By Sharon Begley, STAT Dennis van der Meijden isn’t aiming to see the face of God, feel one with the cosmos, grasp the hidden reality of time and space, or embark on a sacred journey. What the Dutch graphic designer, producer, and rapper (under the professional name Terilekst) wants—and gets—from his twice-weekly “microdoses” of psilocybin is more modest. “It sharpens all the senses, as if the frequencies of all of your atoms and energy field are raised a little bit and are being slightly more conscious,” said van der Meijden, 39, who told STAT he first microdosed psilocybin—the active ingredient in “magic mushrooms”—three years ago. It makes him energetic enough to skip coffee, “as if I’m kicked in some sort of orbit for that day.” If he becomes distracted, “I’m very much aware of that, as if seeing myself from a bird’s eye view, so I can correct myself very fast.” But van der Meijden says he’s careful not to exceed about 0.4 grams, because 0.5 made him “a bit too joyful and a bit too philosophical,” which wasn’t always appropriate. Microdosing involves taking roughly one-tenth the “trip” dose of a psychedelic drug, an amount too little to trigger hallucinations but enough, its proponents say, to sharpen the mind. Psilocybin microdosers (including hundreds on Reddit) report that the mushrooms can increase creativity, calm anxiety, decrease the need for caffeine, and reduce depression. There is enough evidence that trip doses might have the latter effect that, on Wednesday, London-based Compass Pathways received Food and Drug Administration approval for a Phase 2B clinical trial of psilocybin (in larger-than-microdoses) for treatment-resistant depression. But research into microdosing is minimal. © 2018 Scientific American

Keyword: Depression; Drug Abuse
Link ID: 25379 - Posted: 08.25.2018

By Steph Yin Pipefish, along with their cousins sea horses and sea dragons, defy convention in love and fertility. In a striking role reversal, fathers give birth instead of mothers. During courtship, females pursue males with flashy ornaments or elaborate dances, and males tend to be choosy about which females’ eggs they’ll accept. Once pregnant, these gender-bending fathers invest heavily in their young, supplying embryos with nutrients and oxygen through a setup similar to the mammalian placenta. But this investment may also be cruelly conditional, according to a new study in Proceedings of the Royal Society B. Studying pipefish, scientists found evidence that pregnant fathers spontaneously abort or divert fewer resources to their embryos when faced with the prospects of a superior mate — in this case, an exceptionally large female. The researchers named their finding the “woman in red” effect, after the eponymous 1984 Gene Wilder film about a married man’s obsession with a woman in a red dress that becomes damaging to his family life. The reported effect is an interesting instance of sexual conflict, which is ubiquitous among animals, said Sarah Flanagan, a pipefish expert at the University of Canterbury in New Zealand. If you’re a romantic, you might think of mating as harmonious. But in nature, reproduction is more often a vicious power struggle between mothers and fathers with competing interests. A maternal analogue to the “woman in red” effect occurs among mice. Males are willing to kill a female’s offspring, if they are unrelated to him, before mating with her. In anticipation, a pregnant mother may terminate her pregnancy when exposed to a new male, rather than spending resources on doomed offspring. © 2018 The New York Times Company

Keyword: Sexual Behavior; Evolution
Link ID: 25378 - Posted: 08.25.2018

By Susan Pinker If you’ve ever wondered where your memory has gone, ask Brenda Milner. The British-Canadian, who just turned 100, was one of the first researchers to discover how memories are stashed in the brain. Having spent the last 68 years investigating how we consolidate new knowledge, you could say that she knows a thing or two about remembering. Dr. Milner began her career as one of a handful of women admitted to study mathematics at Cambridge University in 1936. Her determination was evident even then. “Cambridge was associated with mathematics and physics—you know Isaac Newton went there. That’s where I wanted to go and nowhere else,” she told me in 2007 (I recently interviewed her again by email). This tenacity served Dr. Milner well when she moved from crunching numbers at the British Defense Ministry to Montreal in 1944, to pursue a Ph.D. in psychology. There she worked with the neurologist Wilder Penfield at McGill’s Montreal Neurological Institute. Their research on the post-surgical brain function of epileptic patients led her to reject the then-fashionable theories that memory was a product of Freudian urges or behaviorist stimulus-response chains. Her key insight was to see memory as a feature of human neurobiology. Dr. Milner is now considered one of the founders of cognitive neuroscience, which links the mind—perceiving, thinking, remembering—to the brain. One of the current leaders in the field, Michael Gazzaniga of the University of California, Santa Barbara, calls her “a true pioneer.” ©2018 Dow Jones & Company, Inc.

Keyword: Learning & Memory
Link ID: 25377 - Posted: 08.25.2018

By Nicholas Bakalar Symptoms of poor cardiovascular health may be linked to an increased risk for Parkinson’s disease, a new study has found. Researchers used data on 17,163,560 South Koreans over 40 years old and found 44,205 cases of Parkinson’s over the course of a five-year follow-up. They looked for five cardiovascular risk factors that define the metabolic syndrome: abdominal obesity, high triglycerides, high cholesterol, high blood pressure and high glucose readings. The study is in PLOS Medicine. After controlling for age, sex, smoking, alcohol consumption, physical activity, income, body mass index and history of stroke, they found that each component of the metabolic syndrome significantly increased the risk for Parkinson’s disease. The more risk factors a person had, the greater the risk. Compared with having none of the risk factors, having all five was associated with a 66 percent increased risk for Parkinson’s disease. The association was particularly strong for people over 65. There are about 60,000 new diagnoses of Parkinson’s each year in the United States, and about a million Americans are living with the disease. “The metabolic syndrome and its components are independent risk factors for Parkinson’s,” the authors wrote. “Future studies are warranted to examine whether control of metabolic syndrome and its components can decrease the risk of Parkinson’s disease development.” © 2018 The New York Times Company

Keyword: Parkinsons
Link ID: 25376 - Posted: 08.25.2018

By Anouk Bercht, Steven Laureys Steven Laureys greets me with a smile as I enter his office overlooking the hills of Lige. Although his phone rings constantly, he takes the time to talk to me about the fine points of what consciousness is and how to identify it in patients who seem to lack it. Doctors from all over Europe send their apparently unconscious patients to Laureys—a clinician and researcher at the University of Lige—for comprehensive testing. To provide proper care, physicians and family members need to know whether patients have some degree of awareness. At the same time, these patients add to Laureys’ understanding. The interview has been edited for clarity. What is consciousness? It is difficult enough to define “life,” even more so to define “conscious” life. There is no single definition. But of course, in clinical practice we need unambiguous criteria. In that setting, everyone needs to know what we mean by an “unconscious” patient. Consciousness is not “all or nothing.” We can be more or less awake, more or less conscious. Consciousness is often underestimated; much more is going on in the brains of newborns, animals and coma patients than we think. So how is it possible to study something as complex as consciousness? There are a number of ways to go about it, and the technology we have at our disposal is crucial in this regard. For example, without brain scanners we would know much, much less than we now do. We study the damaged brains of people who have at least partially lost consciousness. We examine what happens during deep sleep, when people temporarily lose consciousness. © 2018 Scientific American

Keyword: Consciousness
Link ID: 25375 - Posted: 08.24.2018

Laura Sanders Antibodies in the brain can scramble nerve cells’ connections, leading to memory problems in mice. In the past decade, brain-attacking antibodies have been identified as culprits in certain neurological diseases. The details of how antibodies pull off this neuronal hit job, described online August 23 in Neuron, may ultimately lead to better ways to stop the ensuing brain damage. Research on antibodies that target the brain is a “biomedical frontier” that may have implications for a wide range of disorders, says Betty Diamond, an immunologist and rheumatologist at Northwell Health's Feinstein Institute for Medical Research in Manhasset, N.Y. “It’s beyond the idea stage,” she says. “It’s into the ‘It happens. Let’s figure out the why and the when.’ ” Autoantibodies are a type of antibody that mistakenly target a person’s own proteins. One such internal attack comes from autoantibodies that take aim at part of the AMPA receptor, a protein that sits on the outside of nerve cells and detects incoming chemical messages. These autoantibodies interfere with the receptor’s message-sensing job, neurologist Christian Geis of Jena University Hospital in Germany and colleagues found. The team purified autoantibodies from patients suffering from autoimmune encephalitis, a brain inflammation disease that causes confusion, seizures and memory trouble. When the researchers put these human autoantibodies into the brains of mice, the animals began showing memory problems, too. |© Society for Science & the Public 2000 - 2018

Keyword: Learning & Memory; Neuroimmunology
Link ID: 25374 - Posted: 08.24.2018

By Bret Stetka Obesity rates in the U.S. and abroad have soared: The world now has more overweight people than those who weigh too little. One reason relates to the way the body reacts to its own fat stores by setting in motion a set of molecular events that impede the metabolic process that normally puts a damper on hunger. A new study published August 22 in Science Translational Medicine provides details of how this process occurs, giving new insight into why obese individuals have trouble shedding pounds. It also suggests a possible treatment approach that targets obesity in the brain, not in the belly. Scientists have long known that a hormone called leptin is instrumental in regulating the human diet. Produced by fat cells, the molecule communicates with a brain region called the hypothalamus, which reins in hunger cravings when our energy stores are full. Yet as we gain weight our bodies become less sensitive to leptin, and it becomes harder and harder to slim down. In other words, weight gain begets more weight gain. In an experiment using mice that became obese on a high-fat diet, an international team found obesity increases the activity of an enzyme called matrix metalloproteinase-2, or MMP-2. By using a technique called western blot analysis—separating and identifying all the proteins in a tissue sample—the authors found MMP-2 cleaves off a portion of the leptin receptor in the hypothalamus, impairing the hormone’s signaling and its ability to suppress appetite. © 2018 Scientific American

Keyword: Obesity
Link ID: 25373 - Posted: 08.24.2018

Abby Olena Scientists have been looking for years for the proteins that convert the mechanical movement of inner ears’ hair cells into an electrical signal that the brain interprets as sound. In a study published today (August 22) in Neuron, researchers have confirmed that transmembrane channel-like protein 1 (TMC1) contributes to the pore of the so-called mechanotransduction channel in the cells’ membrane. “The identification of the channel has been missing for a long time,” says Anthony Peng, a neuroscientist at the University of Colorado Denver who did not participate in the study. This work “settles the debate as to whether or not [TMC1] is a pore-lining component of the mechanotransduction channel.” When a sound wave enters the cochlea, it wiggles protrusions called stereocilia on both outer hair cells, which amplify the signals, and inner hair cells, which convert the mechanical signals to electric ones and send them to the brain. It’s been tricky to figure out what protein the inner hair cells use for this conversion, because their delicate environment is difficult to recreate in vitro in order to test candidate channel proteins. In 2000, researchers reported on a promising candidate in flies, but it turned out not to be conserved in mammals. In a study published in 2011, Jeffrey Holt of Harvard Medical School and Boston Children’s Hospital and colleagues showed that genes for TMC proteins were necessary for mechanotransduction in mice. This evidence—combined with earlier work from another group showing that mutations in these genes could cause deafness in humans—pointed to the idea that TMC1 formed the ion channel in inner ear hair cells. © 1986 - 2018 The Scientist

Keyword: Hearing
Link ID: 25372 - Posted: 08.24.2018

Leah Rosenbaum A firefly’s blinking behind is more than just a pretty summer sight. It’s known that fireflies flash to attract mates (SN Online: 8/12/15) — but the twinkles may serve another purpose as well. Jesse Barber, a biologist at Boise State University, had a hunch that the lights also warn off potential nighttime predators. He wasn’t the first person with this hypothesis. As far back as 1882, entomologist G.H. Bowles wrote of fireflies: “May not the light then serve … as a warning of their offensiveness to creatures that would devour them?” But the theory hadn’t been tested, until now. “We always assumed that bats don’t use vision for much,” Barber says. Many species of fireflies are “chemically protected,” meaning they taste awful to predators, Barber says. Yet if an insect doesn’t offer a warning of its bad taste, it may get sampled anyway. Barber noticed that, unlike moths, which signal their toxicity to bats with noises, fireflies don’t make a peep (SN Online: 7/3/13). He wondered if lightning bugs were warning bats of their disgusting taste with their blinking lights. Barber and colleagues wanted to see if it took bats longer to learn to avoid fireflies when the flashings were masked. The team began by introducing fireflies to three bats that had never encountered the bugs before. The bats learned to avoid the bright creatures “after just a few interactions,” Barber says. Those early exchanges went something like: catch, taste, drop. Soon, the bats avoided the fireflies completely. |© Society for Science & the Public 2000 - 2018. All rights reserved.

Keyword: Sexual Behavior
Link ID: 25371 - Posted: 08.24.2018

By Joel Achenbach To minimize health risks, the optimal amount of alcohol someone should consume is none. That’s the simple, surprising conclusion of a massive study, co-authored by 512 researchers from 243 institutions, published Thursday in the prestigious journal the Lancet. The researchers built a database of more than a thousand alcohol studies and data sources, as well as death and disability records from 195 countries and territories between 1990 and 2016. The goal was to estimate how alcohol affects the risk of 23 health problems. The number that jumped out, in the end, was zero. Anything more than that was associated with health risks. “What has been underappreciated, what’s surprising, is that no amount of drinking is good for you,” said Emmanuela Gakidou, a professor of global health at the University of Washington and the senior author of the report. “People should no longer think that a drink or two a day is good for you. What’s best for you is to not drink at all,” she said. The report found that 2.8 million people across the globe died in 2016 of alcohol-related causes, which is about the same proportionally as the 2.0 million who died in 1990. For people ages 15 to 49, alcohol is the leading risk factor for experiencing a negative health outcome. This is a sobering report for the roughly 2 billion human beings who drink alcohol. The report challenges the controversial hypothesis that moderate drinking provides a clear health benefit. That notion took hold in the 1990s after news reports on the “French paradox”: The French have relatively low rates of heart disease despite a fatty diet. Some researchers pointed to red wine consumption among the French as potentially protective. © 1996-2018 The Washington Post

Keyword: Drug Abuse
Link ID: 25370 - Posted: 08.24.2018

By Nicholas Bakalar A mother’s depression may have long-term effects on her child’s immune system and psychological health. Israeli researchers followed 125 babies from birth through 10 years. About 43 percent of the mothers had a diagnosis of major depression, and the rest constituted a control group. The study is in Depression & Anxiety. The investigators tested the children’s and mothers’ saliva for cortisol, the stress hormone, as well as for an antibody called secretory immunoglobulin A, or SIgA, high levels of which indicate activation of the immune system. They also visited the families to assess the mother’s emotional health and to observe behavioral problems in children. Compared to controls, depressed mothers had higher cortisol and SIgA levels and tended to exhibit more intrusive and insensitive behaviors toward their children. Children of the depressed mothers had higher levels of SIgA, tended to be more withdrawn and had higher rates of psychiatric symptoms. The senior author, Ruth Feldman, a professor of developmental neuroscience at the Interdisciplinary Center, Herzliya, said that maternal depression may affect the child in various ways. “Children exposed to maternal major depression respond like those under chronic stress,” she said. Depression also increases maternal stress, which impacts a child’s stress levels. And insensitive behaviors by a mother may increase a child’s social withdrawal, which increases the risk for psychiatric disorders. © 2018 The New York Times Company

Keyword: Depression; Development of the Brain
Link ID: 25369 - Posted: 08.24.2018

By Frankie Schembri For many children with autism spectrum disorder (ASD), recognizing and responding to eye contact, body language, and tone of voice is a major challenge. Improving those social skills can take lots of work—putting a strain on caregivers with limited time, resources, and money for therapy. Now, a study shows that just 30 days with an in-home robot that provides social feedback can dramatically improve a child’s interactions with others. Researchers have long known that robots—and games with automated feedback—can change the behavior of children with autism, at least in the short term. Such interactions have been shown to help children pick up on social cues, such as making sustained eye contact, that they might have missed from their caregivers. But translating these new skills into better person-to-person interactions may require longer and more intensive training, and few studies have been large enough—or long enough—to show significant, long-lasting improvements. So Brian Scassellati, a robotics expert and cognitive scientist at Yale University, put together an experiment that gave children a long-term relationship with their bots, one they could share with their families. His team provided 12 families with a tablet computer loaded with social games and a modified version of a commercially sold robot called Jibo, which was programmed to follow along with the games and provide feedback. “As a roboticist, that was one of the most frightening things in the world. Leaving the robots there and hoping they would do the things we’d programmed them to do,” Scassellati says. © 2018 American Association for the Advancement of Science

Keyword: Autism; Robotics
Link ID: 25368 - Posted: 08.23.2018

By Carl Zimmer In a limestone cave nestled high above the Anuy River in Siberia, scientists have discovered the fossil of an extraordinary human hybrid. The 90,000-year-old bone fragment came from a female whose mother was Neanderthal, according to an analysis of DNA discovered inside it. But her father was not: He belonged to another branch of ancient humanity known as the Denisovans. Scientists have been recovering genomes from ancient human fossils for just over a decade. Now, with the discovery of a Neanderthal-Denisovan hybrid, the world as it was tens of thousands of years ago is coming into remarkable new focus: home to a marvelous range of human diversity. In 2010, researchers working in the Siberian cave, called Denisova, announced they had found DNA from a scrap of bone representing an unknown group of humans. Subsequent discoveries in the cave confirmed that the Denisovans were a lineage distinct from modern humans. Scientists can’t yet say what Denisovans looked like or how they behaved, but it’s clear they were separated from Neanderthals and modern humans by hundreds of thousands of years of evolution. Until now, scientists had indirect clues that Neanderthals, Denisovans and modern humans interbred, at least a few times. But the new study, published on Wednesday in the journal Nature, offers clear evidence. “They managed to catch it in the act — it’s an amazing discovery,” said Sharon Browning, a statistical geneticist at the University of Washington who was not involved in the new study. © 2018 The New York Times Company

Keyword: Evolution; Genes & Behavior
Link ID: 25367 - Posted: 08.23.2018

Researchers have identified connections between neurons in brain systems associated with reward, stress, and emotion. Conducted in mice, the new study may help untangle multiple psychiatric conditions, including alcohol use disorder, anxiety disorders, insomnia, and depression in humans. “Understanding these intricate brain systems will be critical for developing diagnostic and therapeutic tools for a broad array of conditions,” said George F. Koob, Ph.D., director of the National Institute on Alcohol Abuse and Alcoholism (NIAAA), which contributed funding for the study. The National Institute of Mental Health (NIMH) also provided major support for the research. NIAAA and NIMH are parts of the National Institutes of Health. A report of the study, by first author Dr. William Giardino and colleagues at Stanford University, appears in the August 2018 issue of Nature Neuroscience. Responding appropriately to aversive or rewarding stimuli is essential for survival. This requires fine-tuned regulation of brain systems that enable rapid responses to changes in the environment, such as those involved in sleep, wakefulness, stress, and reward-seeking. These same brain systems are often dysregulated in addiction and other psychiatric conditions. In the new study, researchers looked at the extended amygdala, a brain region involved in fear, arousal, and emotional processing and which plays a significant role in drug and alcohol addiction. They focused on a part of this structure known as the bed nucleus of stria terminalis (BNST), which connects the extended amygdala to the hypothalamus, a brain region that regulates sleep, appetite, and body temperature.

Keyword: Drug Abuse; Learning & Memory
Link ID: 25366 - Posted: 08.23.2018

Hannah Devlin Science correspondent Lack of sleep has long been linked to obesity, but a new study suggests late night snacking may not be the primary culprit. The latest findings provide the most compelling evidence to date that disrupted sleep alters the metabolism and boosts the body’s ability to store fat. The findings add to mounting scientific evidence on how disrupted sleep influences the usual rhythms of the body clock, raising the risk of a wide range of health problems from heart disease to diabetes. Jonathan Cedernaes, a circadian researcher at Uppsala University in Sweden and the paper’s first author, said the findings pointed to “the irreplaceable function that sleep has”. “Sleep is not just to conserve energy, it has so many functions,” he said. Time and again research has linked shift work and lack of sleep to the risk of obesity and diabetes, but the reasons behind this association are complex and have been difficult to elucidate. Insufficient sleep appears to disrupt hormones that control appetite and feelings of fullness. Those who sleep less have more time to eat, may be too tired to exercise and have less self-control when it comes to resisting the temptation of unhealthy snacks. A previous study by Cedernaes and colleagues showed that even a short period of sleep deprivation led people to eat more and opt for higher calorie food. To complicate matters further, obesity increases the risk of sleep apnoea, a breathing problem that itself disturbs sleep quality. © 2018 Guardian News and Media Limited

Keyword: Sleep; Obesity
Link ID: 25365 - Posted: 08.23.2018

By Nicholas Bakalar Children whose families move homes frequently may be at increased risk for serious psychiatric illness. Researchers followed 1,440,383 children from birth to age 29, including data on residential moves. They found 4,537 cases of psychosis, symptoms of which can include hallucinations and delusions. The more often children under 19 moved, the greater their risk for psychosis. The largest effect was among 16- to 19-year-olds. For them, two or three moves more than tripled the risk for psychosis, and four or more nearly quadrupled the risk. After age 20, there was no association between moving and illness. The study, in JAMA Psychiatry, controlled for sex, foreign background, parental death, parental history of severe mental illness, income and mother’s age at birth, but had no data for bullying or physical or sexual abuse. “Moving once or twice over the course of a childhood won’t have much effect,” said the lead author, James B. Kirkbride, an associate professor at University College London. “But moving once a year for four or five years — it would seem that those kids would face a risk. So we’d want to build a social network for those children who are moving frequently, particularly in late adolescence, when forming friendships can be vital for lifelong resistance to psychotic illness.” © 2018 The New York Times Company

Keyword: Schizophrenia; Development of the Brain
Link ID: 25364 - Posted: 08.23.2018

David Cyranoski Doctors in Japan are poised to implant neural cells made from ‘reprogrammed’ stem cells into the brains of people with Parkinson’s disease. It is only the third clinical application of induced pluripotent stem (iPS) cells, which are developed by reprogramming the cells of body tissues such as skin to revert to an embryonic-like state, from which they can morph into other cell types. Researchers have used the technique to generate precursors to the neurons that make the neurotransmitter dopamine, which degenerate and die in people with Parkinson’s disease. Physicians at Kyoto University Hospital will inject 5 million of these precursor cells into the brains of seven people with the condition. Because dopamine-producing neurons are involved in motor skills, people with the condition typically experience tremors and stiff muscles. Participants will be observed for two years after the transplantation. One of the trial’s leaders, stem-cell scientist Jun Takahashi at the Center for iPS Cell Research and Application in Kyoto, demonstrated in 2017 that the precursor cells differentiated into dopamine-producing neurons in monkeys that had a version of the disease. They also had improved symptoms1. In 2014, ophthalmologist Masayo Takahashi — Takahashi’s wife — at the RIKEN Center for Developmental Biology in Kobe developed an iPS-cell-based therapy to treat retinal disease. And in May, a team at Osaka University received approval to use cells created from iPS cells to treat heart disease. © 2018 Springer Nature Limited

Keyword: Parkinsons; Stem Cells
Link ID: 25363 - Posted: 08.22.2018

By Meredith Wadman VANCOUVER, CANADA—The dark shadow of Huntington disease fell squarely over Michelle Dardengo’s life on the day in 1986 that her 52-year-old father was found floating in the river in Tahsis, the remote Vancouver Island mill town where she grew up. Richard Varney had left his wedding ring, watch, and wallet on the bathroom counter; ridden his bike to a bridge that spans the rocky river; and jumped. The 4.5-meter drop broke his pelvis. The town doctor happened to be fishing below and pulled Varney out as he floated downstream, saving his life. But his tailspin continued. The once funny man who read the Encyclopedia Britannica for pleasure; the good dancer who loved ABBA, the Three Tenors, and AC/DC; the affable volunteer firefighter—that man was disappearing. He was being replaced by an erratic, raging misanthrope wedded to 40-ounce bottles of Bacardi whose legs would not stay still when he reclined in his La-Z-Boy. In 1988, Varney was diagnosed with Huntington disease. That explained his transformation but offered little comfort. Huntington is a brutal brain malady caused by a mutant protein that inexorably robs victims of control of their movements and their minds. Patients are plagued by jerky, purposeless movements called chorea. They may become depressed, irritable, and impulsive. They inevitably suffer from progressive dementia. The slow decline typically begins in midlife and lasts 15 to 20 years, as the toxic protein damages and finally kills neurons. For both families and the afflicted, the descent is agonizing, not least because each child of an affected person has a 50% chance of inheriting the fatal disease. © 2018 American Association for the Advancement of Science

Keyword: Huntingtons
Link ID: 25362 - Posted: 08.22.2018

By Christopher F. Schuetze DOETINCHEM, Netherlands — “We’re lost,” said Truus Ooms, 81, to her friend Annie Arendsen, 83, as they rode a city bus together. “As the driver, you should really know where we are,” Ms. Arendsen told Rudi ten Brink, 63, who sat at the wheel of the bus. But she was joking. The three are dementia patients at a care facility in the eastern Netherlands. Their bus ride — a route on the flat, tree-lined country roads of the Dutch countryside — was a simulation that plays out several times a day on three video screens. It is part of an unorthodox approach to dementia treatment that doctors and caregivers across the Netherlands have been pioneering: harnessing the power of relaxation, childhood memories, sensory aids, soothing music, family structure and other tools to heal, calm and nurture the residents, rather than relying on the old prescription of bed rest, medication and, in some cases, physical restraints. “The more stress is reduced, the better,” said Dr. Erik Scherder, a neuropsychologist at the Vrije Universiteit Amsterdam and one of the country’s best-known dementia care specialists. “If you can lower stress and discomfort, it has a direct physiological effect.” Simulated trips in buses or on beaches — like one in a care facility in Haarlem, not far from a real beach — create a gathering point for patients. The shared experience lets them talk about past trips and take a mini holiday from their daily lives. Dementia, a group of related syndromes, manifests itself in a steep decline in brain functions. The condition steals memories and personalities. It robs families of their loved ones and saps resources, patience and finances. © 2018 The New York Times Company

Keyword: Alzheimers; Learning & Memory
Link ID: 25361 - Posted: 08.22.2018

Inga Vesper The executive director of the European Union’s ambitious — but contentious — Human Brain Project (HBP) has left his post after a disagreement with the institution that coordinates the initiative. The 10-year, €1-billion (US$1.1-billion) project aims to simulate the human brain using computers, and is a flagship science initiative of the EU. In a joint statement on 16 August, Chris Ebell and the HBP’s coordinating institution, the Swiss Federal Institute of Technology in Lausanne, said that they had decided to “separate by common agreement” following “differences of opinion on governance and on strategic orientations”. Ebell became director of the project in 2015, after the HBP disbanded its small executive committee in favour of a 22-member governing board. The HBP, which involves more than 100 partner institutions, had after its inception in 2013 been criticized by some neuroscientists for its scientific direction, its complicated structure and the lack of transparency surrounding its funding decisions. doi: 10.1038/d41586-018-06020-0 © 2018 Springer Nature Limited

Keyword: Brain imaging
Link ID: 25360 - Posted: 08.22.2018