Chapter 5. The Sensorimotor System
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|By Andrea Alfano To scratch an itch is to scratch many itches: placing nails to skin brings sweet yet short-lived relief because it often instigates another bout of itchiness. The unexpected culprit behind this vicious cycle, new research reveals, is serotonin, the so-called happiness hormone. Scientists thought itch was merely a mild form of pain until 2009, when Zhou-Feng Chen and his colleagues at the Center for the Study of Itch at Washington University in St. Louis discovered itch-specific neurons in mice. Though not identical, itch and pain are closely related; they share the same pathways in certain brain areas. Because of the doubling up, activating one suppresses the other, which is why scratching blocks the itch sensation momentarily. The act, however, also triggers the release of the chemical serotonin, which helps to alleviate pain. It is that burst that makes scratching feel good, but recent work by Chen's group showed that it exacerbates the itch-scratch cycle, too. Itch-sensing neurons have a set of receptors that facilitates pain relief and another that induces itch. Serotonin can bind only to the pain-related receptor, but because the two sets sit close to each other and physically interact, the chemical's arrival indirectly enhances the itch pathway. When Chen and his colleagues activated both receptors simultaneously in mice, the rodents scratched much more than if the itch-inducing receptor was turned on alone. In another experiment, mice lacking the cells that produce serotonin scratched less than normal mice when exposed to a skin irritant. The findings were published in the journal Neuron. © 2015 Scientific American
Keyword: Pain & Touch
Link ID: 20793 - Posted: 04.14.2015
Jon Hamilton Researchers have discovered the exact structure of the receptor that makes our sensory nerves tingle when we eat sushi garnished with wasabi. And because the "wasabi receptor" is also involved in pain perception, knowing its shape should help pharmaceutical companies develop new drugs to fight pain. The receptor, which scientists call TRPA1, is "an important molecule in the pain pathway," says David Julius, a professor of physiology at the University of California, San Francisco and an author of a paper published in this week's Nature. "A dream of mine is that some of the work we do will translate into medicines people can take for chronic pain." Julius led a team that discovered the receptor about a decade ago. Since then, researchers have shown that TRPA1 receptors begin sending distress signals to the brain whenever they encounter pungent chemical irritants, including not only wasabi but tear gas and air pollution from cars or wood fires. The receptors also become activated in response to chemicals released by the body itself when tissue becomes inflamed from an injury or a disease like rheumatoid arthritis. © 2015 NPR
Keyword: Pain & Touch
Link ID: 20780 - Posted: 04.10.2015
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 Andy Coghlan Who needs sight to get around when you've got a digital compass in your head? A neuroprosthesis that feeds geomagnetic signals into the brains of blind rats has enabled them to navigate around a maze. The results demonstrate that the rats could rapidly learn to deploy a completely unnatural "sense". It raises the possibility that humans could do the same, potentially opening up new ways to treat blindness, or even to provide healthy people with extra senses. "I'm dreaming that humans can expand their senses through artificial sensors for geomagnetism, ultraviolet, radio waves, ultrasonic waves and so on," says Yuji Ikegaya of the University of Tokyo in Japan, head of the team that installed and tested the 2.5-gram implant. "Ultrasonic and radio-wave sensors may enable the next generation of human-to-human communicationMovie Camera," he says. The neuroprosthesis consists of a geomagnetic compass – a version of the microchip found in smartphones – and two electrodes that fit into the animals' visual cortices, the areas of the brain that process visual information. Whenever the rat positioned its head within 20 degrees either side of north, the electrodes sent pulses of electricity into its right visual cortex. When the rat aligned its head in a southerly direction, the left visual cortex was stimulated. The stimulation allowed blind rats to build up a mental map of their surroundings without any visual cues. During training, blind rats equipped with digital compasses improved at finding food rewards in a five-pronged maze, despite being released from one of three different arms of the maze at random each time. © Copyright Reed Business Information Ltd
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 Catherine Saint Louis Joni Mitchell, 71, was taken to a hospital in Los Angeles on Tuesday after she was found unconscious at her Los Angeles home. In recent years, the singer has complained of a number of health problems, including one particularly unusual ailment: Morgellons disease. People who believe they have the condition report lesions that don’t heal, “fibers” extruding from their skin and uncomfortable sensations like pins-and-needles tingling or stinging. Sufferers may also report fatigue and problems with short-term memory and concentration. But Morgellons is not a medically accepted diagnosis. Scientists have struggled for nearly a decade to find a cause and have come up mostly empty-handed. Researchers at the Centers for Disease Control and Prevention studied 115 people who said they had the condition. In a report published in 2012, they said they were unable to identify an infectious source for the patients’ “unexplained dermopathy.” There was no evidence of an environmental link, and the “fibers” from patients resembled those from clothing that had gotten trapped in a scab or crusty skin. The investigators cast doubt on Morgellons as a distinct condition and said that it might be something doctors were already familiar with: delusional infestation, a psychiatric condition characterized by an unshakable but erroneous belief that one’s skin is infested with bugs or parasites. Drug use can contribute to such delusions, and the investigators noted evidence of drug use — prescription or illicit — in half of the people they examined. Of the 36 participants who completed neuropsychological testing, 11 percent had high scores for depression, and 63 percent, unsurprisingly, were preoccupied with health issues. © 2015 The New York Times Company
Keyword: Pain & Touch
Link ID: 20749 - Posted: 04.02.2015
The commonly-prescribed drug acetaminophen or paracetamol does nothing to help low back pain, and may affect the liver when used regularly, a large new international study has confirmed. Reporting in today's issue of the British Medical Journal researchers also say the benefits of the drug are unlikely to be worth the risks when it comes to treating osteoarthritis in the hip or knee. "Paracetamol has been widely recommended as being a safe medication, but what we are saying now is that paracetamol doesn't bring any benefit for patients with back pain, and it brings only trivial benefits to those with osteoarthritis," Gustavo Machado of The George Institute for Global Health and the University of Sydney, tells the Australian Broadcasting Corporation. "In addition to that it might bring harm to those patients." Most international clinical guidelines recommend acetaminophen as the "first choice" of treatment for low back pain and osteoarthritis of the hip and knee. However, despite a trial last year questioning the use of acetaminophen to treat low back pain, there has never been a systematic review of the evidence for this. Machado and colleagues analyzed three clinical trials and confirmed that acetaminophen is no better than placebo at treating low back pain. An analysis of 10 other clinical trials by the researchers quantified for the first time the effect acetaminophen has on reducing pain from osteoarthritis in the knee and hip. "We concluded that it is too small to be clinically worthwhile," says Machado. He says the effects of acetaminophen on the human body are not well understood and just because it can stop headaches, it doesn't mean the drug will work in all circumstances. ©2015 CBC/Radio-Canada.
Keyword: Pain & Touch
Link ID: 20748 - Posted: 04.02.2015
By Virginia Morell Rats and mice in pain make facial expressions similar to those in humans—so similar, in fact, that a few years ago researchers developed rodent “grimace scales,” which help them assess an animal’s level of pain simply by looking at its face. But scientists have questioned whether these expressions convey anything to other rodents, or if they are simply physiological reactions devoid of meaning. Now, researchers report that other rats do pay attention to the emotional expressions of their fellows, leaving an area when they see a rat that’s suffering. “It’s a finding we thought might be true, and are glad that someone figured out how to do an experiment that shows it,” says Jeffrey Mogil, a neuroscientist at McGill University in Montreal, Canada. Mogil’s lab developed pain grimace scales for rats and mice in 2006, and it discovered that mice experience pain when they see a familiar mouse suffering—a psychological phenomenon known as emotional contagion. According to Mogil, a rodent in pain expresses its anguish through narrowed eyes, flattened ears, and a swollen nose and cheeks. Because people can read these visual cues and gauge the intensity of the animal’s pain, Mogil has long thought that other rats could do so as well. In Japan, Satoshi Nakashima, a social cognition psychologist at NTT Communication Science Laboratories in Kanagawa, thought the same thing. And, knowing that other scientists had recently shown that mice can tell the difference between paintings by Picasso and Renoir, he decided to see if rodents could also discriminate between photographs of their fellows’ expressions. He designed the current experiments as part of his doctoral research. © 2015 American Association for the Advancement of Science
Mo Costandi During the 1960s, neuroscientists Ronald Melzack and Patrick Wall proposed an influential new theory of pain. At the time, researchers were struggling to explain the phenomenon. Some believed that specific nerve fibres carry pain signals up into the brain, while others argued that the pain signals are transmitted by intense firing of non-specific fibres. Neither idea was entirely satisfactory, because they could not explain why spinal surgery often fails to abolish pain, why gentle touch and other innocuous stimuli can sometimes cause excruciating pain, or why intensely painful stimuli are not always experienced as such. Melzack and Wall’s Gate Control Theory stated that inhibitory neurons in the spinal cord control the relay of pain signals into the brain. Despite having some holes in it, the theory provided a revolutionary new framework for understanding the neural basis of pain, and ushered in the modern era of pain research. Now, almost exactly 50 years after the publication of Melzack and Wall’s theory, European researchers provide direct evidence of gatekeeper cells that control the flow of pain and itch signals from the spinal cord to the brain. The experience that we call “pain” is an extremely complex one that often involves emotional aspects. Researchers therefore distinguish it from nociception, the process by which the nervous system detects noxious stimuli. Nociception is mediated by primary sensory neurons, whose cell bodies are clumped together in the dorsal root ganglia that run alongside the spinal cord. Each has a single fibre that splits in two not far from the cell body, sending one branch out to the skin surface and the other into the spinal cord. © 2015 Guardian News and Media Limited
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
Claudia Dreifus Twenty-three states and the District of Columbia have legalized medical marijuana, but scientific research into its appropriate uses has lagged. Dr. Mark Ware would like to change that. Dr. Ware, 50, is the director of the Canadian Consortium for the Investigation of Cannabinoids and the director of clinical research of the Alan Edwards Pain Management Unit of McGill University Health Center. Medical marijuana has been legal in Canada for 16 years, and Dr. Ware, a practicing physician, studies how his patients take the drug and under what conditions it is effective. We spoke for two hours at the recent meeting of the American Association for the Advancement of Science and later by telephone. Our interviews have been condensed and edited for space. Q. How did you become interested in the medical possibilities of cannabis? A. In the late 1990s, I was working in Kingston, Jamaica, at a clinic treating people with sickle cell anemia. My British father and Guyanese mother had raised me in Jamaica, and I’d attended medical school there. One day, an elderly Rastafarian came for his annual checkup. I asked him, “What are your choices of medicines?” He leaned over the table and said, “You must study the herb.” That night, I went back to my office and looked up “cannabis and pain.” What I found were countless anecdotes from patients who’d obtained marijuana either legally or not and who claimed good effect with a variety of pain-related conditions. There were also the eye-opening studies showing that the nervous system had specific receptors for cannabinoids and that these receptors were located in areas related to pain. Everything ended with, “More studies are needed.” So I thought, “This is what I should be doing; let’s go!” © 2015 The New York Times Company
by Emiko Jozuka Touch, says David J. Linden, is something we take for granted. "It's very hard to imagine it gone," he tells WIRED.co.uk. "You can imagine what it's like to be blind or deaf, or have no sense of smell, but there's no way to turn off touch". Touch might not be an obvious starting point for Linden, who is a professor of neuroscience at the John Hopkins University, studying learning and memory. But according to the professor, "the story of the neuroscience underlying touch has yet to be told". Pointing to the advances made in touch research over the last 20 years, Linden tells us that his own interest in the topic was sparked over lunch by colleagues working in the School of Medicine. Making the complex links between the brain and our sense of touch accessible to a wider audience is no easy feat. Yet in his recent book entitled, Touch: The Science of Hand, Heart, and Mind, Linden offers anecdotal and factual ways in to exploring different aspects of touch, whether that be in the form of pain, itches, hot and cold sensations or caresses. "We think of touch as being a one sense modality, but it's many different sensors in the skin acting in parallel," says Linden. He explains how the information in the form of, for example, an itch, pain or caress relays to the brain, dividing them into either discriminative or emotional forms of touch. The discriminative touch allows a person to understand where the body is being touched, or to understand if an object is textured, smooth or 3D. While emotional touch is what makes pain feel emotionally negative, or an orgasm feel positive, says Linden.
Keyword: Pain & Touch
Link ID: 20708 - Posted: 03.21.2015
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