Chapter 11. Motor Control and Plasticity
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By Jerry Adler Smithsonian Magazine | In London, Benjamin Franklin once opened a bottle of fortified wine from Virginia and poured out, along with the refreshment, three drowned flies, two of which revived after a few hours and flew away. Ever the visionary, he wondered about the possibility of incarcerating himself in a wine barrel for future resurrection, “to see and observe the state of America a hundred years hence.” Alas, he wrote to a friend in 1773, “we live in an age too early . . . to see such an art brought in our time to its perfection.” If Franklin were alive today he would find a kindred spirit in Ken Hayworth, a neuroscientist who also wants to be around in 100 years but recognizes that, at 43, he’s not likely to make it on his own. Nor does he expect to get there preserved in alcohol or a freezer; despite the claims made by advocates of cryonics, he says, the ability to revivify a frozen body “isn’t really on the horizon.” So Hayworth is hoping for what he considers the next best thing. He wishes to upload his mind—his memories, skills and personality—to a computer that can be programmed to emulate the processes of his brain, making him, or a simulacrum, effectively immortal (as long as someone keeps the power on). Hayworth’s dream, which he is pursuing as president of the Brain Preservation Foundation, is one version of the “technological singularity.” It envisions a future of “substrate-independent minds,” in which human and machine consciousness will merge, transcending biological limits of time, space and memory. “This new substrate won’t be dependent on an oxygen atmosphere,” says Randal Koene, who works on the same problem at his organization, Carboncopies.org. “It can go on a journey of 1,000 years, it can process more information at a higher speed, it can see in the X-ray spectrum if we build it that way.”
By Brady Dennis In recent months, Pasadena-based Genervon has galvanized many patients with ALS by repeatedly touting the results of 12-week, 12-person trial involving the company's drug, GM604. The company asserted its early results were “statistically significant,” “very robust” and “dramatic.” It also has said it "submitted an accelerated approval application" to the FDA which, if approved, "would allow immediate access" to patients with ALS, also known as Lou Gehrig's disease. But the Wall Street Journal reported Monday that Genervon said in an email that it is “at the point of communicating with FDA about whether [the agency] would accept our formal application” for accelerated approval. In other words, the company has not yet submitted a New Drug Application, a step needed to officially set the FDA approval process in motion. The company's acknowledgement that it has not filed an NDA appears to contradict earlier press releases and statements made by the firm's owners, Winston and Dorothy Ko -- or at least to have sown confusion about the actual status of GM604. In one February press release, for example, the company said that in a meeting with the FDA, "three times during the one-hour meeting we requested that the FDA grant GM604 accelerated approval." Asking, however, is not the same as filing the necessary paperwork and the accompanying data required for the FDA to accept it as sufficient. The difference might seem to be a matter of semantics. But the real-world consequence is that, if Genervon has no application pending at the FDA, there is no imminent decision for the FDA to make about approving GM604.
Keyword: ALS-Lou Gehrig's Disease
Link ID: 20833 - Posted: 04.22.2015
Carl Zimmer In 1998, Dr. Philip A. Starr started putting electrodes in people’s brains. A neurosurgeon at the University of California, San Francisco, Dr. Starr was treating people with Parkinson’s disease, which slowly destroys essential bits of brain tissue, robbing people of control of their bodies. At first, drugs had given his patients some relief, but now they needed more help. After the surgery, Dr. Starr closed up his patients’ skulls and switched on the electrodes, releasing a steady buzz of electric pulses in their brains. For many patients, the effect was immediate. “We have people who, when they’re not taking their meds, can be frozen,” said Dr. Starr. “When we turn on the stimulator, they start walking.” First developed in the early 1990s, deep brain stimulation, or D.B.S., was approved by the Food and Drug Administration for treating Parkinson’s disease in 2002. Since its invention, about 100,000 people have received implants. While D.B.S. doesn’t halt Parkinson’s, it can turn back the clock a few years for many patients. Yet despite its clear effectiveness, scientists like Dr. Starr have struggled to understand what D.B.S. actually does to the brain. “We do D.B.S. because it works,” said Dr. Starr, “but we don’t really know how.” In a recent experiment, Dr. Starr and his colleagues believe they found a clue. D.B.S. may counter Parkinson’s disease by liberating the brain from a devastating electrical lock-step. The new research, published on Monday in Nature Neuroscience, may help scientists develop better treatments for Parkinson’s disease. It may also help researchers adapt D.B.S. for treatment of such brain disorders as depression and obsessive compulsive disorder. © 2015 The New York Times Company
Link ID: 20817 - Posted: 04.18.2015
by Jessica Hamzelou An exoskeleton that enables movement and provides tactile feedback has helped eight paralysed people regain sensation and move previously paralysed muscles "I FELT the ball!" yelled Juliano Pinto as he kicked off the Football World Cup in Brazil last year. Pinto, aged 29 at the time, lost the use of his lower body after a car accident in 2006. "It was the most moving moment," says Miguel Nicolelis at Duke University in North Carolina, head of the Walk Again Project, which developed the thought-controlled exoskeleton that enabled Pinto to make his kick. Since November 2013, Nicolelis and his team have been training Pinto and seven other people with similar injuries to use the exoskeleton – a robotic device that encases the limbs and converts brain signals into movement. The device also feeds sensory information to its wearer, which seems to have partially reawakened their nervous system. When Nicolelis reassessed his volunteers after a year of training, he found that all eight people had regained sensations and the ability to move muscles in their once-paralysed limbs. "Nobody expected it at all," says Nicolelis, who presented the results at the Brain Forum in Lausanne, Switzerland, on 31 March. "When we first saw the level of recovery, there was not a single person in the room with a dry eye." When a person's spinal cord is injured, the connection between body and brain can be damaged, leaving them unable to feel or move parts of their body. If a few spinal nerves remain, people can sometimes regain control over their limbs, although this can involve years of rehabilitation. © Copyright Reed Business Information Ltd.
Link ID: 20805 - Posted: 04.16.2015
by Hal Hodson For a few days last summer, a handful of students walked through a park behind the University of Hannover in Germany. Each walked solo, but followed the same route as the others: made the same turns, walked the same distance. This was odd, because none of them knew where they were going. Instead, their steps were steered from a phone 10 paces behind them, which sent signals via bluetooth to electrodes attached to their legsMovie Camera. These stimulated the students' muscles, guiding their steps without any conscious effort. Max Pfeiffer of the University of Hannover was the driver. His project directs electrical currentMovie Camera into the students' sartorius, the longest muscle in the human body, which runs from the inside of the knee to the top of the outer thigh. When it contracts, it pulls the leg out and away from the body. To steer his test subjects left, Pfeiffer would zap their left sartorius, opening their gait and guiding them in that direction. Pfeiffer hopes his system will free people's minds up for other things as they navigate the world, allowing them to focus on their conversation or enjoy their surroundings. Tourists could keep their eyes on the sights while being imperceptibly guided around the city. Acceptance may be the biggest problem, although it is possible that the rise of wearable computing might help. Pfeiffer says the electrode's current causes a tingling sensation that diminishes the more someone uses the system. Volunteers said they were comfortable with the system taking control of their leg muscles, but only if they felt they could take control back. © Copyright Reed Business Information Ltd
Link ID: 20761 - Posted: 04.06.2015
By Amy Ellis Nutt and Brady Dennis For people with amyotrophic lateral sclerosis, which attacks the body’s motor neurons and renders a person unable to move, swallow or breathe, the search for an effective treatment has been a crushing disappointment. The only drug available for the disease, approved two decades ago, typically extends life just a few months. Then in the fall, a small California biotech company named Genervon began extolling the benefits of GM604, its new ALS drug. In an early-stage trial with 12 patients, the results were “statistically significant,” “very robust” and “dramatic,” the company said in news releases. Such enthusiastic pronouncements are unusual for such a small trial. In February, Genervon took an even bolder step: It applied to the Food and Drug Administration for “accelerated approval,” which allows promising treatments for serious or life-threatening diseases to bypass costly, large-scale efficacy trials and go directly to market. ALS patients responded by pleading with the FDA, in emotional videos and e-mails, to grant broad access to the experimental drug. Online forums lit up, and a Change.org petition calling for rapid approval attracted more than a half-million signatures. “Why would anyone oppose it?” asked ALS patient David Huntley in a letter read aloud in the past week at a rally on Capitol Hill. Huntley, a former triathlete, can no longer speak or travel, so his wife, Linda Clark, flew from San Diego to speak for him.
Keyword: ALS-Lou Gehrig's Disease
Link ID: 20752 - Posted: 04.04.2015
Davide Castelvecchi Boots rigged with a simple spring-and-ratchet mechanism are the first devices that do not require power aids such as batteries to make walking more energy efficient. People walking in the boots expend 7% less energy than they do walking in normal shoes, the devices’ inventors report on 1 April in Nature1. That may not sound like much, but the mechanics of the human body have been shaped by millions of years of evolution, and some experts had doubted that there was room for further improvement in human locomotion, short of skating along on wheels. “It is the first paper of which I’m aware that demonstrates that a passive system can reduce energy expenditure during walking,” says Michael Goldfarb, a mechanical engineer at Vanderbilt University in Nashville, Tennessee, who develops exoskeletons for aiding people with disabilities. As early as the 1890s, inventors tried to boost the efficiency of walking by using devices such as rubber bands, says study co-author Gregory Sawicki, a biomedical engineer and locomotion physiologist at North Carolina State University in Raleigh. More recently, engineers have built unpowered exoskeletons that enable people to do tasks such as lifting heavier weights — but do not cut down the energy they expend. (Biomechanists still debate whether the running ‘blades’ made famous by South African sprinter Oscar Pistorius are more energetically efficient than human feet.2, 3) For their device, Sawicki and his colleagues built a mechanism that parallels human physiology. When a person swings a leg forward to walk, elastic energy is stored mostly in the Achilles tendon of their standing leg. That energy is released when the standing leg's foot pushes into the ground and the heel lifts off, propelling the body forwards. “There is basically a catapult in our ankle,” Sawicki says. © 2015 Nature Publishing Group
Link ID: 20750 - Posted: 04.02.2015
By Maggie Fox and Jane Derenowski A new strain of the polio-like EV-D68 may be causing the rare and mystifying cases of muscle weakness that's affected more than 100 kids across the United States, researchers reported Monday. They say they've found the strongest evidence yet that the virus caused the polio-like syndrome, but they also say it appears to be rare and might have to do with the genetic makeup of the patients. No other germ appears to be responsible, the team reports in the journal Lancet Infectious Diseases. But because most kids were tested many days after they first got sick, it may be impossible to ever know for sure. The body will have cleared the virus itself by then, said Dr. Charles Chiu of the University of California San Francisco, who helped conduct the study. "This is a virus that causes the common cold," Chiu told NBC News. "Parents don't bring their kids in until they are really sick. By that time, typically, the viral levels may be very, very low or undetectable." "Every single virus that we found in the children corresponded to new strain of the virus, called B-1." Enterovirus D68 (EV-D68) is one of about 100 different enteroviruses that infect people. They include polio but also a range of viruses that cause cold-like symptoms. Polio's the only one that is vaccinated against; before widespread vaccination it crippled 35,000 people a year in the United States.
Keyword: Movement Disorders
Link ID: 20739 - Posted: 03.31.2015
Carl Zimmer Scientists in Iceland have produced an unprecedented snapshot of a nation’s genetic makeup, discovering a host of previously unknown gene mutations that may play roles in ailments as diverse as Alzheimer’s disease, heart disease and gallstones. “This is amazing work, there’s no question about it,” said Daniel G. MacArthur, a geneticist at Massachusetts General Hospital who was not involved in the research. “They’ve now managed to get more genetic data on a much larger chunk of the population than in any other country in the world.” In a series of papers published on Wednesday in the journal Nature Genetics, researchers at Decode, an Icelandic genetics firm owned by Amgen, described sequencing the genomes — the complete DNA — of 2,636 Icelanders, the largest collection ever analyzed in a single human population. With this trove of genetic information, the scientists were able to accurately infer the genomes of more than 100,000 other Icelanders, or almost a third of the entire country. “From the technical point of view, these papers are a tour-de-force,” said David Reich, a geneticist at Harvard Medical School who was not involved in the research. While some diseases, like cystic fibrosis, are caused by a single genetic mutation, the most common ones are not. Instead, mutations to a number of different genes can each raise the risk of getting, say, heart disease or breast cancer. Discovering these mutations can shed light on these diseases and point to potential treatments. But many of them are rare, making it necessary to search large groups of people to find them. The wealth of data created in Iceland may enable scientists to begin doing that. In their new study, the researchers at Decode present several such revealing mutations. For example, they found eight people in Iceland who shared a mutation on a gene called MYL4. Medical records showed that they also have early onset atrial fibrillation, a type of irregular heartbeat. © 2015 The New York Times Company
By Kate Baggaley Mutations on a gene necessary for keeping cells clean can cause Lou Gehrig’s disease, scientists report online March 24 in Nature Neuroscience. The gene is one of many that have been connected to the condition. In amyotrophic lateral sclerosis, also known as Lou Gehrig’s disease, nerve cells that control voluntary movement die, leading to paralysis. Scientists have previously identified mutations in 29 genes that are linked with ALS, but these genes account for less than one-third of all cases. To track down more genes, a team of European researchers looked at the protein-coding DNA of 252 ALS patients with a family history of the disease, as well as of 827 healthy people. The team discovered eight mutations on a gene called TBK1 that were associated with ALS. TBK1 normally codes for a protein that controls inflammation and cleans out damaged proteins from cells. “We do not know which of these two principle functions of TBK1 is the more relevant one” to ALS, says coauthor Jochen Weishaupt, a neurologist at Ulm University in Germany. In cells with one of the eight TBK1 mutations, the protein either is missing or lacks components that it needs to interact with other proteins, the researchers found. TBK1 mutations may explain 2 percent of ALS cases that run in families, which make up about 10 percent of all incidences of the disease, Weishaupt says. © Society for Science & the Public 2000 - 2015
By Gary Stix One of the most intriguing new areas of research in neuroscience has to do with the discovery that proteins involved with Alzheimer’s, Parkinson’s and other neurodegenerative illnesses can contort into the wrong shape. The misshapen molecules can spread throughout the brain in a manner akin to prion diseases—the most notorious of which is variant Creutzfeldt-Jakob disease, better known as Mad Cow. Misfolded proteins can lead to a buildup of cellular gunk that then causes damage inside or outside cells. If the process of misfolding observed in Alzheimer’s and Parkinson’s is similar to the one in Mad Cow, the next question is whether these misshapen proteins are transmissible from one organism to another. Last month, an article appeared in Acta Neuropathologica Communications from researchers at the Centre for Biological Threats and Special Pathogens at the Robert Koch-Institut in Berlin that raised questions about whether medical instruments need to be decontaminated if they come into contact with post-mortem brain tissue from Alzheimer’s or Parkinson’s patients. The case for putting in place such prophylaxis is rooted in lab studies that show that injecting deposits of these proteins into an animal brain can initiate a “seeding” process in which one protein causes another to misfold. “Whether those harmful effects can be also caused by transmitted protein particles in humans who express mutated or normal alpha-synuclein, A-beta or tau is still unknown,” the article says. But then it goes on: “…the ability to decontaminate medical instruments from aggregated A-beta, tau and alpha-synuclein may potentially add to patient safety.” © 2015 Scientific American
Jane Brody The Holy Grail in any progressive disease is to find it early enough to start effective treatment before irreversible damage has occurred. For Parkinson’s disease, which afflicts 1.5 million Americans and growing, a new study has brought this goal a little closer. The study, conducted among more than 54,000 British men and women, identified a slew of symptoms that were more likely to be present in people who years later were diagnosed with Parkinson’s. The findings underscore the prevailing view among neurologists that the damage caused by this disease begins long before classic symptoms like tremors, rigidity and an unsteady gait develop and a definite diagnosis can be made. The study, by Dr. Anette Schrag and fellow neurologists at the University College London, was published in The Lancet in January. As many as five years before a diagnosis of Parkinson’s, those who developed it were more likely to have experienced tremor, balance problems, constipation, low blood pressure, dizziness, erectile and urinary dysfunction, fatigue, depression and anxiety. In addition, Dr. Claire Henchcliffe, director of the Parkinson’s Disease and Movement Disorders Institute at Weill Cornell Medical Center, said that REM sleep behavior disorder, characterized by a tendency to act out one’s dreams while asleep, is one of the strongest prediagnostic symptoms, along with a lost sense of smell and subtle changes in cognition. Dr. Melissa J. Nirenberg, a Parkinson’s disease specialist at New York University Medical Center, said, “Up to 80 percent of people with the sleep disorder get Parkinson’s or a similar neurodegenerative disease.” © 2015 The New York Times Company
Jon Hamilton Since his birth 33 years ago, Jonathan Keleher has been living without a cerebellum, a structure that usually contains about half the brain's neurons. This exceedingly rare condition has left Jonathan with a distinctive way of speaking and a walk that is slightly awkward. He also lacks the balance to ride a bicycle. But all that hasn't kept him from living on his own, holding down an office job and charming pretty much every person he meets. "I've always been more into people than anything else," Jonathan tells me when I meet him at his parents' house in Concord, Mass., a suburb of Boston. "Why read a book or why do anything when you can be social and talk to people?" Jonathan is also making an important contribution to neuroscience. By allowing scientists to study him and his brain, he is helping to change some long-held misconceptions about what the cerebellum does. And that, in turn, could help the hundreds of thousands of people whose cerebellums have been damaged by a stroke, infection or disease. For decades, the cerebellum has been the "Rodney Dangerfield of the brain," says Dr. Jeremy Schmahmann, a professor of neurology at Harvard and Massachusetts General Hospital. It gets no respect because most scientists only know about its role in balance and fine motor control. © 2015 NPR
Jon Hamilton A new understanding of the brain's cerebellum could lead to new treatments for people with problems caused by some strokes, autism and even schizophrenia. That's because there's growing evidence that symptoms ranging from difficulty with abstract thinking to emotional instability to psychosis all have links to the cerebellum, says Jeremy Schmahmann, a professor of neurology at Harvard and Massachusetts General Hospital. "The cerebellum has all these functions we were previously unaware of," Schmahmann says. Scientists once thought the cerebellum's role was limited to balance and coordinating physical movements. In the past couple of decades, though, there has been growing evidence that it also plays a role in thinking and emotions. As described in an earlier post, some of the most compelling evidence has come from people like Jonathan Keleher, people born without a cerebellum. "I'm good at routine (activities) and (meeting) people," says Keleher, who is 33. He also has good long-term memory. What he's not good at is strategizing and abstract thinking. But remarkably, Keleher's abilities in these areas have improved dramatically over time. "I'm always working on how to better myself," he says. "And it's a continuous struggle." © 2015 NPR
Jon Hamilton Alzheimer's, Parkinson's and amyotrophic lateral sclerosis ravage the brain in very different ways. But they have at least one thing in common, says Corinne Lasmezas, a neuroscientist and professor at Scripps Research Institute, in Jupiter, Fla. Each spreads from brain cell to brain cell like an infection. "So if we could block this [process], that might prevent the diseases," Lasmezas says. It's an idea that's being embraced by a growing number of researchers these days, including Nobel laureate Dr. Stanley Prusiner, who first recognized in the 1980s the infectious nature of brain proteins that came to be called prions. But the idea that mad cow prions could cause disease in people has its origins in an epidemic of mad cow disease that occurred in Europe and the U.K. some 15 years ago. Back then, Lasmezas was a young researcher in France studying how mad cow, formally known as bovine spongiform encephalopathy, was transmitted. "At that time, nobody knew if this new disease in cows was actually transmissible to humans," she says. In 1996, Lasmezas published a study strongly suggesting that it was. "So that was my first great research discovery," she says. Prions, it turns out, become toxic to brain cells when folded into an abnormal shape. "This misfolded protein basically kills the neurons," Lasmezas says. © 2015 NPR
by Sarah Zielinski Before they grow wings and fly, young praying mantises have to rely on leaps to move around. But these little mantises are really good at jumping. Unlike most insects, which tend to spin uncontrollably and sometimes crash land, juvenile praying mantises make precision leaps with perfect landings. But how do they do that? To find out, Malcolm Burrows of the University of Cambridge in England and colleagues filmed 58 juvenile Stagmomantis theophila praying mantises making 381 targeted jumps. The results of their study appear March 5 in Current Biology. For each test leap, the researchers put a young insect on a ledge with a black rod placed one to two body lengths away. A jump to the rod was fast — only 80 milliseconds, faster than a blink of an eye — but high-speed video captured every move at 1,000 frames per second. That let the scientists see what was happening: First, the insect shook its head from side to side, scanning its path. Then it rocked backwards and curled up its abdomen, readying itself to take a leap. With a push of its legs, the mantis was off. In the air, it rotated its abdomen, hind legs and front legs, but its body stayed level until it hit the target and landed on all four limbs. “The abdomen, front legs and hind legs performed a series of clockwise and anticlockwise rotations during which they exchanged angular momentum at different times and in different combinations,” the researchers write. “The net result … was that the trunk of the mantis spun by 50˚relative to the horizontal with a near-constant angular momentum, aligning itself perfectly for landing with the front and hind legs ready to grasp the target.” © Society for Science & the Public 2000 - 2015
Link ID: 20663 - Posted: 03.07.2015
By Abby Phillip Jan Scheuermann, who has quadriplegia, brings a chocolate bar to her mouth using a robot arm guided by her thoughts. Research assistant Elke Brown watches in the background. (University of Pittsburgh Medical Center) Over at the Defense Advanced Research Projects Agency, also known as DARPA, there are some pretty amazing (and often top-secret) things going on. But one notable component of a DARPA project was revealed by a Defense Department official at a recent forum, and it is the stuff of science fiction movies. According to DARPA Director Arati Prabhakar, a paralyzed woman was successfully able use her thoughts to control an F-35 and a single-engine Cessna in a flight simulator. It's just the latest advance for one woman, 55-year-old Jan Scheuermann, who has been the subject of two years of groundbreaking neurosignaling research. First, Scheuermann began by controlling a robotic arm and accomplishing tasks such as feeding herself a bar of chocolate and giving high fives and thumbs ups. Then, researchers learned that -- surprisingly -- Scheuermann was able to control both right-hand and left-hand prosthetic arms with just the left motor cortex, which is typically responsible for controlling the right-hand side. After that, Scheuermann decided she was up for a new challenge, according to Prabhakar.
Link ID: 20647 - Posted: 03.04.2015
by Hal Hodson Video: Bionic arm trumps flesh after elective amputation Bionic hands are go. Three men with serious nerve damage had their hands amputated and replaced by prosthetic ones that they can control with their minds. The procedure, dubbed "bionic reconstruction", was carried out by Oskar Aszmann at the Medical University of Vienna, Austria. The men had all suffered accidents which damaged the brachial plexus – the bundle of nerve fibres that runs from the spine to the hand. Despite attempted repairs to those nerves, the arm and hand remained paralysed. "But still there are some nerve fibres present," says Aszmann. "The injury is so massive that there are only a few. This is just not enough to make the hand alive. They will never drive a hand, but they might drive a prosthetic hand." This approach works because the prosthetic hands come with their own power source. Aszmann's patients plug their hands in to charge every night. Relying on electricity from the grid to power the hand means all the muscles and nerves need do is send the right signals to a prosthetic. Before the operation, Aszmann's patients had to prepare their bodies and brains. First he transplanted leg muscle into their arms to boost the signal from the remaining nerve fibres. Three months later, after the nerves had grown into the new muscle, the men started training their brains. © Copyright Reed Business Information Ltd.
Link ID: 20617 - Posted: 02.26.2015
By Michelle Roberts Health editor, BBC News online Scientists have proposed a new idea for detecting brain conditions including Alzheimer's - a skin test. Their work, which is at an early stage, found the same abnormal proteins that accumulate in the brain in such disorders can also be found in skin. Early diagnosis is key to preventing the loss of brain tissue in dementia, which can go undetected for years. But experts said even more advanced tests, including ones of spinal fluid, were still not ready for clinic. If they were, then doctors could treatment at the earliest stages, before irreversible brain damage or mental decline has taken place. Brain biomarker Investigators have been hunting for suitable biomarkers in the body - molecules in blood or exhaled breath, for example, that can be measured to accurately and reliably signal if a disease or disorder is present. Dr Ildefonso Rodriguez-Leyva and colleagues from the University of San Luis Potosi, Mexico, believe skin is a good candidate for uncovering hidden brain disorders. Skin has the same origin as brain tissue in the developing embryo and might, therefore, be a good window to what's going on in the mind in later life - at least at a molecular level - they reasoned. Post-mortem studies of people with Parkinson's also reveal that the same protein deposits which occur in the brain with this condition also accumulate in the skin. To test if the same was true in life as after death, the researchers recruited 65 volunteers - 12 who were healthy controls and the remaining 53 who had either Parkinson's disease, Alzheimer's or another type of dementia. They took a small skin biopsy from behind the ear of each volunteer to test in their laboratory for any telltale signs of disease. Specifically, they looked for the presence of two proteins - tau and alpha-synuclein. © 2015 BBC.
By JON PALFREMAN EUGENE, Ore. — FOUR years ago, I was told I had Parkinson’s disease, a condition that affects about one million Americans. The disease is relentlessly progressive; often starting with a tremor in one limb on one side of the body, it spreads. The patient’s muscles become more rigid, frequently leading to a stooped posture, and movements slow down and get smaller and less fluid. As the disease advances — usually over a number of years — the patient becomes more and more disabled, experiencing symptoms from constipation to sleep disorders to cognitive impairment. Can Parkinson’s be slowed, stopped or even reversed? Can the disease be prevented before it starts, like polio and smallpox? More than at any time in history, success seems possible. Having sequenced the human genome, biomedical researchers have now set their sights on the ultimate frontier — the human brain. The formidable puzzle is to figure out how a three-pound lump of mostly fatty matter enables us to perform a seemingly endless number of tasks, like walking, seeing, hearing, smelling, tasting, touching, thinking, loving, hating, speaking and writing ... and why those awesome abilities break down with neurological disease. Many scientists view Parkinson’s as a so-called pathfinder. If they can figure out what causes Parkinson’s, it may open the door to understanding a host of other neurodegenerative diseases — and to making sense of an organ of incredible complexity. In Parkinson’s, the circuitry in a tiny region of the brain called the basal ganglia becomes dysfunctional. Along with the cerebellum, the basal ganglia normally acts as a kind of adviser that helps people learn adaptive skills by classic conditioning — rewarding good results with dopamine bursts and punishing errors by withholding the chemical. Babies rely on the basal ganglia to learn how to deploy their muscles to reach, grab, babble and crawl, and later to accomplish many complex tasks without thinking. For example, when a tennis player practices a stroke over and over again, the basal ganglia circuitry both rewards and “learns” the correct sequence of activities to produce, say, a good backhand drive automatically. © 2015 The New York Times Company
Link ID: 20606 - Posted: 02.24.2015