Chapter 5. The Sensorimotor System

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By Meredith Wadman When people die from overdoses of opioids, whether prescription pain medications or street drugs, it is the suppression of breathing that almost always kills them. The drugs act on neuronal receptors to dull pain, but those in the brain stem also control breathing. When activated, they can signal respiration to slow, and then stop. The results are well-known: an epidemic of deaths—about 64,000 people in the United States alone last year. Countering this lethal side effect without losing opioids' potent pain relief is a challenge that has enticed drug developers for years. Now, for the first time, the U.S. Food and Drug Administration (FDA) in Silver Spring, Maryland, is considering whether to approve an opioid that is as effective as morphine at relieving pain and poses less risk of depressing breathing. Trevena, a firm based in Chesterbrook, Pennsylvania, announced on 2 November that it has submitted oliceridine, an intravenous opioid meant for use in hospitalized patients, to FDA for marketing approval. The drug, which would be marketed under the name Olinvo, is the most advanced of what scientists predict will be a growing crop of pain-relieving "biased agonists"—so called because, in binding a key opioid receptor in the central nervous system, they nudge it into a conformation that promotes a signaling cascade that kills pain over one that suppresses breathing. And in a paper out this week in Cell, a veteran opioid researcher and her colleagues unveil new biased opioid agonists that could surpass oliceridine, though they haven't been tested in people yet. "There are many groups creating [such] biased agonists. And one of them is going to get it right," says Bryan Roth, a molecular pharmacologist at the University of North Carolina in Chapel Hill. "To have a drug you can't die of an overdose with would be a huge lifesaver for tens of thousands of people every year." © 2017 American Association for the Advancement of Science.

Keyword: Drug Abuse; Pain & Touch
Link ID: 24337 - Posted: 11.17.2017

By RONI CARYN RABIN A. Parkinsonism refers to a group of movement abnormalities — such as stiffness, slowness, shuffling of the feet and often tremor — that are classic features of Parkinson’s disease but that can also be caused by medications and other disorders with overlapping symptoms, said Dr. Michael S. Okun, a neurologist and the national medical director of the Parkinson’s Foundation. He said that he makes no assumptions about the cause of parkinsonism “until I see the patient and pinpoint the diagnosis.” Determining the cause of parkinsonism involves asking a series of questions, starting with, “Do we think this is regular Parkinson’s disease?” said Dr. Okun, who is also co-director of the Center for Movement Disorders and Neurorestoration at the University of Florida College of Medicine in Gainesville. Though a diagnosis of Parkinson’s disease strikes fear in patients, Dr. Okun said that the illness, a neurodegenerative brain disorder caused by the loss of dopamine-containing neurons and other cells, progresses slowly in many people and generally responds well to drugs that replenish dopamine in the brain. Some patients whose parkinsonism is not caused by Parkinson’s disease also respond to these drugs, but the medications are most effective for people with Parkinson’s disease, Dr. Okun said. It’s important to rule out other potential causes of parkinsonism, he said. The condition can be triggered by antipsychotic medications that affect dopamine levels in the brain, as well as by other drugs, including stimulants like amphetamines and cocaine. Discontinuing the drugs may stop the symptoms over time, though not always. Parkinsonism may also be caused by repeated injuries to the head, exposure to various toxins or brain lesions. Once doctors rule out Parkinson’s disease, they must consider several other serious neurological disorders. The three most common ones are multiple system atrophy, a degenerative disorder also referred to as Shy-Drager syndrome, which may or may not respond well to Parkinson’s medications; progressive supranuclear palsy, or PSP, which also may respond to high doses of drugs that replace dopamine in the brain; and corticobasal degeneration (CBD). Patients with a form of dementia called Lewy body dementia may also exhibit symptoms of parkinsonism, which may or may not respond to dopamine. Various other movement disorders, called ataxias or dystonias, also may display features of parkinsonism. © 2017 The New York Times Company

Keyword: Parkinsons
Link ID: 24335 - Posted: 11.17.2017

Jon Hamilton The goal is simple: a drug that can relieve chronic pain without causing addiction. But achieving that goal has proved difficult, says Edward Bilsky, a pharmacologist who serves as the provost and chief academic officer at Pacific Northwest University of Health Sciences in Yakima, Wash. "We know a lot more about pain and addiction than we used to," says Bilsky, "But it's been hard to get a practical drug." Bilsky is moderating a panel on pain, addiction and opioid abuse at the Society for Neuroscience meeting in Washington, D.C., this week. Brain scientists have become increasingly interested in pain and addiction as opioid use has increased. About 2 million people in the U.S. now abuse opioids, according to the Centers for Disease Control and Prevention. But at least 25 million people suffer from chronic pain, according to an analysis by the National Institutes of Health. That means they have experienced daily pain for more than three months. The question is how to cut opioid abuse without hurting people who live with pain. And brain scientists think they are getting closer to an answer. One approach is to find drugs that decrease pain without engaging the brain's pleasure and reward circuits the way opioids do, Bilsky says. So far, these drugs have been hampered by dangerous side effects or proved less effective than opioids at reducing pain. But substances related to snail venom look promising, Bilsky says. © 2017 npr

Keyword: Pain & Touch
Link ID: 24321 - Posted: 11.13.2017

By Roni Dengler The bills of even newly hatched ducks might be as sensitive as our hands, as touch sensors in their beaks are as abundant as those in our fingertips and palms. That’s the take-away of new research published today in the Proceedings of the National Academy of Sciences that describes the origins of touchiness in the common duck’s quacker. Researchers knew that duck bills can sense light touch but have muted responsiveness to temperature. This comes in handy (or bill-y) since the birds forage for food in cold, murky bottom waters. Now, researchers find the sensors duck bills use to perceive touch work even before hatching. That likely helps young ducklings scavenge for food alongside adults soon after birth. In keeping with the need to feel for food, the ducks have more nerve cells to relay touch signals than chickens, which rely on eyesight to find sustenance, they report. That means different developmental programs are at work in ducks and chickens, which could help scientists uncover how touch evolved. Because the duck’s touch sensors are similar to mammals’ and their bills aren’t covered in fur, the authors suggest embryonic duck bills might be a better model than standard laboratory rodents to study touch sensation as it applies to us relatively hairless humans. © 2017 American Association for the Advancement of Science

Keyword: Pain & Touch; Development of the Brain
Link ID: 24298 - Posted: 11.07.2017

By Jocelyn Kaiser CENTREVILLE, VIRGINIA—Nothing unusual jumps out upon meeting Evelyn, a bubbly almost-3-year-old with red curls—except that she should not be here, chatting with a visitor in her family’s living room, twirling in her tights to the Pharrell Williams song “Happy.” Evelyn’s older sister Josephine had spinal muscular atrophy type 1 (SMA1), a genetic disease that gradually paralyzes babies. She died at 15 months. Evelyn was an unexpected pregnancy, but her parents decided to have the baby despite one-in-four odds of a second tragedy. Soon after Evelyn was born in December 2014, they were devastated to learn from genetic testing that she, too, had SMA1. “We knew what we were dealing with: We’ll love her for as long as we can,” says her father, Milan Villarreal. But that same night, frantically searching the internet, they learned about a clinical trial in Ohio and sent an email. At 8 weeks old, Evelyn received a gene therapy treatment that gave her body a crucial missing protein. And now here she is, not so different from any healthy toddler. Although she has weak thighs and can’t run normally or jump, she can walk quickly, dance, trace letters, toss foam blocks, carry a small chair, and climb onto her mother Elena’s lap. After the heartbreak of losing their first baby, the Villarreals have watched in amazement as Evelyn has crawled, walked, and talked. “It was just a miracle. Every milestone was like a celebration. We opened a bottle of wine for every little thing she did,” Milan says. © 2017 American Association for the Advancement of Science.

Keyword: Movement Disorders; Genes & Behavior
Link ID: 24280 - Posted: 11.02.2017

By Jessica Hamzelou Can you catch Alzheimer’s disease? Fear has been growing that the illness might be capable of spreading via blood transfusions and surgical equipment, but it has been hard to find any evidence of this happening. Now a study has found that an Alzheimer’s protein can spread between mice that share a blood supply, causing brain degeneration, and suggesting that the disease may transmissible in a similar way to Creutzfeldt-Jacob Disease (CJD). We already know from CJD that misfolded proteins can spread brain diseases. Variant CJD can spread through meat products or blood transfusions infected with so-called prion proteins, for example. Like CJD, Alzheimer’s also involves a misfolded protein called beta-amyloid. Plaques of this protein accumulate in the brains of people with the illness, although we still don’t know if the plaques cause the condition, or are merely a symptom. There has been evidence that beta-amyloid may spread like prions. Around 50 years ago, many people with a growth disorder were treated with growth hormone taken from cadavers. Many of the recipients went on to develop CJD, as these cadavers turned out to be carrying prions. But decades later, it emerged in postmortems that some of these people had also developed Alzheimer’s plaques, despite being 51 or younger at the time. The team behind this work suggested investigating whether beta-amyloid was spreading via blood products or surgical instruments, just as they can spread prions. © Copyright New Scientist Ltd

Keyword: Alzheimers; Prions
Link ID: 24266 - Posted: 10.31.2017

By JANE E. BRODY After two hourlong sessions focused first on body awareness and then on movement retraining at the Feldenkrais Institute of New York, I understood what it meant to experience an incredible lightness of being. Having, temporarily at least, released the muscle tension that aggravates my back and hip pain, I felt like I was walking on air. I had long refrained from writing about this method of countering pain because I thought it was some sort of New Age gobbledygook with no scientific basis. Boy, was I wrong! The Feldenkrais method is one of several increasingly popular movement techniques, similar to the Alexander technique, that attempt to better integrate the connections between mind and body. By becoming aware of how one’s body interacts with its surroundings and learning how to behave in less stressful ways, it becomes possible to relinquish habitual movement patterns that cause or contribute to chronic pain. The method was developed by Moshe Feldenkrais, an Israeli physicist, mechanical engineer and expert in martial arts, after a knee injury threatened to leave him unable to walk. Relying on his expert knowledge of gravity and the mechanics of motion, he developed exercises to help teach the body easier, more efficient ways to move. I went to the institute at the urging of Cathryn Jakobson Ramin, author of the recently published book “Crooked” that details the nature and results of virtually every current approach to treating back pain, a problem that has plagued me on and off (now mostly on) for decades. Having benefited from Feldenkrais lessons herself, Ms. Ramin had good reason to believe they would help me.

Keyword: Pain & Touch; Attention
Link ID: 24259 - Posted: 10.30.2017

A new study published in the journal Neuron sheds light on the normal function of LRRK2, the most common genetic cause for late-onset Parkinson’s disease. The study was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. For more than 10 years, scientists have known that mutations in the LRRK2 gene can lead to Parkinson’s disease, yet both its role in the disease and its normal function in the brain remain unclear. In a study in mice, researchers have now found that LRRK is necessary for the survival of dopamine-containing neurons in the brain, the cells most affected by Parkinson’s. Importantly, this finding could alter the design of treatments against the disease. “Since its discovery, researchers have been trying to define LRRK2 function and how mutations may lead to Parkinson’s disease,” said Beth-Anne Sieber, Ph.D., program director at NINDS. “The findings in this paper emphasize the importance of understanding the normal role for genes associated with neurodegenerative disorders.” LRRK2 is found along with a closely related protein, LRRK1, in the brain. A mutation in LRRK2 alone can eventually produce Parkinson’s disease symptoms and brain pathology in humans as they age. In mice, however, LRRK2 loss or mutation does not lead to the death of dopamine-producing neurons, possibly because LRRK1 plays a complementary or compensatory role during the relatively short, two-year mouse lifespan.

Keyword: Parkinsons
Link ID: 24254 - Posted: 10.28.2017

Bill Chappell It has the power to save lives by targeting opioid overdoses — something that kills more than 140 Americans every day. And now Narcan, the nasal spray that can pull a drug user back from an overdose, is being carried by all of Walgreens' more than 8,000 pharmacies. "By stocking Narcan in all our pharmacies, we are making it easier for families and caregivers to help their loved ones by having it on hand in case it is needed," said Walgreens vice president Rick Gates. The pharmacy chain is making the move as America struggles to respond to an opioid epidemic that President Trump is declaring a national emergency on Thursday, hoping to fight the opioid crisis that has struck families and communities from rural areas to cities. Calling the Walgreens move "an important milestone," Seamus Mulligan, CEO of Narcan maker Adapt Pharma, said that letting people get the medicine "without an individual prescription in 45 states is critical in combating this crisis." In recent years, both Walgreens, the nation's No. 2 pharmacy chain, and CVS, the No. 1 chain, have moved to widen access to Narcan and other products that contain naloxone, a fast-acting overdose antidote. As of last month, CVS reportedly offered prescription-free naloxone in 43 states. The chain has said that its pharmacies "in most communities have naloxone on hand and can dispense it the same day or ordered for the next business day." © 2017 npr

Keyword: Drug Abuse
Link ID: 24249 - Posted: 10.27.2017

As a ballet dancer in a former life, countless rehearsal hours in pointe shoes once landed me in a podiatrist’s office with a particularly inflamed ingrown toenail. To my surprise – and the doctor’s – a typical injection of local anesthesia did nothing to numb the searing pain as his knife dug into my big toe. It was not until a second full injection made my toe the size of a golf ball that I became blissfully unaware of the pain. Was my hair color to blame? It is, after all, a rumor every redhead has heard: we feel more pain and need more painkillers. A look at the published research suggests that the genes that determine my hair color may play a role, but the science itself is murky. What makes a redhead? Our luster-filled locks derive from a pair of mutated genes. For most people, hair color is determined by the melanocortin-1 receptor, or MC1R gene that leads to the production of a brown-black melanin pigment called eumelanin. The more eumelanin created by this gene, the darker and blacker the hair. Most redheads have a recessive version of the MC1R gene caused by the pairing of three possible mutant alleles. The resulting gene expression shuts off eumelanin production, shifting the dominant pigment to the reddish-toned pheomelanin. McGill University behavioral neuroscientist Jeffrey Mogil examined the gene as part of his research on the perception and inhibition of pain. “The purpose of this MC1R gene is to produce dark pigments. If it works, it does, and if it doesn’t, it produces pigment that isn’t dark like it’s supposed to be. So, it really is a dysfunction,” he said.

Keyword: Pain & Touch; Genes & Behavior
Link ID: 24248 - Posted: 10.27.2017

By GRETCHEN REYNOLDS Do brains trump brawn? A remarkable new study of how the human body prioritizes its inner workings found that if you intensely think at the same time as you intensely exercise, your performance in both thinking and moving can worsen. But your muscles’ performance will decline much more than your brain’s will, the study found. The results raise interesting questions about the roles that our body’s wide-ranging abilities may have played in the evolution of humans and also whether a hard workout is the ideal time to be cogitating. Compared to almost all other animals, we humans have disproportionately large brains for our size. Our supersized cranial contents probably provided an advantage during our evolution as a species. Smart creatures presumably could have outwitted predators and outmaneuvered prey, keeping themselves fed, uneaten and winners in the biological sweepstakes to pass on their genes. But most other species eschewed developing similarly outsized brains during evolution, because large brains carry a hefty metabolic cost. Brains are extraordinarily hungry organs, requiring, ounce for ounce, more calories to sustain their operations than almost any other tissue, and these caloric demands rise when the brain is hard at work. Thinking demands considerable bodily fuel. In order to feed and maintain these large brains, early humans’ bodies had to make certain trade-offs, most evolutionary biologists agree. Our digestive systems shrank during evolution, for one thing, since food processing is also metabolically ravenous. But whether a similar trade-off occurred with our muscles has remained in doubt. Muscles potentially provided another route to survival during our species’ early days. With sufficient brawn, animals, including people, could physically overpower prey and sprint from danger. © 2017 The New York Times Company

Keyword: Attention
Link ID: 24243 - Posted: 10.26.2017

By Amina Zafar, CBC News The soothing power of touch eases both physical pain and the sting of hurt feelings, say researchers — a finding that may be increasingly important in our social-media-driven world. When someone hurts an arm, they may brace and rub it to make it feel better. In the past 20 years, scientists have discovered that our hairy skin has cells that respond to a stroking touch. It's a trait we share with other mammals. Now psychologists in England say their work shows, for the first time, that a gentle touch can be a buffer against social rejection, too. In an experiment described in this week's issue of Scientific Reports, researchers recruited 84 healthy women and told them they were going to play a game of Cyberball, an online ball-tossing game. What the women didn't know was that their "opponents" were computer-generated avatars. Participants were told they could throw to anyone they wished, and they believed everyone would play fairly. When participants reported feeling excluded by the other "players," receiving a slow-paced stroke reduced hurt feelings from the perceived rudeness compared with a faster stroke. The study builds on previous ones showing that receiving touch from loved ones after a physical injury is supportive. "In our lab, it's tiny in effect, but the fact that it is significantly, systematically so across many participants is important," said the study's senior author, Katerina Fotopoulou, an associate professor of psychology at University College London ©2017 CBC/Radio-Canada.

Keyword: Pain & Touch
Link ID: 24222 - Posted: 10.20.2017

Expensive medicines can seem to create worse side-effects than cheaper alternatives, suggests a new study that looked at the "nocebo" effect of drugs. The opposite of the placebo effect — perceived improvement when no active medicine is given — nocebo is the perception of negative side-effects from a benign "medication" in a blind trial. These findings about nocebo effects could help improve the design of clinical trials that test new medications, said Dr. Luana Colloca, who wrote a journal commentary about the study. "The main information for patients is that they should be aware that sometimes our brain … reacts as a result of our beliefs and expectations," said Colloca, a pain researcher at University of Maryland School of Nursing. fMRI Researchers used a functional MRI scanner to identify areas along the spinal cord that became activated during the nocebo effect. (Alexandra Tinnermann and Tim Dretzler/University Medical Center Hamburg-Eppendorf) The study, published recently in the journal Science, focused on the pain perceptions of patients who were treated with creams they believed had anti-itch properties but actually contained no active ingredients. Researchers in Germany studied 49 people, randomly assigning some to receive a "cheap" cream and others to receive an "expensive" cream. Those in the expensive group received cream packaged in a colourful box labelled Solestan Creme. The others received cream packaged in a drab box labelled with the more generic sounding name Imotadil-LeniPharma Creme. ©2017 CBC/Radio-Canada.

Keyword: Pain & Touch
Link ID: 24218 - Posted: 10.19.2017

Laura Sanders Hydrogen peroxide, a molecule produced by cells under duress, may be a common danger signal, helping to alert animals to potential harm and send them scurrying. New details from planarian flatworms of how this process works may deepen scientists’ understanding of how people detect pain, and may ultimately point to better ways to curb it. “Being able to get a big-picture view of how these systems are built and what they’re cuing in on is always really helpful,” says biologist Paul Garrity of Brandeis University in Waltham, Mass. And by finding cellular similarities among planarians, fruit flies and people, the new study, published online October 16 in Nature Neuroscience, provides hints about how this threat-detecting system might have operated hundreds of millions of years ago. The results center on a protein called TRPA1, a well-known pain detector in people. Embedded in the outside of cells, TRPA1 helps many different animals detect (and ultimately escape) harmful chemicals, physical injuries and extreme temperatures. In humans, mutations in the TRPA1 gene can cause syndromes marked by intense pain. But scientists have puzzled over TRPA1’s seemingly inconsistent behavior in different animals. In Caenorhabditis elegans worms, for instance, the protein is activated by cold. But in other animals such as mosquitoes, TRPA1 is activated by heat. “The more people started looking at activation of TRPA1 in different species, the more the puzzle became complicated,” says study coauthor Marco Gallio of Northwestern University in Evanston, Ill. © Society for Science & the Public 2000 - 2017.

Keyword: Pain & Touch; Evolution
Link ID: 24211 - Posted: 10.18.2017

Jules Montague Steve Thomas and I are talking about brain implants. Bonnie Tyler’s Holding Out For a Hero is playing in the background and for a moment I almost forget that a disease has robbed Steve of his speech. The conversation breaks briefly; now I see his wheelchair, his ventilator, his hospital bed. Steve, a software engineer, was diagnosed with ALS (amyotrophic lateral sclerosis, a type of motor neurone disease) aged 50. He knew it was progressive and incurable; that he would soon become unable to move and, in his case, speak. He is using eye-gaze technology to tell me this (and later to turn off the sound of Bonnie Tyler); cameras pick up light reflection from his eye as he scans a screen. Movements of his pupils are translated into movements of a cursor through infrared technology and the cursor chooses letters or symbols. A speech-generating device transforms these written words into spoken ones – and, in turn, sentences and stories form. Eye-gaze devices allow some people with limited speech or hand movements to communicate, use environmental controls, compose music, and paint. That includes patients with ALS – up to 80% have communication difficulties, cerebral palsy, strokes, multiple sclerosis and spinal cord injuries. It’s a far cry from Elle editor-in-chief Jean-Dominique Bauby, locked-in by a stroke in 1995, painstakingly blinking through letters on an alphabet board. His memoir, written at one word every two minutes, later became a film, The Diving Bell and the Butterfly. Although some still use low-tech options (not everyone can meet the physical or cognitive requirements for eye-gaze systems; occasionally, locked-in patients can blink but cannot move their eyes), speech-to-text and text-to-speech functionality on smartphones and tablets has revolutionised communication. © 2017 Guardian News and Media Limited

Keyword: Robotics
Link ID: 24200 - Posted: 10.16.2017

Victoria Lorrimar Michael Burdett The idea of dangerous, inhumane artificial intelligence taking over the world is familiar to many of us, thanks to cautionary tales such as the Matrix and Terminator franchises. But what about the more sympathetic portrayals of robots? The benevolence of Arnold Schwarzenegger’s Terminator character in the later movies of the franchise may have been the exception in older portrayals of AI, but human-like machines are often represented more positively in contemporary films. Think of Ex Machina, Chappie or A.I. Artificial Intelligence. This shift is very likely representative of a wider shift in how we think about these technologies in reality. Blade Runner 2049, long-anticipated sequel to the original 1982 Blade Runner film, is a part of this shift. The ability of science fiction to inspire technological innovation is well-known. A lot of science fiction writers are scientists and technologists (Arthur C Clarke and Geoffrey Landis are two examples), and ideas from science fiction have sparked more serious scientific research (touch screens and tablet computers are common examples). But science fiction serves other purposes too. It can be a tool for exploring the social and ethical implications of technologies being developed now – a fictional laboratory for testing possible futures. It can also prepare us to deal with certain technologies as they arise in the real world. © 2010–2017, The Conversation US, Inc.

Keyword: Consciousness; Robotics
Link ID: 24160 - Posted: 10.07.2017

By Michael Price Expensive medications tend to make us feel better, even when they’re no different than cheap generics. But they can also make us feel worse, according to a new study. Researchers have found that we’re more likely to experience negative side effects when we take a drug we think is pricier—a flip side of the placebo effect known as the “nocebo” effect. The work could help doctors decide whether to recommend brand-name or generic drugs depending on each patient’s expectations. In the study, researchers asked 49 people to test out a purported anti-itch cream that, in reality, contained no active ingredient. Some got “Solestan® Creme,” a fake brand name in a sleek blue box designed to look like other expensive brands on the market. Others received “Imotadil-LeniPharma Creme”—another fake, this time housed in a chintzier orange box resembling those typically used for generic drugs. “I put a lot of effort into making the designs convincing,” says study leader Alexandra Tinnermann, a neuroscientist at University Medical Center Hamburg-Eppendorf in Germany. The researchers rubbed one of the two creams on the volunteers’ forearms and waited a few minutes for it soak in. They told the participants that the cream could cause increased sensitivity to pain—a known side effect of real medications called hyperalgesia. Then the scientists affixed a small device to the volunteers’ arms that delivered a brief flash of heat up to about 45°C (or 113°F). © 2017 American Association for the Advancement of Science.

Keyword: Pain & Touch
Link ID: 24154 - Posted: 10.06.2017

By GRETCHEN REYNOLDS Because we can never have enough reasons to keep exercising, a new study with mice finds that physical activity not only increases the number of new neurons in the brain, it also subtly changes the shape and workings of these cells in ways that might have implications for memory and even delaying the onset of dementia. As most of us have heard, our brains are not composed of static, unchanging tissue. Instead, in most animals, including people, the brain is a dynamic, active organ in which new neurons and neural connections are created throughout life, especially in areas of the brain related to memory and thinking. This process of creating new neurons, called neurogenesis, can be altered by lifestyle, including physical activity. Many past studies have shown that in laboratory rodents, exercise doubles or even triples the number of new cells produced in adult animals’ brains compared to the brains of animals that are sedentary. But it has not been clear whether the new brain cells in active animals are somehow different from comparable new neurons in inactive animals or if they are just more numerous. That question has long interested scientists at the Laboratory of Neurosciences at the National Institute on Aging, who have been examining how running alters the brains and behavior of lab animals. Last year, in an important study published in NeuroImage, the researchers found for the first time that young brain cells in adult mice that spent a month with running wheels in their cages did seem to be different from those in animals that did not run. For the experiment, the scientists injected a modified rabies vaccine into the animals, where it entered the nervous system and brain. They then tracked and labeled connections between brain cells and learned that compared to the sedentary animals’ brain cells, the runners’ newborn neurons had more and longer dendrites, the snaky tendrils that help to connect the cells into the neural communications network. They also found that more of these connections led to portions of the brain that are important for spatial memory, which is our internal map of where we have been and how we got there. © 2017 The New York Times Company

Keyword: Neurogenesis; Development of the Brain
Link ID: 24145 - Posted: 10.04.2017

By Dan Stark I used to tell people considering deep brain stimulation — which involves the surgical implantation of electrodes into the brain — that it gave the typical Parkinson’s sufferer perhaps 10 years of relief, during which the symptoms would be relatively minor. The bet — this is, after all, brain surgery that carries some risk of serious adverse results — would be that sometime during that decade, researchers would come up with a real solution. In other words, DBS was a way to buy time. Still, 10 years is no small period, particularly for those who have no other hope. My experience is typical. I had DBS just under 12 years ago. Things went so well that I became a huge fan of the procedure. But DBS works on only some Parkinson’s symptoms. (Drooling, for example, is not affected.) For slightly more than a decade, DBS performed wonders on me, eliminating the shakes that had accompanied my attempts to beat back Parkinson’s symptoms with medicine alone. But because DBS masks the symptoms while not affecting the underlying disease, in the end it will fail the Parkinson’s patient. For me, the failure was in the form of a one-two punch. The first blow was self-inflicted. In April, one of the batteries powering my neural implants died. That was my fault; one should monitor the batteries and replace them in advance. Because I hadn’t, I got a taste of what life would be like without the stimulators. © 1996-2017 The Washington Post

Keyword: Parkinsons
Link ID: 24132 - Posted: 10.02.2017

By GRETCHEN REYNOLDS For most of us, temptations are everywhere, from the dessert buffet to the online shoe boutique. But a new study suggests that exercise might be a simple if unexpected way to increase our willpower and perhaps help us to avoid making impulsive choices that we will later regret. Self-control is one of those concepts that we all recognize and applaud but do not necessarily practice. It requires forgoing things that entice us, which, let’s face it, is not fun. On the other hand, lack of self-control can be consequential for health and well-being, often contributing to problems like weight gain, depression or money woes. Given these impacts, scientists and therapists have been interested in finding ways to increase people’s self-restraint. Various types of behavioral therapies and counseling have shown promise. But such techniques typically require professional assistance and have for the most part been used to treat people with abnormally high levels of impulsiveness. There have been few scientifically validated options available to help those of us who might want to be just a little better at resisting our more devilish urges. So for the new study, which was published recently in Behavior Modification, a group of researchers at the University of Kansas in Lawrence began wondering about exercise. Exercise is known to have considerable psychological effects. It can raise moods, for example, and expand people’s sense of what they are capable of doing. So perhaps, the researchers speculated, exercise might alter how well people can control their impulses. To find out, the scientists decided first to mount a tiny pilot study, involving only four men and women. © 2017 The New York Times Company

Keyword: Obesity; Attention
Link ID: 24119 - Posted: 09.28.2017