showed it stopped the build up of toxic proteins and cell death. Prof Julie Andersen, of the Buck Institute, said trials in people to determine the correct dosage could start soon. © Copyright of Telegraph Media Group Limited 2011
by Wendy Zukerman A hooked herb, root extract and a dash of bark – it may sound like a witches' brew, but these compounds could provide treatments for diseases that have so far foiled western doctors, such as Parkinson's and irritable bowel syndrome. For over 2000 years Chinese doctors have treated "the shakes" – now known as Parkinson's disease – with gou teng, a herb with hook-like branches. Early this year, 115 people with Parkinson's were given a combination of traditional Chinese medical herbs, including gou teng, or a placebo for 13 weeks. At the end of the study, volunteers who had taken the herbs slept better and had more fluent speech than those taking the placebo. Parkinson's symptoms, such as muscle tremors, slowness of movement and rigidity, are caused by the progressive destruction of brain cells that produce dopamine. Previous work has suggested that an abundance of a protein called alpha-synuclein may be to blame. Current treatments aim to boost levels of dopamine, which only partly alleviates symptoms and does not affect the protein clusters. It is thought that clumps of alpha-synuclein accumulate because brain cells cannot remove them through autophagy – a type of programmed cell death. Mice without the genes needed for autophagy quickly develop Parkinson's-like symptoms. © Copyright Reed Business Information Ltd.
By Pallab Ghosh Science correspondent, BBC News Researchers in Oxford have begun creating a bank of artificially grown brain cells from Parkinson's patients, BBC news has learned. They are using a new stem cell technique that allows them to turn a small piece of skin from the patient into a small piece of brain. This is the first time this has been done in a large-scale study aimed at finding cures for the disease. Researchers say they can analyse nerve cells as they start to deteriorate. The first batch of nerve cells have been grown from a 56-year-old Oxfordshire man, Derek Underwood. He had to take early retirement because of the progression of the disease. Mr Underwood will be the first of 50 patients whose skin cells will be grown into brain cells as part of a five year study. According Dr Richard Wade Martins of Oxford University, who is leading the study, the aim is to build up a "brain bank" which will enable researchers to study how the disease develops in unprecedented detail. "The brain is an inaccessible organ and you can't get bits of people's brain to study very easily," he said. BBC © 2011
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: 15454 - Posted: 06.18.2011
By JANE E. BRODY Dr. Karen Jaffe, an obstetrician-gynecologist in Cleveland, was only 48 when she learned she had Parkinson’s disease. Four years later, she continues to maintain a full-time medical and surgical practice, even performing ritual circumcisions. “I’m doing everything I can to stay healthy,” she told me in an interview. “My medications and exercises control my tremor, so doing surgery is not a problem.” For patients with Parkinson’s disease, like Dr. Jaffe, there still is no cure. But researchers have begun to make progress in identifying causes of the disease, and a new study promises to help identify better treatments. Until then, many patients are getting by on grit and determination. In speaking recently with several of them, two common threads emerged: an initial unwillingness to believe or reveal the diagnosis, followed by acceptance and a determination to pursue whatever it takes to remain as healthy and functional as possible. In addition to taking medication designed to replace the brain chemical, dopamine, that is diminished in this neurological disease, each person I spoke with is dedicated to regular, often vigorous physical activity that can minimize the disabilities caused by Parkinson’s. One, David Wolf, 51, of Buffalo, has even taken up fencing, saying (in jest, I hope), “There’s nothing like running someone through with a sword to make your day.” Another, Rena Bulkin, 68, of Manhattan, goes to a gym several times a week to do aerobics, stretching and range-of-motion and balance exercises. “If I don’t work out, my symptoms are much worse,” she said. © 2011 The New York Times Company
By Tina Hesman Saey NEW ORLEANS — Brain cells may be the latest victim of a bacterial bad guy already charged with causing ulcers and stomach cancer. Helicobacter pylori, a bacterium that lives in the stomachs of about half the people in the world, may help trigger Parkinson’s disease, researchers reported May 22 at a meeting of the American Society for Microbiology. Parkinson’s disease is a neurological disorder that kills dopamine-producing cells in some parts of the brain. People with the disease have trouble controlling their movements. About 60,000 new cases of the disease are diagnosed each year in the United States. Some previous studies have suggested that people with Parkinson’s disease are more likely than healthy people to have had ulcers at some point in their lives and are more likely to be infected with H. pylori. But until now those connections between the bacterium and the disease have amounted to circumstantial evidence. Now researchers are gathering evidence that may pin at least some blame for Parkinson’s disease on the notorious bacterium. Middle-aged mice infected with the ulcer-causing bacterium developed abnormal movement patterns over several months of infection, said Traci Testerman, a microbiologist at Louisiana State University Health Sciences Center in Shreveport. Young mice infected with the bacterium didn’t show any signs of movement problems. Testerman’s colleague, neuroscientist Michael Salvatore, found that Helicobacter-infected mice make less dopamine in parts of the brain that control movement, possibly indicating that dopamine-making cells are dying just as they do in Parkinson’s disease patients. © Society for Science & the Public 2000 - 2011
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
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
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.
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
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.
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
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.
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