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By Jessica Hamzelou Feel like you’ve read this before? Most of us have experienced the eerie familiarity of déjà vu, and now the first brain scans of this phenomenon have revealed why – it’s a sign of our brain checking its memory. Déjà vu was thought to be caused by the brain making false memories, but research by Akira O’Connor at the University of St Andrews, UK, and his team now suggests this is wrong. Exactly how déjà vu works has long been a mystery, partly because its fleeting and unpredictable nature makes it difficult to study. To get around this, O’Connor and his colleagues developed a way to trigger the sensation of déjà vu in the lab. The team’s technique uses a standard method to trigger false memories. It involves telling a person a list of related words – such as bed, pillow, night, dream – but not the key word linking them together, in this case, sleep. When the person is later quizzed on the words they’ve heard, they tend to believe they have also heard “sleep” – a false memory. To create the feeling of déjà vu, O’ Connor’s team first asked people if they had heard any words beginning with the letter “s”. The volunteers replied that they hadn’t. This meant that when they were later asked if they had heard the word sleep, they were able to remember that they couldn’t have, but at the same time, the word felt familiar. “They report having this strange experience of déjà vu,” says O’Connor. © Copyright Reed Business Information Ltd.
By Gary Stix In recent decades neuroscience has emerged as a star among the biological disciplines. But its enormous popularity as an academic career choice has been accompanied by a drop in the percentage of trained neuroscientists who actually work in academic research positions—largely because of a lack of funding. In 2014 the National Academies organized a workshop to ponder the question of whether this trend bodes well for the scientists-to-be who are now getting their Ph.D.s. The findings were published this summer in Neuron. Steven Hyman of the Broad Institute of the Massachusetts Institute of Technology and Harvard University, who helped to plan the workshop and was recently president of the Society for Neuroscience (SfN), welcomes the flood of doctoral students choosing the field but warns: “Insofar as talented young people are discouraged from academic careers by funding levels so low that they produce debilitating levels of competition or simply foreclose opportunities, the U.S. and the world are losing an incredibly precious resource.” Because there are not enough academic positions to go around, it is now the responsibility of professors to prepare students for alternative careers, says Huda Akil of the University of Michigan Medical School, lead author of the paper. “It's not just academia and industry” where trained neuroscientists can make contributions to society, says Akil, also a former SfN president: “It's nonprofits. It's social policy. It's science writing. It's man-machine interfaces. It's Big Data, or education, or any area where knowledge of the brain is relevant.” © 2016 Scientific American
Link ID: 22564 - Posted: 08.17.2016
by Helen Thompson Some guys really know how to kill a moment. Among Mediterranean fish called ocellated wrasse (Symphodus ocellatus), single males sneak up on mating pairs in their nest and release a flood of sperm in an effort to fertilize some of the female’s eggs. But female fish may safeguard against such skullduggery through their ovarian fluid, gooey film that covers fish eggs. Suzanne Alonzo, a biologist at Yale University, and her colleagues exposed sperm from both types of males to ovarian fluid from female ocellated wrasse in the lab. Nesting males release speedier sperm in lower numbers (about a million per spawn), while sneaking males release a lot of slower sperm (about four million per spawn). Experiments showed that ovarian fluid enhanced sperm velocity and motility and favored speed over volume. Thus, the fluid gives a female’s chosen mate an edge in the race to the egg, the researchers report August 16 in Nature Communications. While methods to thwart unwanted sperm are common in species that fertilize within the body, evidence from Chinook salmon previously hinted that external fertilizers don’t have that luxury. However, these new results suggest otherwise: Some female fish retain a level of control over who fathers their offspring even after laying their eggs. Male ocellated wrasse come in three varieties: sneaky males (shown) that surprise mating pairs with sperm but don’t help raise offspring; nesting males that build algae nests and court females; and satellite males, which protect nests from sneakers but staying out of parenting. |© Society for Science & the Public 2000 - 2016
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 Marlene Cimons Former president Jimmy Carter, 91, told the New Yorker recently that 90 percent of the arguments he has with Rosalynn, his wife of 70 years, are about hearing. “When I tell her, ‘Please speak more loudly,’ she absolutely refuses to speak more loudly, or to look at me when she talks,” he told the magazine. In response, the former first lady, 88, declared that having to repeat things “drives me up the wall.” Yet after both went to the doctor, much to her surprise, “I found out it was me!” she said. “I was the one who was deaf.” Hearing loss is like that. It comes on gradually, often without an individual’s realizing it, and it prompts a range of social and health consequences. “You don’t just wake up with a sudden hearing loss,” says Barbara Kelley, executive director of the Hearing Loss Association of America. “It can be insidious. It can creep up on you. You start coping, or your spouse starts doing things for you, like making telephone calls.” An estimated 25 percent of Americans between ages 60 and 69 have some degree of hearing loss, according to the President’s Council of Advisors on Science and Technology. That percentage grows to more than 50 percent for those age 70 to 79, and to almost 80 percent of individuals older than 80. That’s about 30 million people, a number likely to increase as our population ages. Behind these statistics are disturbing repercussions such as social isolation and the inability to work, travel or be physically active.
Link ID: 22561 - Posted: 08.16.2016
Are you a giver or a taker? Brain scans have identified a region of the cerebral cortex responsible for generosity – and some of us are kinder than others. The area was identified using a computer game that linked different symbols to cash prizes that either went to the player, or one of the study’s other participants. The volunteers readily learned to score prizes that helped other people, but they tended to learn how to benefit themselves more quickly. Read more: The kindness paradox: Why be generous? MRI scanning revealed that one particular brain area – the subgenual anterior cingulate cortex – seemed to be active when participants chose to be generous, prioritising benefits for someone else over getting rewards for themselves. But Patricia Lockwood, at the University of Oxford, and her team found that this brain area was not equally active in every volunteer. People who rated themselves as having higher levels of empathy learned to benefit others faster, and these people had more activity in this particular brain area, says Lockwood. This finding may lead to new ways to identify and understand anti-social and psychopathic behavior. Journal reference: PNAS, DOI: 10.1073/pnas.1603198113 © Copyright Reed Business Information Ltd.
By Roni Caryn Rabin Dementia is a general term for a set of symptoms that includes severe memory loss, a significant decline in reasoning and severely impaired communication skills; it most commonly strikes elderly people and used to be referred to as “senility.” Alzheimer’s disease is a specific illness that is the most common cause of dementia. Though many diseases can cause dementia, Alzheimer’s accounts for 60 percent to 80 percent of dementia cases, “which is why you’ll often hear the terms used interchangeably,” said Heather Snyder, the senior director of medical and scientific operations for the Alzheimer’s Association. She said the question comes up frequently because patients may receive an initial diagnosis of dementia followed by an evaluation that yields the more specific diagnosis of Alzheimer’s disease, and they may be confused. The second most common form of dementia is vascular dementia, which is caused by a stroke or poor blood flow to the brain. Other diseases that can lead to dementia include Huntington’s disease, Parkinson’s disease and Creutzfeldt-Jakob disease. Some patients may have more than one form of dementia. Dementia is caused by damage to brain cells. In the case of Alzheimer’s disease, that damage is characterized by telltale protein fragments or plaques that accumulate in the space between nerve cells and twisted tangles of another protein that build up inside cells. In Alzheimer’s disease, dementia gets progressively worse to the point where patients cannot carry out daily activities and cannot speak, respond to their environment, swallow or walk. Although some treatments may temporarily ease symptoms, the downward progression of disease continues and it is not curable. © 2016 The New York Times Company
Link ID: 22559 - Posted: 08.16.2016
By Anna Azvolinsky Sets of neurons in the brain that behave together—firing synchronously in response to sensory or motor stimuli—are thought to be functionally and physiologically connected. These naturally occurring ensembles of neurons are one of the ways memories may be programmed in the brain. Now, in a paper published today (August 11) in Science, researchers at Columbia University and their colleagues show that it is possible to stimulate visual cortex neurons in living, awake mice and induce a new ensemble of neurons that behave as a group and maintain their concerted firing for several days. “This work takes the concept of correlated [neuronal] firing patterns in a new and important causal direction,” David Kleinfeld, a neurophysicist at the University of California, San Diego, who was not involved in the work told The Scientist. “In a sense, [the researchers] created a memory for a visual feature that does not exist in the physical world as a proof of principal of how real visual memories are formed.” “Researchers have previously related optogenetic stimulation to behavior [in animals], but this study breaks new ground by investigating the dynamics of neural activity in relation to the ensemble to which these neurons belong,” said Sebastian Seung, a computational neuroscientist at the Princeton Neuroscience Institute in New Jersey who also was not involved in the study. Columbia’s Rafael Yuste and colleagues stimulated randomly selected sets of individual neurons in the visual cortices of living mice using two-photon stimulation while the animals ran on a treadmill. © 1986-2016 The Scientist
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
By Sunpreet Singh Every day people are exposed to hours of artificial light from a variety of sources – computers, video games, office lights and, for some, 24-hour lighting in hospitals and nursing homes. Now new research in animals shows that excessive exposure to “light pollution” may be worse for health than previously known, taking a toll on muscle and bone strength. Researchers at Leiden University Medical Center in the Netherlands tracked the health of rats exposed to six months of continuous light compared to a control group of rats living under normal light-dark conditions — 12 hours of light, followed by 12 hours of dark. During the study, the rats exposed to continuous light had less muscle strength and developed signs of early-stage osteoporosis. They also got fatter and had higher blood glucose levels. Several markers of immune system health also worsened, according to the report published in the medical journal Current Biology. While earlier research has suggested excessive light exposure could affect cognition, the new research was surprising in that it showed a pronounced effect on muscles and bones. While it’s not clear why constant light exposure took a toll on the motor functions of the animals, it is known that light and dark cues influence a body’s circadian rhythms, which regulate many of the body’s physiological processes. “The study is the first of its kind to show markers of negatively-affected muscle fibers, skeletal systems and motor performances due to the disruption of circadian clocks, remarkably in only a few months,” said Chris Colwell, a psychiatry professor and sleep specialist at the University of California, Los Angeles, who was not part of the study. “They found that not only did motor performance go down on tests, but the muscles themselves just atrophied, and mice physically became weaker under just two months under these conditions.” © 2016 The New York Times Company
Keyword: Biological Rhythms
Link ID: 22556 - 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
Ramin Skibba Scientists and medical researchers in the United States have been studying the health benefits and risks of marijuana for decades. But despite the increasing availability of legal marijuana, scientists have been forced to obtain the drug from a single source — the University of Mississippi in Oxford, which grows pot for research on a campus farm under a contract with the National Institute on Drug Abuse (NIDA). Now, the university’s monopoly is coming to an end. In an unexpected move, the US Drug Enforcement Administration (DEA) announced on 11 August that it will allow any institution to apply for permission to grow marijuana for research. Nature explains how the policy could transform the study of marijuana. Why do researchers want to study pot — and how do they get it? Researchers have been extracting cannabinoids — chemical compounds found in cannabis — and developing strains of varying strength to test whether they could alleviate chronic pain and treat or mitigate the effects of ailments such as seizures and other neurological disorders. Approved medical-marijuana consumers may buy pot from dispensaries in more than half the country, and recreational marijuana use is permitted in a few states. But researchers are limited to the handful of strains grown by the University of Mississippi farm. © 2016 Macmillan Publishers Limited
Keyword: Drug Abuse
Link ID: 22554 - Posted: 08.13.2016
By THE EDITORIAL BOARD Supporters of a saner marijuana policy scored a small victory this week when the Obama administration said it would authorize more institutions to grow marijuana for medical research. But the government passed up an opportunity to make a more significant change. The Drug Enforcement Administration on Thursday turned down two petitions — one from the governors of Rhode Island and Washington and the other from a resident of New Mexico — requesting that marijuana be removed from Schedule 1 of the Controlled Substances Act. Drugs on that list, which include heroin and LSD, are deemed to have no medical use; possession is illegal under federal law, and researchers have to jump through many hoops to obtain permission to study them and obtain samples to study. Having marijuana on that list is deeply misguided since many scientists and President Obama have said that it is no more dangerous than alcohol. Over the years, Congress and attorneys general have deferred to the expertise of the D.E.A., which is the part of the Justice Department that enforces the nation’s drug laws. So the D.E.A. has amassed extensive control over drug policy making. It determines who gets to grow marijuana for research and which scholars are allowed to study it, for example. It has strongly resisted efforts by scientists, state officials and federal lawmakers to reclassify marijuana by rejecting or refusing to acknowledge evidence that marijuana is not nearly as harmful as federal law treats it. Since 1968, the University of Mississippi has been the only institution allowed to grow the plant for research. This has severely limited availability. The D.E.A. now says that because researchers are increasingly interested in studying marijuana, it will permit more universities to grow the cannabis plant and supply it to researchers who have been approved to conduct studies on it. This should make it easier for researchers to obtain varieties of marijuana with varying concentrations of different compounds. © 2016 The New York Times Company
Keyword: Drug Abuse
Link ID: 22553 - Posted: 08.13.2016
Ed Yong At the age of seven, Henry Gustav Molaison was involved in an accident that left him with severe epilepsy. Twenty years later, a surgeon named William Scoville tried to cure him by removing parts of his brain. It worked, but the procedure left Molaison unable to make new long-term memories. Everyone he met, every conversation he had, everything that happened to him would just evaporate from his mind. These problems revolutionized our understanding of how memory works, and transformed Molaison into “Patient H.M.”—arguably the most famous and studied patient in the history of neuroscience. That’s the familiar version of the story, but the one presented in Luke Dittrich’s new book Patient H.M.: A Story of Memory, Madness, and Family Secrets is deeper and darker. As revealed through Dittrich’s extensive reporting and poetic prose, Molaison’s tale is one of ethical dilemmas that not only influenced his famous surgery but persisted well beyond his death in 2008. It’s a story about more than just the life of one man or the root of memory; it’s also about how far people are willing to go for scientific advancement, and the human cost of that progress. And Dittrich is uniquely placed to consider these issues. Scoville was his grandfather. Suzanne Corkin, the scientist who worked with Molaison most extensively after his surgery, was an old friend of his mother’s. I spoke to him about the book and the challenges of reporting a story that he was so deeply entwined in. Most of this interview was conducted on July 19th. Following a New York Times excerpt published on August 7th, and the book’s release two weeks later, many neuroscientists have expressed “outrage” at Dittrich’s portrayal of Corkin. The controversy culminated in a statement from MIT, where Corkin was based, rebutting three allegations in the book. Dittrich has himself responded to the rebuttals, and at the end of this interview, I talk to him about the debate. © 2016 by The Atlantic Monthly Group.
Keyword: Learning & Memory
Link ID: 22552 - Posted: 08.13.2016
Like many students of neuroscience, I first learned of patient HM in a college lecture. His case was so strange yet so illuminating, and I was immediately transfixed. HM was unable to form new memories, my professor explained, because a surgeon had removed a specific part of his brain. The surgery froze him in time. HM—or Henry Molaison, as his name was revealed to be after his death in 2008—might be the most famous patient in the history of brain research. He is now the subject of the new book, Patient HM: A Story of Memory, Madness, and Family Secrets. An excerpt from the book in the New York Times Magazine, which details MIT neuroscientist Sue Corkin’s custody fight over HM’s brain after his death, has since sparked a backlash. Should you wish to go down that particular rabbit hole, you can read MIT’s response, the book author’s response to the response, and summaries of the back and forth. Why HM’s brain was worth fighting over should be obvious; he was probably the most studied individual in neuroscience while alive. But in the seven years since scientists sectioned HM’s brain into 2,401 slices, it has yielded surprisingly little research. Only two papers examining his brain have come out, and so far, physical examinations have led to no major insights. HM’s scientific potential remains unfulfilled—thanks to delays from the custody fight and the limitations of current neuroscience itself. Corkin, who made her career studying HM, confronted her complicated emotions about his death in her own 2013 book. She describes being “ecstatic to see his brain removed expertly from his skull.” Corkin passed away earlier this year.
Keyword: Learning & Memory
Link ID: 22551 - Posted: 08.13.2016
Cassie Martin Understanding sea anemones’ exceptional healing abilities may help scientists figure out how to restore hearing. Proteins that the marine invertebrates use to repair damaged cells can also repair mice’s sound-sensing cells, a new study shows. The findings provide insights into the mechanics of hearing and could lead to future treatments for traumatic hearing loss, researchers report in the Aug. 1 Journal of Experimental Biology. “This is a preliminary step, but it’s a very useful step in looking at restoring the structure and function of these damaged cells,” says Lavinia Sheets, a hearing researcher at Harvard Medical School who was not involved in the study. Tentacles of starlet sea anemones (Nematostella vectensis) are covered in tiny hairlike cells that sense vibrations in the water from prey swimming nearby.The cells are similar to sound-sensing cells found in the ears of humans and other mammals. When loud noises damage or kill these hair cells, the result can range from temporary to permanent hearing loss. Anemones’ repair proteins restore their damaged hairlike cells, but landlubbing creatures aren’t as lucky. Glen Watson, a biologist at the University of Louisiana at Lafayette, wondered if anemones’ proteins — which have previously been shown to mend similar cells in blind cave fish — might also work in mammals. |© Society for Science & the Public 2000 - 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
Rachel Ehrenberg Pulling consecutive all-nighters makes some brain areas groggier than others. Regions involved with problem solving and concentration become especially sluggish when sleep-deprived, a new study using brain scans reveals. Other areas keep ticking along, appearing to be less affected by a mounting sleep debt. The results might lead to a better understanding of the rhythmic nature of symptoms in certain psychiatric or neurodegenerative disorders, says study coauthor Derk-Jan Dijk. People with dementia, for instance, can be afflicted with “sundowning,” which worsens their symptoms at the end of the day. More broadly, the findings, published August 12 in Science, document the brain’s response to too little shut-eye. “We’ve shown what shift workers already know,” says Dijk, of the University of Surrey in England. “Being awake at 6 a.m. after a night of no sleep, it isn’t easy. But what wasn’t known was the remarkably different response of these brain areas.” The research reveals the differing effects of the two major factors that influence when you conk out: the body’s roughly 24-hour circadian clock, which helps keep you awake in the daytime and put you to sleep when it’s dark, and the body’s drive to sleep, which steadily increases the longer you’re awake. Dijk and collaborators at the University of Liege in Belgium assessed the cognitive function of 33 young adults who went without sleep for 42 hours. Over the course of this sleepless period, the participants performed some simple tasks testing reaction time and memory. The sleepy subjects also underwent 12 brain scans during their ordeal and another scan after 12 hours of recovery sleep. Throughout the study, the researchers also measured participants’ levels of the sleep hormone melatonin, which served as a way to track the hands on their master circadian clocks. |© Society for Science & the Public 2000 - 2016
Link ID: 22548 - Posted: 08.12.2016
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 Sharon Begley, The Massachusetts Institute of Technology brain sciences department and, separately, a group of some 200 neuroscientists from around the world have written letters to The New York Times claiming that a book excerpt in the newspaper’s Sunday magazine this week contains important errors, misinterpretations of scientific disputes, and unfair characterizations of an MIT neuroscientist who did groundbreaking research on human memory. In particular, the excerpt contains a 36-volley verbatim exchange between author Luke Dittrich and MIT’s Suzanne Corkin in which she says that key documents from historic experiments were “shredded.” “Most of it has gone, is in the trash, was shredded,” Corkin is quoted as telling Dittrich before she died in May, explaining, “there’s no place to preserve it.” Destroying files related to historic scientific research would raise eyebrows, but Corkin’s colleagues say it never happened. “We believe that no records were destroyed and, to the contrary, that professor Corkin worked in her final days to organize and preserve all records,” said the letter that Dr. James DiCarlo, head of the MIT Department of Brain and Cognitive Sciences, sent to the Times late Tuesday. Even as Corkin fought advanced liver cancer, he wrote, “she instructed her assistant to continue to organize, label, and maintain all records” related to the research, and “the records currently remain within our department.” © 2016 Scientific American
Keyword: Learning & Memory
Link ID: 22546 - Posted: 08.11.2016