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By Emily Underwood It is famous for robbing Lou Gehrig of his life and Stephen Hawking of his mobility and voice, but just how amyotrophic lateral sclerosis (ALS) destroys motor neurons in the brain and spinal cord remains a mystery. Now, scientists are converging on an explanation, at least for a fraction of the ALS cases caused by a specific mutation. In cells with the mutation, the new work shows, pores in the membrane separating the nucleus and cytoplasm become clogged, preventing vital molecules from passing through and creating a fatal cellular traffic jam. For now, the work applies only to the mutation dubbed C9orf72—a DNA stutter in which a short nucleotide sequence, GGGGCC, is repeated hundreds to thousands of times in a gene on chromosome 9. Nor do the multiple labs reporting results this week agree on exactly what plugs those nuclear pores and how the cells die. Still, the work is “a major breakthrough” in ALS research, says Amelie Gubitz, program director of the neurodegeneration division at the National Institute of Neurological Disorders in Bethesda, Maryland. The groups worked independently, starting with different hypotheses and experimental designs, yet reached similar conclusions, making the finding more convincing. And it suggests that boosting traffic through nuclear pores could be a new strategy for treating some cases of ALS and frontotemporal dementia (FTD), another neurodegenerative condition C9orf72 can cause. Based on past work by their own and other groups, neuroscientists Jeff Rothstein and Tom Lloyd at Johns Hopkins University in Baltimore, Maryland, suspected that the long strands of excess RNA produced by C9orf72 cause neurodegeneration by binding to, and thus sequestering, key cellular proteins. The team tested the idea in fruit flies with the mutation, which display damage in the nerve cells of their eyes and in motor neurons. © 2015 American Association for the Advancement of Science
By Felicity Muth You might have heard of serotonin as one of the ‘happy’ hormones in humans. Indeed, mood disorders like anxiety and depression are associated with low levels of serotonin. However, this neurotransmitter also has other functions. One of the more interesting ones in humans is its role in cooperation. Lowering the serotonin levels of people increases peoples’ reactions to unfairness and makes them less cooperative. On the other hand, increasing the level of serotonin in people makes people less argumentative and more communicative and cooperative. Serotonin also plays a role in peoples’ intimate relationships, for example men and women who were fed tryptophan (necessary for serotonin production) were more likely to judge photos of couples as intimate and romantic than people who had not been fed tryptophan. Humans are of course not the only animals that form intimate relationships or cooperate with each other. One of the best examples of unrelated animals cooperating comes from cleaner fish, who form relationships with ‘clients’ (visiting reef fish) where they clean their bodies, gills and even mouths. This relationship is very cooperative: the cleaner fish would rather eat the mucus from the skin of their clients than the ectoparasites (it’s yummier, apparently), but they usually keep this particular urge under control. In return, the clients don’t eat the cleaner fish, even when they are cleaning the inside of their mouths and one might think that it would be pretty tempting just to swallow one. Of course, cleaner fish do ‘cheat’ occasionally, taking a bite from the skin of a client, making the client jolt away and probably choose not to return to that particular cleaner again. © 2015 Scientific American
By James Gallagher Health editor, BBC News website Close your eyes and imagine walking along a sandy beach and then gazing over the horizon as the Sun rises. How clear is the image that springs to mind? Most people can readily conjure images inside their head - known as their mind's eye. But this year scientists have described a condition, aphantasia, in which some people are unable to visualise mental images. Niel Kenmuir, from Lancaster, has always had a blind mind's eye. He knew he was different even in childhood. "My stepfather, when I couldn't sleep, told me to count sheep, and he explained what he meant, I tried to do it and I couldn't," he says. "I couldn't see any sheep jumping over fences, there was nothing to count." Our memories are often tied up in images, think back to a wedding or first day at school. As a result, Niel admits, some aspects of his memory are "terrible", but he is very good at remembering facts. And, like others with aphantasia, he struggles to recognise faces. Yet he does not see aphantasia as a disability, but simply a different way of experiencing life. Take the aphantasia test It is impossible to see what someone else is picturing inside their head. Psychologists use the Vividness of Visual Imagery Questionnaire, which asks you to rate different mental images, to test the strength of the mind's eye. The University of Exeter has developed an abridged version that lets you see how your mind compares. © 2015 BBC.
Christopher Joyce Male treehoppers make their abdomens thrum like tuning forks to transmit very particular vibrating signals that travel down their legs and along leaf stems to other bugs — male and female. Male treehoppers make their abdomens thrum like tuning forks to transmit very particular vibrating signals that travel down their legs and along leaf stems to other bugs — male and female. Courtesy of Robert Oelman Animals, including humans, feel sound as well as hear it, and some of the most meaningful audio communication happens at frequencies that people can't hear. Elephants, for example, use these low-frequency rumbles to, among other things, find family or a mate across long distances. Whales do it, too. But you don't have to weigh a ton to rumble. In fact, you don't have to be bigger than a pea. Consider, for example, the treehopper, a curious little sap-sucking insect that lives on the stems of leaves. Or the tree cricket, which communicates by rubbing together tooth-like structures on its wings, the way you might draw your thumb across the teeth of a comb. University of Missouri biologist Rex Cocroft has spent much of his career listening closely to treehoppers. In 1999, a team from NPR's Radio Expeditions program rendezvoused with Cocroft at a locust tree in a backyard in Virginia. Soft-spoken and bespectacled, he was pressing a phonograph needle up against the stem of a leaf. © 2015 NPR
By Elizabeth Kolbert C57BL/6J mice are black, with pink ears and long pink tails. Inbred for the purposes of experimentation, they exhibit a number of infelicitous traits, including a susceptibility to obesity, a taste for morphine, and a tendency to nibble off their cage mates’ hair. They’re also tipplers. Given access to ethanol, C57BL/6J mice routinely suck away until the point that, were they to get behind the wheel of a Stuart Little-size roadster, they’d get pulled over for D.U.I. Not long ago, a team of researchers at Temple University decided to take advantage of C57BL/6Js’ bad habits to test a hunch. They gathered eighty-six mice and placed them in Plexiglas cages, either singly or in groups of three. Then they spiked the water with ethanol and videotaped the results. Half of the test mice were four weeks old, which, in murine terms, qualifies them as adolescents. The other half were twelve-week-old adults. When the researchers watched the videos, they found that the youngsters had, on average, outdrunk their elders. More striking still was the pattern of consumption. Young male C57BL/6Js who were alone drank roughly the same amount as adult males. But adolescent males with cage mates went on a bender; they spent, on average, twice as much time drinking as solo boy mice and about thirty per cent more time than solo girls. The researchers published the results in the journal Developmental Science. In their paper, they noted that it was “not possible” to conduct a similar study on human adolescents, owing to the obvious ethical concerns. But, of course, similar experiments are performed all the time, under far less controlled circumstances. Just ask any college dean. Or ask a teen-ager.
By Melinda Wenner Moyer As many as four out of every five pregnant women say that they suffer from “pregnancy brain”—deficits in memory and cognitive ability that arise during pregnancy, making women more forgetful and slow-witted. Yet studies on the phenomenon have generally not supported these claims: although some have found evidence of problems on certain types of tasks, others, including a recent paper published by researchers in Utah, have found no signs of cognitive problems at all. Some experts believe that pregnancy brain and its postnatal cousin, “baby brain,” could largely be a product of confirmation bias: pregnant women and new moms expect to experience brain fog and therefore believe they are actually affected. Others argue that the mental symptoms might simply be too difficult to confirm in a laboratory setting. In the most recent study, researchers at Brigham Young University gave cognitive and neuropsychological tests to 21 women in their third trimester of pregnancy and then tested them again six months after they gave birth. They administered the same tests at similar intervals to 21 women who had never been pregnant. They found no differences between the groups no matter when they were tested, including before and after giving birth. These findings mesh with those from a 2003 study, which found that pregnant women did not score differently from nonpregnant women on tests of verbal memory, divided attention and focused attention. “There is variety in the results, but overall most studies suggest there are few to no memory impairments associated with pregnancy,” says Michael Larson, a psychologist at Brigham Young and a co-author of the recent paper. He thinks the reason the myth persists may be that women selectively look for evidence that supports the cultural expectation. © 2015 Scientific American
By Simon Worrall, National Geographic How do we know we exist? What is the self? These are some of the questions science writer Anil Ananthaswamy asks in his thought-provoking new book, The Man Who Wasn’t There: Investigations Into the Strange New Science of the Self. The answers, he says, may lie in medical conditions like Cotard’s syndrome, Alzheimer’s or body integrity identity disorder, which causes some people to try and amputate their own limbs. Speaking from Berkeley, California, he explains why Antarctic explorer Ernest Shackleton fell victim to the doppelgänger effect; how neuroscience is rewriting our ideas about identity; and how a song by George Harrison of the Beatles offers a critique of the Western view of the self. You dedicate the book to “those of us who want to let go but wonder, who is letting go and of what?” Explain that statement. We always hear within popular culture that we have to “let go,” as a way of dealing with certain situations in our lives. And in some sense you have to wonder about that statement because the person or thing doing the letting go is also probably what has to be let go. In the book, I am trying to get behind the whole issue of what the self is that has to do the letting go; and what aspects of the self have to be let go of. You start your book with Alzheimer’s. Tell us about the origin of the condition and what it tells us about “the autobiographical self.” Alzheimer’s is a very severe condition, especially during the mid- to late stages, which starts robbing people of their ability to remember anything that’s happening to them. They also start forgetting the people they are close to. © 1996-2015 National Geographic Society
Link ID: 21343 - Posted: 08.27.2015
Dan Charles Ah, sugar — we love the sweetness, but not the calories. For more than a century, food technologists have been on a quest for the perfect, guilt-free substitute. Ah, sugar — we love the sweetness, but not the calories. For more than a century, food technologists have been on a quest for the perfect, guilt-free substitute. Ryan Kellman/NPR There's a new candidate in the century-old quest for perfect, guiltless sweetness. I encountered it at the annual meeting of the Institute of Food Technologists, a combination of Super Bowl, Mecca, and Disneyland for the folks who put the processing in processed food. It was right in the middle of the vast exhibition hall, at the Tate & Lyle booth. This is the company that introduced the British Empire to the sugar cube, back in 1875. A century later, it invented sucralose, aka Splenda. "We have a deep understanding of sweetening," says Michael Harrison, Tate & Lyle's vice president of new product development. This year, his company launched its latest gift to your sweet tooth. It's called allulose. "This is a rare sugar. A sugar that's found in nature," Harrison explains. Chemically speaking, it's almost identical to ordinary sugar. It has the same chemical formula as fructose and glucose, but the atoms of hydrogen and oxygen are arranged slightly differently. © 2015 NPR
Sara Reardon Some of the people who survived Hurricane Katrina lost loved ones, and many were made homeless by the storm. New Orleans still bears the scars of Hurricane Katrina, ten years later. More than 500,000 people fled when the storm hit, and many never returned. Large swathes of the city are sparsely populated, particularly in the poor neighbourhoods that suffered the most severe flood damage. Psychological scars linger, too. Many hurricane survivors continue to experience mental-health problems related to the storm, whether or not they returned to New Orleans, say researchers tracking Katrina’s psychological aftermath. Such work could ultimately aid people affected by future disasters, by identifying factors — such as lack of a social-support network and unstable environments for children — that seem to increase risk of mental-health trauma. “What’s unique about this disaster is the magnitude of it,” says Joy Osofsky, a clinical psychologist at Louisiana State University in New Orleans. Katrina, a category 3 hurricane when it made landfall on 29 August 2005, ultimately damaged an area the size of the United Kingdom. In New Orleans, it destroyed basic resources such as schools and health clinics to a degree unparalleled in recent US history. Osofsky saw the devastation and despair first hand. With their clinics flooded after the storm, she and other mental-health experts set up treatment centres for emergency responders on cruise ships docked nearby on the Mississippi River, and an emergency psychology unit at the city’s central command centre. Osofsky says that the centres treated thousands of displaced and traumatized people. © 2015 Nature Publishing Group
While some research suggests that a diet high in omega-3 fatty acids can protect brain health, a large clinical trial by researchers at the National Institutes of Health found that omega-3 supplements did not slow cognitive decline in older persons. With 4,000 patients followed over a five-year period, the study is one of the largest and longest of its kind. It was published today in the Journal of the American Medical Association. “Contrary to popular belief, we didn’t see any benefit of omega-3 supplements for stopping cognitive decline,” said Emily Chew, M.D., . Dr. Chew leads the Age-Related Eye Disease Study (AREDS), which was designed to investigate a combination of nutritional supplements for slowing age-related macular degeneration (AMD), a major cause of vision loss among older Americans. That study established that daily high doses of certain antioxidants and minerals — called the AREDS formulation — can help slow the progression to advanced AMD. A later study, called AREDS2, tested the addition of omega-3 fatty acids to the AREDS formula. But the omega-3’s made no difference. Omega-3 fatty acids are made by marine algae and are concentrated in fish oils; they are believed to be responsible for the health benefits associated with regularly eating fish, such as salmon, tuna, and halibut.*Where studies have surveyed people on their dietary habits and health, they’ve found that regular consumption of fish is associated with lower rates of AMD, cardiovascular disease, and possibly dementia. “We’ve seen data that eating foods with omega-3 may have a benefit for eye, brain, and heart health,” Dr. Chew explained.
Link ID: 21340 - Posted: 08.26.2015
By Michelle Roberts Health editor, BBC News online People genetically prone to low vitamin-D levels are at increased risk of multiple sclerosis, a large study suggests. The findings, based on the DNA profiles of tens of thousands of people of European descent, add weight to the theory that the sunshine vitamin plays a role in MS. Scientists are already testing whether giving people extra vitamin D might prevent or ease MS. Experts say the jury is still out. It is likely that environmental and genetic factors are involved in this disease of the nerves in the brain and spinal cord, they say. And if you think you may not be getting sufficient vitamin D from sunlight or your diet, you should discuss this with your doctor. Taking too much vitamin D can also be dangerous. Research around the world already shows MS is more common in less sunny countries, further from the equator. But it is not clear if this relationship is causal - other factors might be at play. To better understand the association, investigators at McGill University in Canada compared the prevalence of MS in a large group of Europeans with and without a genetic predisposition to low vitamin D. © 2015 BBC.
Keyword: Multiple Sclerosis
Link ID: 21339 - Posted: 08.26.2015
By Laura Sanders By tweaking a single gene, scientists have turned average mice into supersmart daredevils. The findings are preliminary but hint at therapies that may one day ease the symptoms of such disorders as Alzheimer’s disease and schizophrenia, scientists report August 14 in Neuropsychopharmacology. The altered gene provides instructions for a protein called phosphodiesterase-4B, or PDE4B, which has been implicated in schizophrenia. It’s too early to say whether PDE4B will turn out to be a useful target for drugs that treat these disorders, cautions pharmacologist Ernesto Fedele of the University of Genoa in Italy. Nonetheless, the protein certainly deserves further investigation, he says. The genetic change interfered with PDE4B’s ability to do its job breaking down a molecular messenger called cAMP. Mice designed to have this disabled form of PDE4B showed a suite of curious behaviors, including signs of smarts, says study coauthor Alexander McGirr of the University of British Columbia. Compared with normal mice, these mice more quickly learned which objects in a cage had been moved to a new location, for instance, and could better recognize a familiar mouse after 24 hours. “The system is primed and ready to learn, and it doesn’t require the same kind of input as a normal mouse,” McGirr says. These mice also spent more time than usual exploring brightly lit spaces, spots that normal mice avoid. But this devil-may-care attitude sometimes made the “smart” mice blind to risky situations. The mice were happy to spend time poking around an area that had been sprinkled with bobcat urine. “Not being afraid of cat urine is not a good thing for a mouse,” McGirr says. © Society for Science & the Public 2000 - 2015
By Jessica Schmerler In the modern age of technology it is not uncommon to come home after a long day at work or school and blow off steam by reading an e-book or watching television. Lately, however, scientists have been cautioning against using light-emitting devices before bed. Why? The light from our devices is “short-wavelength-enriched,” meaning it has a higher concentration of blue light than natural light—and blue light affects levels of the sleep-inducing hormone melatonin more than any other wavelength. Changes in sleep patterns can in turn shift the body’s natural clock, known as its circadian rhythm. Recent studies have shown that shifts in this clock can have devastating health effects because it controls not only our wakefulness but also individual clocks that dictate function in the body’s organs. In other words, stressors that affect our circadian clocks, such as blue-light exposure, can have much more serious consequences than originally thought. How did you become interested in the effects of light on sleep? Brainard: I was interested in the effects of light on animals as a teenager. I never planned to be a scientist—I wanted to be a writer! So I learned more about the topic out of pure curiosity. When I began my career as a journalist, I interviewed researchers on the topic who encouraged me to pursue a career in science. So I returned to school to get my doctorate and studied the effects of different wavelengths and intensities of light on rodents. I have exclusively studied the effects of light on humans for the past 30 years. © 2015 Scientific American
A placebo can make you feel a little better – and now we know how to boost the effect. Drugs based on hormones that make us more cooperative seem to enhance the placebo effect. The finding could lead to changes in the way some trials are performed. Sometimes a sugar pill can be all you need, even when you know it doesn’t contain any medicine. We’re still not entirely sure why. The brain’s natural painkillers, such as dopamine and opioids, seem to be involved, but other factors may be at work too. Evidence that a compassionate, trustworthy carer can speed recovery suggests that there is also a social dimension to the placebo effect. “This interaction between the patient and care provider seems to be based on a more complex system,” says Luana Colloca at the University of Maryland in Baltimore. Hormones that modulate our social behaviour might play a role. Last year, a team led by Ulrike Bingel of the University Duisburg-Essen in Germany, found that oxytocin – the so-called “cuddle chemical” that is thought to help us trust, bond and form relationships – seems to boost the placebo effect, at least in men. In the study, Bingel’s team applied an inert ointment to the arms of male volunteers. Half of them were told that the cream would reduce the degree of pain caused by the painfully hot stimulus subsequently applied. Men who were told that they were receiving pain relief said that the heat was less painful than those who knew that the cream was inert. When oxytocin was squirted up volunteers’ noses, the men reported being in even less pain. The team didn’t test oxytocin in women. © Copyright Reed Business Information Ltd.
Aaron E. Carroll If there is one health myth that will not die, it is this: You should drink eight glasses of water a day. It’s just not true. There is no science behind it. And yet every summer we are inundated with news media reports warning that dehydration is dangerous and also ubiquitous. These reports work up a fear that otherwise healthy adults and children are walking around dehydrated, even that dehydration has reached epidemic proportions. Let’s put these claims under scrutiny. I was a co-author of a paper back in 2007 in the BMJ on medical myths. The first myth was that people should drink at least eight 8-ounce glasses of water a day. This paper got more media attention (even in The Times) than pretty much any other research I’ve ever done. It made no difference. When, two years later, we published a book on medical myths that once again debunked the idea that we need eight glasses of water a day, I thought it would persuade people to stop worrying. I was wrong again. Many people believe that the source of this myth was a 1945 Food and Nutrition Board recommendation that said people need about 2.5 liters of water a day. But they ignored the sentence that followed closely behind. It read, “Most of this quantity is contained in prepared foods.” Water is present in fruits and vegetables. It’s in juice, it’s in beer, it’s even in tea and coffee. Before anyone writes me to tell me that coffee is going to dehydrate you, research shows that’s not true either. Although I recommended water as the best beverage to consume, it’s certainly not your only source of hydration. You don’t have to consume all the water you need through drinks. You also don’t need to worry so much about never feeling thirsty. The human body is finely tuned to signal you to drink long before you are actually dehydrated. © 2015 The New York Times Company
Link ID: 21335 - Posted: 08.25.2015
By Esther Landhuis The birth of a child leaves its mark on the brain. Most investigations of these changes have focused on mothers, but scientists have recently begun looking more closely at fathers. Neural circuits that support parental behaviors appear more robust in moms a few weeks after the baby is born, whereas in dads the growth can take several months. A study in Social Neuroscience analyzed 16 dads several weeks after their baby's birth and again a few months later. At each check, the researchers administered a multiple-choice test to check for signs of depression and used MRI to image the brain. Compared with the earlier scans, MRI at three to four months postpartum showed growth in the hypothalamus, amygdala and other regions that regulate emotion, motivation and decision making. Furthermore, dads with more growth in these brain areas were less likely to show depressive symptoms, says first author Pilyoung Kim, who directs the Family and Child Neuroscience Lab at the University of Denver. Although some physiological brain changes are similar in new moms and dads, other changes seem different and could relate to the roles of each parent, says senior author James Swain, a psychiatrist at the University of Michigan (brain diagrams below). A 2014 behavioral study of expectant fathers showed that midpregnancy ultrasound imaging was a “magic moment” in the dads' emerging connection with their baby. Yet the emotional bond was different than it is in expectant moms. Instead of thinking about cuddling or feeding the baby, dads-to-be focused on the future: they imagined saving money for a college fund or walking down the aisle at their daughter's wedding. © 2015 Scientific American
By JOAN RAYMOND Rita Gunther McGrath, a Columbia Business School professor, is one of those business travelers who do not care about delays, cancellations or navigating a new location. What does concern her is the seeming inability to conquer jet lag, and the accompanying symptoms that leave her groggy, unfocused and feeling, she says, “like a dishrag.” “Jet lag has always been an issue for me,” says Ms. McGrath, who has been a business traveler for more than two decades and has dealt with itineraries that take her from New York to New Zealand to Helsinki to Hong Kong all within a matter of days. She has scoured the Internet for “jet lag cures,” and has tried preventing or dealing with the misery by avoiding alcohol, limiting light exposure or blasting her body with sunlight and “doing just about anything and everything that experts tell you to do,” Ms. McGrath said. “Jet lag is not conducive to the corporate environment,” she said. “There has to be some kind of help that actually works for those of us that travel a lot, but I sure can’t find it.” Although science is closer to understanding the basic biological mechanisms that make many travelers feel so miserable when crossing time zones, research has revealed that, at least for now, there is no one-size fits-all recommendation for preventing or dealing with the angst of jet lag. Recommendations to beat jet lag include adjusting sleep schedules, short-term use of medications to sleep or stay awake, melatonin supplements and light exposure timing, among others, said Col. Ian Wedmore, an emergency medicine specialist for the Army. © 2015 The New York Times Company
Keyword: Biological Rhythms
Link ID: 21333 - Posted: 08.25.2015
By Hanae Armitage The libido enhancement drug flibanserin (trade name Addyi) took center stage last week after winning long-sought approval from the U.S. Food and Drug Administration (FDA). The coverage from advocates and nonbelievers has run the gamut—advice, caution, and criticism likely to confuse undecided—but curious—onlookers. But exactly how Addyi drums up sex drive is still murky. The drug has a long backstory. It was originally investigated in 1995 by pharmacologist Franco Borsini and a team of researchers at Boehringer Ingelheim Italia in Milan as an antidepressant because of its ability to regulate neurotransmitters—the brain’s chemical-signaling molecules. In particular, the team suspected that the drug regulated three key neurotransmitters thought to influence mood: serotonin, dopamine, and norepinephrine. A clinical trial found it did little to alleviate depression, but did seem to have an effect on mood. It just wasn’t the mood the researchers were expecting. These early trials tipped clinicians to flibanserin’s more prominent role in sexual health, as female subjects had higher scores on the Arizona Sexual Experience Scale, a survey that asks participants to rate their satisfaction on a variety of sexual health topics, like how often participants felt sexual desire and how intense that desire was. A separate group of researchers, also at Boehringer Ingelheim, completed their first clinical trials to explore flibanserin as a libido-enhancer in 2008. They measured levels of desire through a journal-based evaluation in which subjects recorded their levels of sexual drive on a daily basis. But FDA twice concluded that the resulting increases in libido were not statistically significant, and regulators were wary of potentially dangerous side effects like dizziness, sleepiness, nausea, and fainting. © 2015 American Association for the Advancement of Science
Keyword: Sexual Behavior
Link ID: 21332 - Posted: 08.25.2015
By NINA STROHMINGER and SHAUN NICHOLS WHEN does the deterioration of your brain rob you of your identity, and when does it not? Alzheimer’s, the neurodegenerative disease that erodes old memories and the ability to form new ones, has a reputation as a ruthless plunderer of selfhood. People with the disease may no longer seem like themselves. Neurodegenerative diseases that target the motor system, like amyotrophic lateral sclerosis, can lead to equally devastating consequences: difficulty moving, walking, speaking and eventually, swallowing and breathing. Yet they do not seem to threaten the fabric of selfhood in quite the same way. Memory, it seems, is central to identity. And indeed, many philosophers and psychologists have supposed as much. This idea is intuitive enough, for what captures our personal trajectory through life better than the vault of our recollections? But maybe this conventional wisdom is wrong. After all, the array of cognitive faculties affected by neurodegenerative diseases is vast: language, emotion, visual processing, personality, intelligence, moral behavior. Perhaps some of these play a role in securing a person’s identity. The challenge in trying in determine what parts of the mind contribute to personal identity is that each neurodegenerative disease can affect many cognitive systems, with the exact constellation of symptoms manifesting differently from one patient to the next. For instance, some Alzheimer’s patients experience only memory loss, whereas others also experience personality change or impaired visual recognition. The only way to tease apart which changes render someone unrecognizable is to compare all such symptoms, across multiple diseases. And that’s just what we did, in a study published this month in Psychological Science. © 2015 The New York Times Company
Link ID: 21331 - Posted: 08.24.2015
Jon Hamilton More than 50 million adults in the U.S. have a disorder such as insomnia, restless leg syndrome or sleep apnea, according to an Institute of Medicine report. And it's now clear that a lack of sleep "not only increases the risk of errors and accidents, it also has adverse effects on the body and brain," according to Charles Czeisler, chief of the division of sleep and circadian disorders at Brigham and Women's hospital in Boston. Research in the past couple of decades has shown that a lack of sleep increases a person's risk for cardiovascular disease, diabetes, infections, and maybe even Alzheimer's disease. Yet most sleep disorders go untreated. Michael Arnott, of Cambridge, Massachusetts, says he used to have terrible trouble staying awake on long drives. Sleep specialists discovered he has obstructive sleep apnea, though not for the most common reasons — he isn't overweight, and doesn't smoke or take sedatives. "I would get groggy and feel like I've got to keep talking, open the window," Arnott says. His wife, Mary White, says being a passenger on those drives could be scary. "All of a sudden there'd be a change in the speed and I'd look over, and his eyes would be starting to close," she remembers. White thought her husband might have sleep apnea, which interferes with breathing. But Arnott was in denial. He figured he was free of most risk factors for apnea. He wasn't overweight, he didn't smoke or take sedatives, and he has always stayed in great shape. So his wife took the initiative. "I asked him to see a doctor and he wouldn't," she says. In 2012, though, White persuaded him to take part in a sleep research study that paid for his participation, and took place at a sleep lab in Boston –not too far from the couple's home in Cambridge. © 2015 NPR
Link ID: 21330 - Posted: 08.24.2015