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By Emily Underwood In 2003, neurologist Helen Mayberg of Emory University in Atlanta began to test a bold, experimental treatment for people with severe depression, which involved implanting metal electrodes deep in the brain in a region called area 25. The initial data were promising; eventually, they convinced a device company, St. Jude Medical in Saint Paul, to sponsor a 200-person clinical trial dubbed BROADEN. This month, however, Lancet Psychiatry reported the first published data on the trial’s failure. The study stopped recruiting participants in 2012, after a 6-month study in 90 people failed to show statistically significant improvements between those receiving active stimulation and a control group, in which the device was implanted but switched off. Although that decision was “game over” for BROADEN, the story wasn’t finished for some 44 patients who asked to keep the implants in their brains, and the clinicians responsible for their long-term care, Mayberg explained last week to colleagues at a meeting on the ethical dilemmas of brain stimulation research at the National Institutes of Health (NIH) in Bethesda, Maryland. The episode highlights a tricky dilemma for companies and research teams involved in deep brain stimulation (DBS) research: If trial participants want to keep their implants, who will take responsibility—and pay—for their ongoing care? And participants in last week’s meeting said it underscores the need for the growing corps of DBS researchers to think long-term about their planned studies. © 2017 American Association for the Advancement of Science.

Keyword: Depression
Link ID: 24276 - Posted: 11.01.2017

Rachael Lallensack It takes a village to teach a bat how to communicate. Baby Egyptian fruit bats learn calls from their mothers, but research now shows that they can learn new dialects, or the pitch of their vocalizations, from the colony members around them. Learning to communicate by repeating the noises that others make is something only a few mammal groups — including humans, whales and dolphins — are known to do. Researchers call this vocal learning, and it's something that they're starting to study in bats. Findings published on 31 October in PLOS Biology1 show that bats can also pick things up from the group around them, a process that the authors dub crowd vocal learning. Bats are becoming the best organism to use in studies of how mammals learn to vocalize, because they’re more easily manipulated in the lab than whales or dolphins. The latest research underscores their importance, says neuroscientist Michael Yartsev of the University of California, Berkeley, who was not involved with the work. Egyptian fruit bats (Rousettus aegyptiacus) are highly social and live in colonies with dozens to thousands of other bats. To see how the pups learn dialects, researchers caught 15 pregnant Egyptian fruit bats and took them into the lab. To control for potential genetic effects, they ensured that the mothers weren't closely related. The team then split the mothers into three groups of five and put each group into one of three chambers, where the mothers gave birth to their young. The scientists used recordings of wild Egyptian fruit bat colonies that were low in frequency, high or a mix of both frequencies, and then piped one pitch into each chamber. © 2017 Macmillan Publishers Limited,

Keyword: Animal Communication; Language
Link ID: 24275 - Posted: 11.01.2017

Using an innovative “NeuroGrid” technology, scientists showed that sleep boosts communication between two brain regions whose connection is critical for the formation of memories. The work, published in Science, was partially funded by the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative, a project of the National Institutes of Health devoted to accelerating the development of new approaches to probing the workings of the brain. “Using new technologies advanced by the BRAIN Initiative, these researchers made a fundamental discovery about how the brain creates and stores new memories,” said Nick Langhals, Ph.D., program director at NIH’s National Institute of Neurological Disorders and Stroke. A brain structure called the hippocampus is widely thought to turn new information into permanent memories while we sleep. Previous work by the new study’s senior author, New York University School of Medicine professor György Buzsáki, M.D., Ph.D., revealed high-frequency bursts of neural firing called ripples in the hippocampus during sleep and suggested they play a role in memory storage. The current study confirmed the presence of ripples in the hippocampus during sleep and found them in certain parts of association neocortex, an area on the brain’s surface involved in processing complex sensory information. “When we first observed this, we thought it was incorrect because it had never been observed before,” said Dion Khodagholy, Ph.D., the study’s co-first author and assistant professor at Columbia University in New York.

Keyword: Learning & Memory
Link ID: 24274 - Posted: 11.01.2017

Teens are getting less sleep than they did before smartphones became commonplace, prompting concerns about potentially serious health consequences, researchers say. A study published in the current issue of the journal Sleep Medicine examined data from two surveys of U.S. adolescents conducted over many years and including questions about how many hours of sleep they got. Almost 370,000 adolescents participated. The researchers focused on how much sleep teens reported getting in the years from 2009 to 2015, "when the mobile technology really saturated the market among adolescents," said Zlatan Krizan, a psychologist specializing in sleep and social behaviour at Iowa State University and co-author of the study. Zlatan Krizan, a psychology researcher specializing in sleep, personality and social behaviour at Iowa State University, was one of the authors of a recent study that showed a trend of teens getting less sleep over the years they started using smartphones. (Iowa State University) Krizan and his colleagues found that teens were 16 to 17 per cent more likely to report getting less than seven hours of sleep a night in 2015 than they were in 2009. The recommended amount of sleep for 13 to 18-year-olds is eight to 10 hours per night, according to the U.S. Centers for Disease Control and Prevention. ©2017 CBC/Radio-Canada.

Keyword: Sleep; Development of the Brain
Link ID: 24273 - Posted: 11.01.2017

By Dr Michael Mosley BBC Thanks to the clocks going back, many of us managed to grab a little bit of extra shut-eye over the weekend. And that's no bad thing because, as a country, we seem to be chronically sleep-deprived. According to the Sleep Council, the average Briton gets six-and-a-half hours sleep a night, which for most people is not enough. Lots of studies have shown that cutting back on sleep, deliberately or otherwise, can have a serious impact on our bodies. A few nights of bad sleep can really mess with our blood sugar control and encourage us to overeat. It even messes with our DNA. A few years ago, Trust Me I'm a Doctor did an experiment with Surrey University, asking volunteers to cut down on their sleep by an hour a night for a week. Dr Simon Archer, who helped run the experiment, found that getting an hour's less sleep a night affected the activity of a wide range of our volunteers' genes (around 500 in all) including some which are associated with inflammation and diabetes. Disturbed nights So the negative effects on our bodies of sleep deprivation are clear. But what effect does lack of sleep have on our mental health? To find out Trust Me teamed up with sleep scientists at the University of Oxford to run a small experiment. This time, we recruited four volunteers who normally sleep soundly. We fitted them with devices to accurately monitor their sleep and then, for the first three nights of our study, let them get a full, undisturbed eight hours. For the next three nights, however, we restricted their sleep to just four hours.

Keyword: Sleep
Link ID: 24272 - Posted: 11.01.2017

Susan Milius Kleptopredation klep-toe-preh-day-shun n. A food-gathering strategy of eating an organism and the meal it just ate. A wily sea slug has a way to get two meals in one: It gobbles up smaller predators that have recently gulped in their own prey. “Kleptopredation” is the term Trevor Willis of the University of Portsmouth in England and his colleagues propose for this kind of food theft by well-timed predation. Researchers knew that the small Mediterranean nudibranch Cratena peregrina, with a colorful mane of streamers rippling off its body, climbs and preys on pipe cleaner‒skinny, branched colonies of Eudendrium racemosum hydroids, which are distant relatives of corals. The nudibranchs devour the individual hydroid polyps and, new tests show, prefer them well fed. In experimental buffets with fed or hungry polyps, the nudibranchs ate faster when polyps were fat with just-caught plankton. In this way, at least half of a nudibranch’s diet is plankton. This quirk explains why some biochemical signatures that distinguish predators from prey don’t work out clearly for nudibranchs and hydroids, the researchers report November 1 in Biology Letters. A weird echo of this meal-stealing strategy shows up in certain jumping spiders. The arachnids don’t have the biology to drink vertebrate blood themselves. Instead, they catch a lot of female mosquitoes that have just tanked up (SN: 10/15/05, p. 246). |© Society for Science & the Public 2000 - 2017. All rights reserved.

Keyword: Aggression
Link ID: 24271 - Posted: 11.01.2017

Sara Reardon Human genome databases are enabling researchers to take a deeper dive into the evolution of psychiatric disorders. Psychiatric disorders can be debilitating and often involve a genetic component, yet, evolution hasn’t weeded them out. Now, recent work is beginning to reveal the role of natural selection — offering a peek at how the genetic underpinnings of mental illness has changed over time. Many psychiatric disorders are polygenic: they can involve hundreds or thousands of genes and DNA mutations. It can be difficult to track how so many genetic regions evolved, and such studies require large genome data sets. But the advent of massive human genome databases is enabling researchers to look for possible connections between mental illnesses and the environmental and societal conditions that might have driven their emergence and development. Others are looking to Neanderthal genetic sequences to help inform the picture of these disorders, as well as cognitive abilities, in humans. Several of these teams presented their findings at the American Society of Human Genetics (ASHG) meeting in Orlando, Florida, in late October. One project found that evolution selected for DNA variants thought to protect against schizophrenia. The study, led by population geneticist Barbara Stranger of the University of Chicago in Illinois, looked at hundreds of thousands of human genomes using a statistical method that identified signals of selection over the past 2,000 years1. There were no signs of selection in genetic regions associated with any other mental illness. Many of schizophrenia's symptoms, such as auditory hallucinations and jumbling sentences, involve brain regions tied to speech, says Bernard Crespi, an evolutionary biologist at Simon Fraser University in Burnaby, Canada. Over the course of hominid evolution, he says, the ability to speak could have outweighed the small, but unavoidable risk that the genes involved in language could malfunction and result in schizophrenia in a small percentage of the population. © 2017 Macmillan Publishers Limited

Keyword: Schizophrenia; Depression
Link ID: 24270 - Posted: 10.31.2017

Jon Hamilton People who are thinking about killing themselves appear to have distinctive brain activity that can now be measured by a computer. In these people, words like "death" and "trouble" produce a distinctive "neural signature" not found in others, scientists report in the journal Nature Human Behavior. More than 44,000 people commit suicide in the U.S. each year. "There really is a difference in the way [suicidal] people think about certain concepts," says Marcel Just, an author of the paper and the D. O. Hebb professor of cognitive neuroscience at Carnegie Mellon University. That difference allowed a computer program to distinguish people who thought about suicide from people who did not more than 90 percent of the time. It also allowed the computer program to distinguish people who had attempted suicide from people who had only thought about it. The results come from a study of just 34 young adults and will need to be replicated, says Barry Horwitz, chief of brain imaging and modeling at the National Institute on Deafness and Other Communication Disorders. But he says they hint at a future in which brain scans and computers can help assess a person's mental health. Horwitz was not involved in the study. "Just looking at behavior is probably inadequate for a lot of purposes," he says. "It's much better to be able to see what the brain is doing." © 2017 npr

Keyword: Depression
Link ID: 24269 - Posted: 10.31.2017

Christopher French, Alice M Gregory and Dan Denis Of all the sleep disorders, “exploding head syndrome” (EHS) has arguably the most intriguing name. EHS has been described as “a sensory parasomnia characterised by the perception of loud noises and/or a sense of explosion in the head when transitioning to or from sleep. These noises are not associated with significant pain, but lead to abrupt arousal and feelings of fright”. Although this phenomenon was first described as long ago as 1876, it was not given its colourful title until 1988. Despite its long history, it has received very little systematic research attention, with most of our knowledge being based upon small samples of case histories as opposed to large-scale investigations. We, the authors of this piece, along with the world’s leading authority on EHS, Dr Brian Sharpless of Argosy University, Northern Virginia, are hoping to rectify that situation by carrying out a large-scale survey of EHS. We’re also interested in the equally intriguing phenomenon of sleep paralysis, which involves a temporary period of paralysis occurring between sleep and wakefulness, often accompanied by hallucinations. If you have ever experienced either EHS or sleep paralysis, or even if you haven’t, we would love to hear from you. In addition to explosions, other types of loud noise perceived during episodes of EHS include gunshots, fireworks, thunder, doors slamming, clapping, shouting, and the clash of cymbals. There can also be beeps, buzzing and video static. This may be accompanied by “electrical” sensations, palpitations, breathing difficulties, sweating, seeing a flash of light, and twitching. Perhaps unsurprisingly, intense fear caused by the belief that something is seriously wrong is often reported. © 2017 Guardian News and Media Limited

Keyword: Sleep
Link ID: 24268 - Posted: 10.31.2017

By GINA KOLATA It is a question that plagues all who struggle with weight: Why do some of us manage to keep off lost pounds, while others regain them? Now, a study of 14 participants from the “Biggest Loser” television show provides an answer: physical activity — and much more of it than public health guidelines suggest. On average, those who managed to maintain a significant weight loss had 80 minutes a day of moderate activity, like walking, or 35 minutes a day of vigorous exercise, like running. The researchers conducting the new study did not distinguish between purposeful exercise, like going to the gym and working out, and exercise done over the course of the day, like walking to work or taking the stairs. Guidelines from the Centers for Disease Control and Prevention, by comparison, call for at least 150 minutes a week of moderate exercise, or 75 minutes a week of vigorous exercise for healthy adults. The study was published on Tuesday in the journal Obesity. The lead author, Kevin Hall, chief of the Integrative Physiology Section at the National Institute of Diabetes and Digestive and Kidney Diseases, and his colleagues also presented their work at the Obesity Society’s annual meeting. Although the study is very small and must be replicated, Dr. Hall said, it is the first to assess obese people years after they lost weight with state-of-the-art methods to measure the calories they had consumed and the amount of exercise they had done. The researchers did their measurements when the contestants were chosen, and again at six weeks, thirty weeks and six years after the contest began. “The findings here are important,” said Rena Wing, a psychiatry professor at Brown University and a founder of the National Weight Control Registry, which includes more than 10,000 people. The food eaten “is the key determinant of initial weight loss. And physical activity is the key to maintenance,” she said. © 2017 The New York Times Company

Keyword: Obesity
Link ID: 24267 - Posted: 10.31.2017

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

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

There is no good evidence that a nutrient drink being sold online in the UK to "help" people with early Alzheimer's actually slows the disease, say experts. Latest trial results in patients who took Souvenaid did not find it preserves memory and thinking. The authors say in Lancet Neurology that bigger studies are needed to show if the product can work as hoped. And consumers should be aware that the £3.49 per bottle drink "is not a cure". Manufacturer Nutricia says its drink should only be taken under the direction of a doctor, specialist nurse or pharmacist. Souvenaid comes in strawberry or vanilla flavour and contains a combination of fatty acids, vitamins and other nutrients. Taken once daily, the idea is that the boost of nutrients it provides will help keep Alzheimer's at bay in people with the earliest signs of this type of dementia. But the latest phase two clinical trial results do not prove this. What the trial found The study involved 311 patients with very early Alzheimer's or mild cognitive impairment. All of them were asked to take a daily drink, but only half were given Souvenaid - the other half received one with no added nutrients. After two years of participating, the patients were reassessed to see if there was any difference between the two groups in terms of dementia progression, measured by various memory and cognitive tests. The treatment did not appear to offer an advantage, although patients in the Souvenaid group did have slightly less brain shrinkage on scans, which the researchers say is promising because shrinkage in brain regions controlling memory is seen with worsening dementia. But experts remain cautious. Prof Tara Spires-Jones, a dementia expert at the University of Edinburgh, said: "Some of the other tests of brain structure and function were promising, but overall this study indicates that a specific change in nutrition is unlikely to make a large difference to people with Alzheimer's, even in the early stages. © 2017 BBC.

Keyword: Alzheimers
Link ID: 24265 - Posted: 10.31.2017

By Nicholas Kristof The colored parts of the image above, prepared by Columbia University scientists, indicate where a child’s brain is physically altered after exposure to this pesticide. This chemical, chlorpyrifos, is hard to pronounce, so let’s just call it Dow Chemical Company’s Nerve Gas Pesticide. Even if you haven’t heard of it, it may be inside you: One 2012 study found that it was in the umbilical cord blood of 87 percent of newborn babies tested. And now the Trump administration is embracing it, overturning a planned ban that had been in the works for many years. The Environmental Protection Agency actually banned Dow’s Nerve Gas Pesticide for most indoor residential use 17 years ago — so it’s no longer found in the Raid you spray at cockroaches (it’s very effective, which is why it’s so widely used; then again, don’t suggest this to Dow, but sarin nerve gas might be even more effective!). The E.P.A. was preparing to ban it for agricultural and outdoor use this spring, but then the Trump administration rejected the ban. That was a triumph for Dow, but the decision stirred outrage among public health experts. They noted that Dow had donated $1 million for President Trump’s inauguration. So Dow’s Nerve Gas Pesticide will still be used on golf courses, road medians and crops that end up on our plate. Kids are told to eat fruits and vegetables, but E.P.A. scientists found levels of this pesticide on such foods at up to 140 times the limits deemed safe. © 2017 The New York Times Company

Keyword: Neurotoxins; Development of the Brain
Link ID: 24264 - Posted: 10.30.2017

Nick Fraser I was just finishing a talk about documentaries I was giving in Soho. I’d been asked a question about why so many films are seriously depressing. I remember that I talked about the great neurosurgeon Henry Marsh and the documentary about him, The English Surgeon. The film followed him to Ukraine as he helped and taught the local surgeons, who often resorted to using rusty domestic power tools to work on their patients’ skulls. I’d talked about him for some time, enthusiastically explaining how awed Henry said he felt every time he opened a patient’s head, and about how beautiful the brain is. I wanted to say more – but suddenly I sat down, and couldn’t say or think anything. Something had happened to me. I had gone into a different world of not making sense. I was taken by ambulance to University College hospital and given a head CT scan. There was a blood clot on my brain. I’d had a stroke, a brain attack. Time is all-important to stroke patients, and fortunately I was within the time frame to be given serious clot-busting drugs. There was something else they could do, the doctor said, a procedure called a thrombectomy. UCH offered the procedure up until 6pm. The time was then around 8pm, but the doctor heroically fought through NHS protocols and secured me a trip to St George’s hospital in south-west London, the only UK location open 24/7 for thrombectomies. I was lucky. I remember meeting the neuro-radiologist who, after putting me under mild sedation, performed the extraordinary procedure that involved sending a very thin wire from my groin to my brain, and removing one small clot and one larger one from the left side of my brain. I could understand the details of the operation, but I couldn’t say anything. I wondered if I would be all right. © 2017 Guardian News and Media Limited o

Keyword: Stroke; Language
Link ID: 24263 - Posted: 10.30.2017

By KYLE SPENCER As other college students head out to party on a Saturday night, Julie Linneman, a sophomore at Villanova University, rides the subway to a small rowhouse in West Philadelphia to meet with “her people,” a posse of students who understand what it’s like to be taken down by opioids. Ms. Linneman is a bespectacled 22-year-old who favors shredded jeans. She is a fan of cooking shows, fantasy fiction and Paul McCartney. She spent her first attempt at sophomore year — the one at Northern Kentucky University — in her dorm room, high on heroin. Coming to terms with a habit that nearly killed her, she has found support at the Haven at Drexel, Drexel University’s housing for students in recovery. Seven students from colleges in the Philadelphia area — including the University of Pennsylvania, Temple and Villanova — live, eat and socialize here, where they can abstain without temptation. More converge during these Saturday night meetings. “Sometimes you just need to be around other students who know what you have gone through,” Ms. Linneman said. They share snacks, drink water instead of beer, and talk about their life-threatening addictions. Ms. Linneman, who agreed to be named because she hopes to pursue a career in recovery advocacy, got her first pills — Vyvanse and Adderall, stimulants for attention deficit hyperactivity disorder — in high school from the boy with the locker next to hers. She soon moved on to prescription painkillers like Percocet. The “warm blanket” effect alleviated debilitating anxiety and loneliness. Once at college, she replaced pills with bags of cheap heroin. Her roommate moved out. The drug rendered her friendless. “It was one of the most lonely times of my life,” she recalled. She grew thin and pale. She would sit in the cafeteria alone, barely eating, occasionally nodding off. The workers would ask, “Are you O.K.?” © 2017 The New York Times Company

Keyword: Drug Abuse
Link ID: 24262 - Posted: 10.30.2017

By Angela Clow, Nina Smyth, October is a dismal time of year. The clocks go back, which accelerates the onset of darker evenings and the “shorter days” inevitably lead to calls for the tradition of putting clocks forward or backward to stop. Of course, the annual return to Greenwich Mean Time (GMT) from British Summer Time (BST) doesn’t make the days any shorter, it merely shifts an hour of available daylight from the evening to the morning. For many, lighter evenings are a priority and little attention is given to the benefits of lighter mornings. Arguments over clock changes tend to revolve around benefits for easier travel in lighter evenings. Nevertheless research suggests that holding onto lighter mornings might have hitherto unforeseen advantages. Light in the morning – more than any other time of day – leads to powerful brain-boosting effects, helping us to function as best we can, despite the approaching winter. All life on Earth has evolved around the 24-hour cycle of light and dark. An obvious sign is our desire for night-time sleep, but most biological functions are fine-tuned around day and night. Our bodies are honed to environmental light via a biological chain reaction. Light intensity is detected by special cells in the retina and this information is relayed to the internal body clock, located deep in a part of the brain called the suprachiasmatic nucleus. This sits in the hypothalamus, responsible for regulation of internal body processes using the endocrine system, which is linked to hormone secretion, via the pituitary gland. We are unaware of these light messages as they have nothing to do with conscious vision. Their sole job is to internalise information about environmental light intensity. © 2017 Scientific American,

Keyword: Biological Rhythms
Link ID: 24261 - Posted: 10.30.2017

By Michael Ellenbogen Twenty years ago, at age 39, I began having memory and cognitive problems. My primary-care doctor and my neurologists said I was stressed and depressed. I also was diagnosed with mild cognitive impairment, or MCI. Ten years later, I received another diagnosis. Well, really two. One doctor said I had Alzheimer’s disease, and another thought it was semantic dementia. Alzheimer’s is a devastating chronic neurodegenerative disease. It is a progressive mental deterioration that advances to affect bodily functions such as walking and swallowing, and always leads to death. Semantic dementia leads to losses of vocabulary, fluency of speech and meanings of familiar words. It also is progressive. After another year of testing, physicians decided that I had Alzheimer’s. While it was a relief to finally get a diagnosis, I realized that I had been given a death sentence. There is no prevention or cure for Alzheimer’s, and no survivors. Overwhelmed, I decided to help the search for a cure by advocating for Alzheimer’s and dementia. I got involved with clinical trials and advocacy. My huge network on LinkedIn allowed me to connect with advocates and information. It gave me access to many tests, including gene tests, free. Two contacts — health-care professionals — even read my medical records and scans and gave me their opinions. Alzheimer’s is a complex disease to diagnose. The science is just not there yet. Sixty to 80 percent of dementia cases are said to be due to Alzheimer’s. But postmortem tests of elderly patients have found that dementia has several causes. s. © 1996-2017 The Washington Post

Keyword: Alzheimers
Link ID: 24260 - Posted: 10.30.2017

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

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

Sara Reardon The 70 million neurons in the mouse brain look like a tangled mess, but researchers are beginning to unravel the individual threads that carry messages across the organ. A 3D brain map released on 27 October, called MouseLight, allows researchers to trace the paths of single neurons and could eventually reveal how the mind assembles information. The map contains 300 neurons and researchers plan to add another 700 in the next year. “A thousand is just beginning to scratch the surface,” says Nelson Spruston, a neuroscientist at the Howard Hughes Medical Institute (HHMI) Janelia Research Campus in Ashburn, Virginia. To create the maps, Spruston and HHMI neuroscientist Jayaram Chandrashekar injected mouse brains with viruses that infect only a few cells at a time, prompting them to produce fluorescent proteins1. The team made the organs transparent using a sugar-alcohol treatment to obtain an unobstructed view of the glowing neurons, and then scanned each brain with a high-resolution microscope. Computer programs created 3D models of the glowing neurons and their projections, called axons, which can be half a metre long and branch like a tree. MouseLight has already revealed new information, including the surprisingly extensive number of brain regions that a single axon can reach. For instance, four neurons associated with taste stretch into the region that controls movement and another area related to touch. Chandrashekar says the group is now working on identifying which genes each neuron expresses, which will help to pin down their function. © 2017 Macmillan Publishers Limited,

Keyword: Brain imaging
Link ID: 24258 - Posted: 10.28.2017

By MARK LUKACH For my son Jonas’s first Halloween, when he was 5 months old, I dressed the two of us as matching lumberjacks. For the second, we were characters from the movie “Up.” I was Carl, the old man, my wife was Ellie, and Jonas was Russell, the enthusiastic Wilderness Explorer. We tied a dozen balloons to our bulldog’s collar, to make him the house. In our version, the wife didn’t die at the beginning of the movie, and we all lived happily ever after. The next Halloween, Jonas wanted to be an elephant. He loved the scene in “The Jungle Book” where Mowgli tries to march with the elephants. We resisted, since we like family costumes and didn’t want to buy three elephant outfits, but conceded. We displayed his elephant costume in his room the week before Halloween so he could look at it in anticipation of the big day. My wife, Giulia, wasn’t there for the lumberjack Halloween. She was in the hospital. Giulia was there for the “Up” Halloween. But as we approached the elephant Halloween, I suspected she wasn’t going to dress up. Because, once again, she was going psychotic. Giulia was 27 when the first psychotic episode happened. It came out of nowhere. She got nervous about her new job; she lost her appetite; she stopped sleeping; she began having delusions. The first delusions were encouraging. She said she spoke to God, who told her that she was going to be fine. Giulia had never been very religious, so I was alarmed, but at least she was hearing things that were comforting. But then the delusions turned on her. The voices said she wasn’t going to make it, there was no point in even trying, she was better off not being here. That’s how she ended up in the hospital the first time. They gave her medication. The delusions eventually went away. She was depressed for a long time afterward. They gave her more medication, and then she got better. © 2017 The New York Times Company

Keyword: Schizophrenia
Link ID: 24257 - Posted: 10.28.2017