Chapter 5. The Sensorimotor System
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By Robin Wylie Scientists have been searching for a genetic explanation for athletic ability for decades. So far their efforts have focused largely on genes related to physical attributes, such as muscular function and aerobic efficiency. But geneticists have also started to investigate the neurologicalbasis behind what makes someone excel in sports—and new findings implicate dopamine, a neurotransmitter responsible for the feelings of reward and pleasure. Dopamine is also involved in a host of other mental functions, including the ability to deal with stress and endure pain. Consequently, the new research supports the idea that the mental—not just the physical—is what sets elite athletes above the rest. In an effort to piece together what makes a great athlete great, researchers at the University of Parma in Italy collected DNA from 50 elite athletes (ones who had achieved top scores at an Olympic Games or other international competition) and 100 nonprofessional athletes (ones who played sports regularly, but below competitive level). They then compared four genes across the two groups that had previously been suggested as linked to athletic ability: one related to muscle development, one involved with transporting dopamine in the brain, another that regulates levels of cerebral serotonin and one involved in breaking down neurotransmitters. The researchers found a significant genetic difference between the two groups in only one of the genes: the one involved in transporting dopamine. Two particular variants of this gene (called the dopamine active transporter, or DAT) were significantly more common among the elite athletes than in the control group. One variant was almost five times more prevalent in the elite group (occurring in 24 percent of the elites versus 5 percent of the rest); the other variant was approximately 1.7 times more prevalent (51 percent versus 30 percent). The results were published in Journal of Biosciences. © 2016 Scientific American
Neuroscientists peered into the brains of patients with Parkinson’s disease and two similar conditions to see how their neural responses changed over time. The study, funded by the NIH’s Parkinson’s Disease Biomarkers Program and published in Neurology, may provide a new tool for testing experimental medications aimed at alleviating symptoms and slowing the rate at which the diseases damage the brain. “If you know that in Parkinson’s disease the activity in a specific brain region is decreasing over the course of a year, it opens the door to evaluating a therapeutic to see if it can slow that reduction,” said senior author David Vaillancourt, Ph.D., a professor in the University of Florida’s Department of Applied Physiology and Kinesiology. “It provides a marker for evaluating how treatments alter the chronic changes in brain physiology caused by Parkinson’s.” Parkinson’s disease is a neurodegenerative disorder that destroys neurons in the brain that are essential for controlling movement. While many medications exist that lessen the consequences of this neuronal loss, none can prevent the destruction of those cells. Clinical trials for Parkinson’s disease have long relied on observing whether a therapy improves patients’ symptoms, but such studies reveal little about how the treatment affects the underlying progressive neurodegeneration. As a result, while there are treatments that improve symptoms, they become less effective as the neurodegeneration advances. The new study could remedy this issue by providing researchers with measurable targets, called biomarkers, to assess whether a drug slows or even stops the progression of the disease in the brain. “For decades, the field has been searching for an effective biomarker for Parkinson’s disease,” said Debra Babcock, M.D., Ph.D., program director at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS).
By Helen Thomson Take a walk while I look inside your brain. Scientists have developed the first wearable PET scanner – allowing them to capture the inner workings of the brain while a person is on the move. The team plans to use it to investigate the exceptional talents of savants, such as perfect memory or exceptional mathematical skill. All available techniques for scanning the deeper regions of our brains require a person to be perfectly still. This limits the kinds of activities we can observe the brain doing, but the new scanner will enable researchers to study brain behaviour in normal life, as well providing a better understanding of the tremors of Parkinson’s disease, and the effectiveness of treatments for stroke. Positron emission tomography scanners track radioactive tracers, injected into the blood, that typically bind to glucose, the molecule that our cells use for energy. In this way, the scanners build 3D images of our bodies, enabling us to see which brain areas are particularly active, or where tumours are guzzling glucose in the body. To adapt this technique for people who are moving around, Stan Majewski at West Virginia University in Morgantown and his colleagues have constructed a ring of 12 radiation detectors that can be placed around a person’s head. This scanner is attached to the ceiling by a bungee-cord contraption, so that the wearer doesn’t feel the extra weight of the scanner. © Copyright Reed Business Information Ltd
Keyword: Brain imaging
Link ID: 22557 - Posted: 08.13.2016
David R. Jacobs, We all know that exercise improves our physical fitness, but staying in shape can also boost our brainpower. We are not entirely sure how, but evidence points to several explanations. First, to maintain normal cognitive function, the brain requires a constant supply of oxygen and other chemicals, delivered via its abundant blood vessels. Physical exercise—and even just simple activities such as washing dishes or vacuuming—helps to circulate nutrient-rich blood efficiently throughout the body and keeps the blood vessels healthy. Exercise increases the creation of mitochondria—the cellular structures that generate and maintain our energy—both in our muscles and in our brain, which may explain the mental edge we often experience after a workout. Studies also show that getting the heart rate up enhances neurogenesis—the ability to grow new brain cells—in adults. Regardless of the mechanism, mounting evidence is revealing a robust relation between physical fitness and cognitive function. In our 2014 study, published in Neurology, we found that physical activity has an extensive, long-lasting influence on cognitive performance. We followed 2,747 healthy people between the ages of 18 and 30 for 25 years. In 1985 we evaluated their physical fitness using a treadmill test: the participants walked up an incline that became increasingly steep every two minutes. On average, they walked for about 10 minutes, reaching 3.4 miles per hour at an 18 percent incline (a fairly steep hill). Low performers lasted for only seven minutes and high performers for about 13 minutes. A second treadmill test in 2005 revealed that our participants' fitness levels had declined with age, as would be expected, but those who were in better shape in 1985 were also more likely to be fit 20 years later. © 2016 Scientific American
Link ID: 22555 - Posted: 08.13.2016
Tim Radford Eight paraplegics – some of them paralysed for more than a decade by severe spinal cord injury – have been able to move their legs and feel sensation, after help from an artificial exoskeleton, sessions using virtual reality (VR) technology and a non-invasive system that links the brain with a computer. In effect, after just 10 months of what their Brazilian medical team call “brain training” they have been able to make a conscious decision to move and then get a response from muscles that have not been used for a decade. Of the octet, one has been able to leave her house and drive a car. Another has conceived and delivered a child, feeling the contractions as she did so. The extent of the improvements was unexpected. The scientists had intended to exploit advanced computing and robotic technology to help paraplegics recover a sense of control in their lives. But their patients recovered some feeling and direct command as well. The implication is that even apparently complete spinal cord injury might leave some connected nerve tissue that could be reawakened after years of inaction. The patients responded unevenly, but all have reported partial restoration of muscle movement or skin sensation. Some have even recovered visceral function and are now able to tell when they need the lavatory. And although none of them can walk unaided, one woman has been able to make walking movements with her legs, while suspended in a harness, and generate enough force to make a robot exoskeleton move. © 2016 Guardian News and Media Limited
In a global study of myasthenia gravis, an autoimmune disease that causes muscle weakness and fatigue, researchers found that surgical removal of an organ called the thymus reduced patients’ weakness, and their need for immunosuppressive drugs. The study, published in the New England Journal of Medicine, was partially funded by the National Institutes of Health. “Our results support the idea that thymectomy is a valid treatment option for a major form of myasthenia gravis,” said Gil Wolfe, M.D., Professor and Irvin and Rosemary Smith Chair of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, New York, and a leader of the study. The Thymectomy Trial in Non-Thymomatous Myasthenia Gravis Patients Receiving Prednisone (MGTX) was a randomized, controlled study conducted on 126 patients aged 18-65 between 2006 and 2012. The researchers compared the combination of surgery and immunosuppression with the drug prednisone with prednisone treatment alone. They performed extended transternal thymectomies on 57 patients. This major surgical procedure aims to remove most of the thymus, which requires opening of a patient’s chest. On average the researchers found that the combination of surgery and prednisone treatment reduced overall muscle weakness more than prednisone treatment alone. After 36 months of prednisone treatment, both groups of patients had better QMG scores, a measure of muscle strength. Scores for the patients who had thymectomies and prednisone were 2.84 points better than patients who were on prednisone alone.
By ABBY GOODNOUGH TUSCALOOSA, Ala. — Roslyn Lewis was at work at a dollar store here in Tuscaloosa, pushing a heavy cart of dog food, when something popped in her back: an explosion of pain. At the emergency room the next day, doctors gave her Motrin and sent her home. Her employer paid for a nerve block that helped temporarily, numbing her lower back, but she could not afford more injections or physical therapy. A decade later, the pain radiates to her right knee and remains largely unaddressed, so deep and searing that on a recent day she sat stiffly on her couch, her curtains drawn, for hours. The experience of African-Americans, like Ms. Lewis, and other minorities illustrates a problem as persistent as it is complex: Minorities tend to receive less treatment for pain than whites, and suffer more disability as a result. While an epidemic of prescription opioid abuse has swept across the United States, African-Americans and Hispanics have been affected at much lower rates than whites. Researchers say minority patients use fewer opioids, and they offer a thicket of possible explanations, including a lack of insurance coverage and a greater reluctance among members of minority groups to take opioid painkillers even if they are prescribed. But the researchers have also found evidence of racial bias and stereotyping in recognizing and treating pain among minorities, particularly black patients. “We’ve done a good job documenting that these disparities exist,” said Salimah Meghani, a pain researcher at the University of Pennsylvania. “We have not done a good job doing something about them.” Dr. Meghani’s 2012 analysis of 20 years of published research found that blacks were 34 percent less likely than whites to be prescribed opioids for conditions such as backaches, abdominal pain and migraines, and 14 percent less likely to receive opioids for pain from traumatic injuries or surgery. © 2016 The New York Times Company
Meghan Rosen Exercise may not erase old memories, as some studies in animals have previously suggested. Running on an exercise wheel doesn’t make rats forgetprevious trips through an underwater maze, Ashok Shetty and colleagues report August 2 in the Journal of Neuroscience. Exercise or not, four weeks after learning how to find a hidden platform, rats seem to remember the location just fine, the team found. The results conflict with two earlier papers that show that running triggers memory loss in some rodents by boosting the birth of new brain cells. Making new brain cells rejiggers memory circuits, and that can make it hard for animals to remember what they’ve learned, says Paul Frankland, a neuroscientist at the Hospital for Sick Children in Toronto. He has reported this phenomenon in mice, guinea pigs and degus (SN: 6/14/14, p. 7). Maybe rats are the exception, he says, “but I’m not convinced.” In 2014, Frankland and colleagues reported that brain cell genesis clears out fearful memories in three different kinds of rodents. Two years later, Frankland’s team found similar results with spatial memories. After exercising, mice had trouble remembering the location of a hidden platform in a water maze, the team reported in February in Nature Communications. Again, Frankland and colleagues pinned the memory wipeout on brain cell creation — like a chalkboard eraser that brushes away old information. The wipe seemed to clear the way for new memories to form. Shetty, a neuroscientist at Texas A&M Health Science Center in Temple, wondered if the results held true in rats, too. “Rats are quite different from mice,” he says. “Their biology is similar to humans.” |© Society for Science & the Public 2000 - 2016. All rights reserved.
Keyword: Learning & Memory
Link ID: 22510 - Posted: 08.03.2016
By Libby Copeland Don’t get him wrong: Dean Burnett loves the brain as much as the next neuroscientist. But if he’s being honest, it’s “really quite rubbish in a lot of ways,” he says. In his new book, Idiot Brain, Burnett aims to take our most prized organ down a peg or two. Burnett is most fascinated by the brain’s tendency to trip us up when it’s just trying to help. His book explores many of these quirks: How we edit our own memories to make ourselves look better without knowing it; how anger persuades us we can take on a bully twice our size; and what may cause us to feel like we’re falling and jerk awake just as we’re falling asleep. (It could have something to do with our ancestors sleeping in trees.) We caught up with Burnett, who is also a science blogger for The Guardian and a stand-up comic, to ask him some of our everyday questions and frustrations with neuroscience. Why is it that we get motion sickness when we’re traveling in a plane or a car? We haven’t evolved, obviously, to ride in vehicles; that’s a very new thing in evolutionary terms. So the main theory as to why we get motion sickness is that it’s essentially a conflict in the senses that are being relayed to the subcortical part of the brain where the senses are integrated together. The body and the muscles are saying we are still. Your eyes are saying the environment is still. The balance sense in the ears are detecting movement. The brain is getting conflicting messages from the fundamental senses, and in evolutionary terms there’s only one thing that can cause that, which is a neurotoxin. And as a result the brain thinks it’s been poisoned and what do you do when you’ve been poisoned? Throw up.
Link ID: 22508 - Posted: 08.03.2016
Nisha Gaind Most people in the United States are more worried than enthusiastic about the prospect of scientific advances such as gene editing and brain-chip implants, a survey of thousands suggests. The Pew Research Center in Washington DC asked 4,726 US people about the potential uses of three biomedical technologies that it classified as ‘potential human enhancement’: gene editing to reduce disease risk in babies; brain implants to enhance concentration and brain processes, and transfusions of synthetic blood to improve strength and stamina. (None of these procedures are a reality, but the underlying technologies are being researched.) Those who took the survey were overwhelmingly wary about all of the ideas. In each case, more than 60% said that they would be worried about the technologies, and fewer than half expressed enthusiasm about them — with the prospect of brain implants prompting the most concern and least excitement. More than 70% thought that the procedures would become available before they were well understood or officially deemed safe. Around one-third thought the technologies were morally unacceptable, and about 70% were concerned that such enhancements would widen social divides — for instance, because initially only wealthy people would be able to afford them. © 2016 Macmillan Publishers Limited
Link ID: 22505 - Posted: 08.02.2016
Ian Sample and Nicky Woolf When Bill Gates pulled on a red and white-striped cord to upturn a bucket of iced water positioned delicately over his head, the most immediate thought for many was not, perhaps, of motor neurone disease. But the ice bucket challenge, the charity campaign that went viral in the summer of 2014 and left scores of notable persons from Gates and Mark Zuckerberg to George W. Bush and Anna Wintour shivering and drenched, has paid off in the most spectacular way. Dismissed by some at the time as “slacktivism” - an exercise that appears to do good while achieving very little - the ice bucket challenge raised more than $115m (£88m) for motor neurone disease in a single month. Now, scientists funded with the proceeds have discovered a gene variant associated with the condition. In the near term the NEK1 gene variant, described in the journal Nature Genetics this week, will help scientists understand how the incurable disorder, known also as Amyotrophic Lateral Sclerosis (ALS) or Lou Gehrig’s disease, takes hold. Once the mechanisms are more clearly elucidated, it may steer researchers on a path towards much-needed treatments. The work may never have happened were it not for the curious appeal of the frozen water drenchings. The research grants that scientists are awarded do not get close to the €4m the study required. Instead, Project MinE, which aims to unravel the genetic basis of the disease and ultimately find a cure, was funded by the ALS Association through ice bucket challenge donations. © 2016 Guardian News and Media Limited
By Gretchen Reynolds Learning requires more than the acquisition of unfamiliar knowledge; that new information or know-how, if it’s to be more than ephemeral, must be consolidated and securely stored in long-term memory. Mental repetition is one way to do that, of course. But mounting scientific evidence suggests that what we do physically also plays an important role in this process. Sleep, for instance, reinforces memory. And recent experiments show that when mice and rats jog on running wheels after acquiring a new skill, they learn much better than sedentary rodents do. Exercise seems to increase the production of biochemicals in the body and brain related to mental function. Researchers at the Donders Institute for Brain, Cognition and Behavior at Radboud University in the Netherlands and the University of Edinburgh have begun to explore this connection. For a study published this month in Current Biology, 72 healthy adult men and women spent about 40 minutes undergoing a standard test of visual and spatial learning. They observed pictures on a computer screen and then were asked to remember their locations. Afterward, the subjects all watched nature documentaries. Two-thirds of them also exercised: Half were first put through interval training on exercise bicycles for 35 minutes immediately after completing the test; the others did the same workout four hours after the test. Two days later, everyone returned to the lab and repeated the original computerized test while an M.R.I. machine scanned their brain activity. Those who exercised four hours after the test recognized and recreated the picture locations most accurately. Their brain activity was subtly different, too, showing a more consistent pattern of neural activity. The study’s authors suggest that their brains might have been functioning more efficiently because they had learned the patterns so fully. But why delaying exercise for four hours was more effective than an immediate workout remains mysterious. By contrast, rodents do better in many experiments if they work out right after learning. © 2016 The New York Times Company
Keyword: Learning & Memory
Link ID: 22486 - Posted: 07.28.2016
By KATHARINE Q. SEELYE PORTLAND, Me. — A woman in her 30s was sitting in a car in a parking lot here last month, shooting up heroin, when she overdosed. Even after the men she was with injected her with naloxone, the drug that reverses opioid overdoses, she remained unconscious. They called 911. Firefighters arrived and administered oxygen to improve her breathing, but her skin had grown gray and her lips had turned blue. As she lay on the asphalt, the paramedics slipped a needle into her arm and injected another dose of naloxone. In a moment, her eyes popped open. Her pupils were pinpricks. She was woozy and disoriented, but eventually got her bearings as paramedics put her on a stretcher and whisked her to a hospital. Every day across the country, hundreds, if not thousands, of people who overdose on opioids are being brought back to life with naloxone. Hailed as a miracle drug by many, it carries no health risk; it cannot be abused and, if given mistakenly to someone who has not overdosed on opioids, does no harm. More likely, it saves a life. As a virulent opioid epidemic continues to ravage the country, with 78 people in the United States dying of overdoses every day, naloxone’s use has increasingly moved out of medical settings, where it has been available since the 1970s, and into the homes and hands of the general public. But naloxone, also known by the brand name Narcan, has also had unintended consequences. Critics say that it gives drug users a safety net, allowing them to take more risks as they seek higher highs. Indeed, many users overdose more than once, some multiple times, and each time, naloxone brings them back. © 2016 The New York Times Company
By Maia Szalavitz When a family member, spouse or other loved one develops an opioid addiction — whether to pain relievers like Vicodin or to heroin — few people know what to do. Faced with someone who appears to be driving heedlessly into the abyss, families often fight, freeze or flee, unable to figure out how to help. Families are sometimes overwhelmed with conflicting advice about what should come next. Much of the advice given by treatment groups and programs ignores what the data says in a similar way that anti-vaccination or climate skeptic websites ignore science. The addictions field is neither adequately regulated nor effectively overseen. There are no federal standards for counseling practices or rehab programs. In many states, becoming an addiction counselor doesn’t require a high school degree or any standardized training. “There’s nothing professional about it, and it’s not evidence-based,” said Dr. Mark Willenbring, the former director of treatment research at the National Institute on Alcohol Abuse and Alcoholism, who now runs a clinic that treats addictions. Consequently, families are often given guidance that bears no resemblance to what the research evidence shows — and patients are commonly subjected to treatment that is known to do harm. People who are treated as experts firmly proclaim that they know what they are doing, but often turn out to base their care entirely on their own personal and clinical experience, not data. “Celebrity Rehab with Dr. Drew,” which many people see as an example of the best care available, for instance, used an approach that is not known to be effective for opioid addiction. More than 13 percent of its participants died after treatment,1 mainly of overdoses that could potentially have been prevented with evidence-based care. Unethical practices such as taking kickbacks for patient referrals are also rampant.
By Diana Kwon Few things feel worse than not knowing when your next paycheck is coming. Economic insecurity has been shown to have a whole host of negative effects, including low self-esteem and impaired cognitive functioning. It turns out financial stress can also physically hurt, according to a paper published in February in Psychological Science. Eileen Chou, a public policy professor at the University of Virginia, and her collaborators began by analyzing a data set of 33,720 U.S. households and found that those with higher levels of unemployment were more likely to purchase over-the-counter painkillers. Then, using a series of experiments, the team discovered that simply thinking about the prospect of financial insecurity was enough to increase pain. For example, people reported feeling almost double the amount of physical pain in their body after recalling a financially unstable time in their life as compared with those who thought about a secure period. In another experiment, university students who were primed to feel anxious about future employment prospects removed their hand from an ice bucket more quickly (showing less pain tolerance) than those who were not. The researchers also found that economic insecurity reduced people's sense of control, which, in turn, increased feelings of pain. Chou and her colleagues suggest that because of this link between financial insecurity and decreased pain tolerance, the recent recession may have been a factor in fueling the prescription painkiller epidemic. Other experts are cautious about taking the findings that far. “I think the hypothesis [that financial stress causes pain] has a lot of merit, but it would be helpful to see additional rigorous evidence in a real-world environment,” says Heather Schofield, an economist at the University of Pennsylvania who was not involved in the study. © 2016 Scientific American,
By Sara Chodosh There has long been debate about a link between serious blows to the head and the development of neurodegenerative diseases later in life. Research has made cases for and against a relationship between traumatic brain injuries and neurological ailments such as Alzheimer’s, Parkinson’s and general dementia. Now the question is drawing ever more scrutiny as the alarming extent of these injuries becomes better known—and new research is finally casting some light on this murky and often quietly terrifying topic. A large-scale analysis of three separate studies published this week in JAMA Neurology found no association between unconsciousness-causing traumatic brain injuries (TBI) and Alzheimer’s disease or general dementia—but it did find a strong association between TBI and Parkinson’s disease. “I can’t decide if the positive or negative findings are more surprising,” says one of the study’s investigators, physician and Alzheimer’s researcher Paul Crane at the University of Washington. The positive association his team found between Parkinson’s and TBI was not entirely novel, but Crane says the magnitude of the link was unexpected. The researchers found the risk of Parkinson’s rose threefold for people whose head injuries had caused them to go unconscious for more than an hour. The more contentious finding is the lack of an association between TBI and Alzheimer’s. Prior research has been divided on whether there is a link, but many of the previous studies have been smaller in scale and conducted less-comprehensive analyses. “Although early studies suggested a clear link between TBI and an increased risk for Alzheimer’s disease, this has not been replicated,” explains Frances Corrigan at the University of Adelaide, who studies how TBI influences neurodegeneration. © 2016 Scientific American,
By Gretchen Reynolds To strengthen your mind, you may first want to exert your leg muscles, according to a sophisticated new experiment involving people, mice and monkeys. The study’s results suggest that long-term endurance exercise such as running can alter muscles in ways that then jump-start changes in the brain, helping to fortify learning and memory. I often have written about the benefits of exercise for the brain and, in particular, how, when lab rodents or other animals exercise, they create extra neurons in their brains, a process known as neurogenesis. These new cells then cluster in portions of the brain critical for thinking and recollection. Even more telling, other experiments have found that animals living in cages enlivened with colored toys, flavored varieties of water and other enrichments wind up showing greater neurogenesis than animals in drab, standard cages. But animals given access to running wheels, even if they don’t also have all of the toys and other party-cage extras, develop the most new brain cells of all. These experiments strongly suggest that while mental stimulation is important for brain health, physical stimulation is even more potent. But so far scientists have not teased out precisely how physical movement remakes the brain, although all agree that the process is bogglingly complex. Fascinated by that complexity, researchers at the National Institutes of Health recently began to wonder whether some of the necessary steps might be taking place far from the brain itself, and specifically, in the muscles, which are the body part most affected by exercise. Working muscles contract, burn fuel and pump out a wide variety of proteins and other substances. The N.I.H. researchers suspected that some of those substances migrated from the muscles into the bloodstream and then to the brain, where they most likely contributed to brain health. © 2016 The New York Times Company
Keyword: Learning & Memory
Link ID: 22429 - Posted: 07.13.2016
By Aviva Rutkin At first glance, she was elderly and delicate – a woman in her 90s with a declining memory. But then she sat down at the piano to play. “Everybody in the room was totally startled,” says Eleanor Selfridge-Field, who researches music and symbols at Stanford University. “She looked so frail. Once she sat down at the piano, she just wasn’t frail at all. She was full of verve.” Selfridge-Field met this woman, referred to as ME to preserve her privacy, at a Christmas party around eight years ago. ME, who is now aged 101, has vascular dementia: she rarely knows where she is, and doesn’t recognise people she has met in the last few decades. But she can play nearly 400 songs by ear – a trick that depends on tapping into a memory of previously stored musical imprints – and continues to learn new songs just by listening to them. She has even composed an original piece of her own. ME’s musical talent, despite her cognitive impairments, inspired Selfridge-Field to spend the last six years observing her, and she presented her observations today at the International Conference on Music Perception and Cognition in San Francisco, California. ME experienced a stroke-like attack when she was in her 80s, and a few years later was diagnosed with vascular dementia. She struggles most to remember events and encounters that are recent, and her memory is selective, focusing on specific periods – such as her childhood between the ages of 3 and 8. She can recognise people that she met before the age of about 75 to 80. She is never quite sure of her surroundings. © Copyright Reed Business Information Ltd.
Link ID: 22420 - Posted: 07.11.2016
Beatrice Alexandra Golomb, Statins can indeed produce neurological effects. These drugs are typically prescribed to lower cholesterol and thereby reduce the risk of heart attack and stroke. Between 2003 and 2012 roughly one in four Americans aged 40 and older were taking a cholesterol-lowering medication, according to the Centers for Disease Control and Prevention. But studies show that statins can influence our sleep and behavior—and perhaps even change the course of neurodegenerative conditions, including dementia. The most common adverse effects include muscle symptoms, fatigue and cognitive problems. A smaller proportion of patients report peripheral neuropathy—burning, numbness or tingling in their extremities—poor sleep, and greater irritability and aggression. Interestingly, statins can produce very different outcomes in different patients, depending on an individual's medical history, the statin and the dose. Studies show, for instance, that statins generally reduce the risk of ischemic strokes—which arise when a blocked artery or blood clot cuts off oxygen to a brain region—but can also increase the risk of hemorrhagic strokes, or bleeding into the brain. Statins also appear to increase or decrease aggression. In 2015 my colleagues and I observed that women taking statins, on average, showed increased aggression; men typically showed less, possibly because of reduced testosterone levels. Some men in our study did experience a marked increase in aggression, which was correlated with worsening sleep. © 2016 Scientific American
Andrew Orlowski Special Report If the fMRI brain-scanning fad is well and truly over, then many fashionable intellectual ideas look like collateral damage, too. What might generously be called the “British intelligentsia” – our chattering classes – fell particularly hard for the promise that “new discoveries in brain science” had revealed a new understanding of human behaviour, which shed new light on emotions, personality and decision making. But all they were looking at was statistical quirks. There was no science to speak of, the results of the experiments were effectively meaningless, and couldn’t support the (often contradictory) conclusions being touted. The fMRI machine was a very expensive way of legitimising an anecdote. This is an academic scandal that’s been waiting to explode for years, for plenty of warning signs were there. In 2005, Ed Vul, now a psychology professor at UCSD, and Hal Pashler – then and now at UCSD – were puzzled by a claim being made in a talk by a neuroscience researcher. He was explaining study that purported to report a high correlation between a test subject’s brain activity and the speed with which they left the room after the study. “It seemed unbelievable to us that activity in this specific brain area could account for so much of the variance in walking speed,” explained Vul. “Especially so, because the fMRI activity was measured some two hours before the walking happened. So either activity in this area directly controlled motor action with a delay of two hours — something we found hard to believe — or there was something fishy going on.” IT © 1998–2016
Keyword: Brain imaging
Link ID: 22410 - Posted: 07.08.2016