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By Andy Coghlan It tastes foul and makes people vomit. But ayahuasca, a hallucinogenic concoction that has been drunk in South America for centuries in religious rituals, may help people with depression that is resistant to antidepressants. Tourists are increasingly trying ayahuasca during holidays to countries such as Brazil and Peru, where the psychedelic drug is legal. Now the world’s first randomised clinical trial of ayahuasca for treating depression has found that it can rapidly improve mood. The trial, which took place in Brazil, involved administering a single dose to 14 people with treatment-resistant depression, while 15 people with the same condition received a placebo drink. A week later, those given ayahuasca showed dramatic improvements, with their mood shifting from severe to mild on a standard scale of depression. “The main evidence is that the antidepressant effect of ayahuasca is superior to the placebo effect,” says Dráulio de Araújo of the Brain Institute at the Federal University of Rio Grande do Norte in Natal, who led the trial. Shamans traditionally prepare the bitter, deep-brown brew of ayahuasca using two plants native to South America. The first, Psychotria viridis, is packed with the mind-altering compound dimetheyltryptamine (DMT). The second, the ayahuasca vine (Banisteriopsis caapi), contains substances that stop DMT from being broken down before it crosses the gut and reaches the brain. © Copyright Reed Business Information Ltd.
Sarah Boseley in Amsterdam The city of Amsterdam is leading the world in ending the obesity epidemic, thanks to a radical and wide-reaching programme which is getting results even among the poorest communities that are hardest to reach. Better known for tulips and bicycles, Amsterdam has the highest rate of obesity in the Netherlands, with a fifth of its children overweight and at risk of future health problems. The programme appears to be succeeding by hitting multiple targets at the same time – from promoting tap water to after-school activities to the city refusing sponsorship to events that take money from Coca Cola or McDonalds. It is led by a dynamic deputy mayor with the unanimous backing of the city’s politicians. From 2012 to 2015, the number of overweight and obese children has dropped by 12%. Even more impressive, Amsterdam has done what nobody else has managed, because the biggest fall has been amongst the lowest socio-economic groups. It is in neighbourhoods like the Bijlmer in the south-east that the programme is changing lives. The Bijlmer is notorious, says Wilbert Sawat, coordinator and PE teacher at De Achtsprong primary school, and that’s why he wanted to work there. Other teachers do too, he says. “Here we can make a difference.
Link ID: 23493 - Posted: 04.15.2017
Laurel Hamers Earth’s magnetic field helps eels go with the flow. The Gulf Stream fast-tracks young European eels from their birthplace in the Sargasso Sea to the European rivers where they grow up. Eels can sense changes in Earth’s magnetic field to find those highways in a featureless expanse of ocean — even if it means swimming away from their ultimate destination at first, researchers report in the April 13 Current Biology. European eels (Anguilla anguilla) mate and lay eggs in the salty waters of the Sargasso Sea, a seaweed-rich region in the North Atlantic Ocean. But the fish spend most of their adult lives living in freshwater rivers and estuaries in Europe and North Africa. Exactly how eels make their journey from seawater to freshwater has baffled scientists for more than a century, says Nathan Putman, a biologist with the National Oceanic and Atmospheric Administration in Miami. The critters are hard to track. “They’re elusive,” says study coauthor Lewis Naisbett-Jones, a biologist now at the University of North Carolina at Chapel Hill. “They migrate at night and at depth. The only reason we know they spawn in the Sargasso Sea is because that’s where the smallest larvae have been collected.” |© Society for Science & the Public 2000 - 2017.
Keyword: Animal Migration
Link ID: 23492 - Posted: 04.14.2017
By James Gallagher Health and science reporter, BBC News website Toddlers who spend time playing on smartphones and tablets seem to get slightly less sleep than those who do not, say researchers. The study in Scientific Reports suggests every hour spent using a touchscreen each day was linked to 15 minutes less sleep. However, those playing with touchscreens do develop their fine motor skills more quickly. Experts said the study was "timely" but parents should not lose sleep over it. There has been an explosion in touchscreens in the home, but understanding their impact on early childhood development has been lacking. The study by Birkbeck, University of London, questioned 715 parents of children under three years old. It asked how often their child played with a smartphone or tablet and about the child's sleep patterns. It showed that 75% of the toddlers used a touchscreen on a daily basis, with 51% of those between six and 11 months using one, and 92% of those between 25 and 36 months doing so as well. But children who did play with touchscreens slept less at night and more in the day. Overall they had around 15 minutes less sleep for every hour of touchscreen use. Not before bedtime? Dr Tim Smith, one of the researchers, told the BBC News website: "It isn't a massive amount when you're sleeping 10-12 hours a day in total, but every minute matters in young development because of the benefits of sleep." © 2017 BBC.
Link ID: 23491 - Posted: 04.14.2017
By CATHERINE SAINT LOUIS Halfway through February, I could no longer sleep through the night. At 2 a.m., I’d find myself chugging milk from the carton to extinguish a fire at the top of my rib cage. The gnawing feeling high in my stomach alternated with nausea so arresting I kept a bucket next to my laptop and considered taking a pregnancy test, even though I was 99 percent sure I wasn’t expecting. One day on the subway platform, I doubled over and let out a groan so pathetic it prompted a complete stranger to ask, “Are you all right?” Then I knew it was time to seek medical attention. New Yorkers don’t address strangers on the subway, I told myself. It’s like breaking the fourth wall. The next day, my primary care doctor told me I probably had an ulcer, a raw spot or sore in the lining of the stomach or small intestine. Here are some of the things I learned about ulcers during the odyssey that followed. ■ Anyone Can Get an Ulcer. Back in the 1980s, when doctors and most everyone else thought psychological stress or spicy foods led to ulcers, two Australian scientists discovered that the main culprit was actually a bacterium called Helicobacter pylori. That discovery eventually won them a Nobel Prize in 2005, and ushered in an era of using antibiotics to cure ulcers. But that didn’t wipe out ulcers altogether. Far from it. Indeed, my tribe of fellow sufferers are legion. Nearly 16 million adults nationwide reported having an ulcer in 2014,according to the Centers for Disease Control and Prevention’s National Center for Health Statistics. The largest group, roughly 6.2 million, were 45 to 64 years old. Those 18 to 44 accounted for 4.6 million, 65- to 74-year-olds for 2.6 million, and those 75 and older for 2.4 million. I got a blood test to see if I was infected with H. pylori; the test came back negative, so I didn’t need antibiotics. Regular use of nonsteroidal anti-inflammatory drugs, like ibuprofen or aspirin, can also lead to an ulcer, but I wasn’t taking those medicines. My ulcer turned out to be “idiopathic,” which is a fancy way of saying that doctors have no idea why it happened. © 2017 The New York Times Company
Link ID: 23490 - Posted: 04.14.2017
By Pascal Wallisch One of psychologist Robert Zajonc’s lasting contributions to science is the “mere exposure effect,” or the observation that people tend to like things if they are exposed to them more often. Much of advertising is based on this notion. But it was sorely tested in late February 2015, when “the dress” broke the internet. Within days, most people were utterly sick of seeing or talking about it. I can only assume that now, two years later, you have very limited interest in being here. (Thank you for being here.) But the phenomenon continues to be utterly fascinating to vision scientists like me, and for good reason. The very existence of “the dress” challenged our entire understanding of color vision. Up until early 2015, a close reading of the literature could suggest that the entire field had gone somewhat stale—we thought we basically knew how color vision worked, more or less. The dress upended that idea. No one had any idea why some people see “the dress” differently than others—we arguably still don’t fully understand it. It was like discovering a new continent. Plus, the stimulus first arose in the wild (in England, no less), making it all the more impressive. (Most other stimuli used by vision science are generally created in labs.) Even outside of vision scientists, most people just assume everyone sees the world in the same way. Which is why it’s awkward when disagreements arise—it suggests one party either is ignorant, is malicious, has an agenda, or is crazy. We believe what we see with our own eyes more than almost anything else, which may explain the feuds that occurred when “the dress” first struck and science lacked a clear explanation for what was happening.
Link ID: 23489 - Posted: 04.14.2017
By Andy Coghlan Using a virus to reprogram cells in the brain could be a radical way to treat Parkinson’s disease. People with Parkinson’s have difficulty controlling their movements due to the death of neurons that make dopamine, a brain signalling chemical. Transplants of fetal cells have shown promise for replacing these dead neurons in people with the disease, and a trial is currently under way. But the transplant tissue comes from aborted pregnancies, meaning it is in short supply, and some people may find this ethically difficult. Recipients of these cells have to take immunosuppressant drugs too. Ernest Arenas, at the Karolinska Institute in Stockholm, Sweden, and his team have found a new way to replace lost dopamine-making neurons. They injected a virus into the brains of mice whose dopamine neurons had been destroyed. This virus had been engineered to carry four genes for reprogramming astrocytes – the brain’s support cells – into dopamine neurons. Five weeks later, the team saw improvements in how the mice moved. “They walked better and their gait showed less asymmetry than controls,” says Arenas. This is the first study to show that reprogramming cells in the living brain can lead to such improvements, he says. © Copyright Reed Business Information Ltd.
Link ID: 23488 - Posted: 04.14.2017
Tina Hesman Saey Some Pakistani people are real knockouts, a new DNA study finds. Knockouts in this sense doesn’t refer to boxing or a stunning appearance, but to natural mutations that inactivate, or “knock out” certain genes. The study suggests that human knockouts could prove valuable evidence for understanding how genes work and for developing drugs. Among 10,503 adults participating in a heart disease study in Pakistan, 1,843 people have at least one gene of which both copies have been knocked out, researchers report online April 12 in Nature. Researchers also drew blood from many of the participants and used medical records to study more than 200 traits, such as heart rate, blood pressure and blood levels of sugar, cholesterol, hormones or other substances. Studying how the knockout mutations affect those traits and health could point to genes that are potentially safe and effective targets for new drugs. Combining genetic data with medical information will provide “a rich dataset for many applications,” says Robert Plenge, a human geneticist formerly with the pharmaceutical company Merck. Scientists have traditionally learned about genes’ roles by deleting the genes from mice and then cataloging abnormalities in how those mice developed and behaved. Such animal research will always be needed, but studies of people naturally lacking certain genes “will change the nature of the scientific investigation of the genetic basis of human disease,” Plenge wrote in a commentary in the same issue of Nature. Often, a person will inherit a broken copy of a gene from one parent and a healthy copy from the other. But 39 percent of the people in this study had parents who were closely related — often first cousins — increasing the odds of inheriting two mutant copies of a gene. Of this study’s 1,843 participants, 1,504 had both copies of a single gene knocked out. The rest had more than one gene knocked out, including one person in whom six genes were predicted to be completely nonfunctional. |© Society for Science & the Public 2000 - 2017.
In two studies of mice, researchers showed that a drug, engineered to combat the gene that causes spinocerebellar ataxia type 2 (SCA2), might also be used to treat amyotrophic lateral sclerosis (ALS). Both studies were published in the journal Nature with funding from National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “Our results provide hope that we may one day be able to treat these devastating disorders,” said Stefan M. Pulst, M.D., Dr. Med., University of Utah, professor and chair of neurology and a senior author of one the studies. In 1996, Dr. Pulst and other researchers discovered that mutations in the ataxin 2 gene cause spinocerebellar ataxia type 2, a fatal inherited disorder that primarily damages a part of the brain called the cerebellum, causing patients to have problems with balance, coordination, walking and eye movements. For this study his team found that they could reduce problems associated with SCA2 by injecting mouse brains with a drug programmed to silence the ataxin 2 gene. In the accompanying study, researchers showed that injections of the same type of drug into the brains of mice prevented early death and neurological problems associated with ALS, a paralyzing and often fatal disorder. “Surprisingly, the ataxin 2 gene may act as a master key to unlocking treatments for ALS and other neurological disorders,” said Aaron Gitler, Ph.D., Stanford University, associate professor and senior author of the second study. In 2010, Dr. Gitler and colleagues discovered a link between ataxin 2 mutations and ALS.
By Simon Makin When the now-famous neurological patient Henry Molaison had his brain’s hippocampus surgically sectioned to treat seizures in 1953, science’s understanding of memory inadvertently received perhaps its biggest boost ever. Molaison lost the ability to form new memories of events, and his recollection of anything that had happened during the preceding year was severely impaired. Other types of memory such as learning physical skills were unaffected, suggesting the hippocampus specifically handles the recall of events—known as “episodic” memories. Further research on other patients with hippocampal damage confirmed recent memories are more impaired than distant ones. It appears the hippocampus provides temporary storage for new information whereas other areas may handle long-term memory. Events that we are later able to remember appear to be channeled for more permanent storage in the cortex (the outer layers of the brain responsible for higher functions such as planning and problem-solving). In the cortex these memories form gradually, becoming integrated with related information to build lasting knowledge about ourselves and the world. Episodic memories that are intended for long-term storage accumulate to form the “autobiographical” memory that is so essential for our sense of identity. Neuroscientists know a lot about how short-term memories are formed in the brain but the processes underlying long-term storage are still not well understood. © 2017 Scientific American,
Keyword: Learning & Memory
Link ID: 23485 - Posted: 04.13.2017
By Jyoti Madhusoodanan For three consecutive winters, starting in 2011, researchers at the University of Birmingham asked healthy men and women over the age of 65 to come in to clinics across the western Midlands in the U.K. for a seasonal influenza vaccination at specific times of day—either between 9 and 11 a.m., or between 3 and 5 p.m. Blood drawn a month later revealed that participants, who totaled nearly 300 over the three years, had higher levels of anti-flu antibodies if they’d received their vaccinations in the morning.1 The results suggested that daily rhythms of people’s bodies tweaked the vaccine’s effectiveness. Lead author Anna Phillips Whittaker had suspected as much, after observing similar trends in her studies on behavioral factors such as exercise that affect vaccination responses, and in the wake of a growing body of literature suggesting that a little timing can go a long way when it comes to health. Many hormones and immune signals are produced rhythmically in 24-hour cycles. Cortisol, for example, which is known to suppress inflammation and regulate certain T cell–mediated immune responses, peaks early in the morning and ebbs as the day progresses. Other facets of the immune system undergo similar cycles that could underlie the differences in antibody responses Phillips observed among people receiving the flu vaccine. Much more work is required to nail down the immune mechanisms responsible for such variation and exploit them appropriately, she says. But timing flu vaccine delivery would be straightforward to implement. “It’s such a simple, low-risk intervention that’s free to do, and could have massive implications for vulnerable populations.” © 1986-2017 The Scientist
Keyword: Biological Rhythms
Link ID: 23484 - Posted: 04.13.2017
By Niall Firth The firing of every neuron in an animal’s body has been recorded, live. The breakthrough in imaging the nervous system of a hydra – a tiny, transparent creature related to jellyfish – as it twitches and moves has provided insights into how such simple animals control their behaviour. Similar techniques might one day help us get a deeper understanding of how our own brains work. “This could be important not just for the human brain but for neuroscience in general,” says Rafael Yuste at Columbia University in New York City. Instead of a brain, hydra have the most basic nervous system in nature, a nerve net in which neurons spread throughout its body. Even so, researchers still know almost nothing about how the hydra’s few thousand neurons interact to create behaviour. To find out, Yuste and colleague Christophe Dupre genetically modified hydra so that their neurons glowed in the presence of calcium. Since calcium ions rise in concentration when neurons are active and fire a signal, Yuste and Dupre were able to relate behaviour to activity in glowing circuits of neurons. For example, a circuit that seems to be involved in digestion in the hydra’s stomach-like cavity became active whenever the animal opened its mouth to feed. This circuit may be an ancestor of our gut nervous system, the pair suggest. © Copyright Reed Business Information Ltd.
By Partha Mitra Intricate, symmetric patterns, in tiles and stucco, cover the walls and ceilings of Alhambra, the “red fort,” the dreamlike castle of the medieval Moorish kings of Andalusia. Seemingly endless in variety, the two dimensionally periodic patterns are nevertheless governed by the mathematical principles of group theory and can be classified into a finite number of types: precisely seventeen, as shown by Russian crystallographer Evgraf Federov. The artists of medieval Andalusia are unlikely to have been aware of the mathematics of space groups, and Federov was unaware of the art of Alhambra. The two worlds met in the 1943 PhD thesis of Swiss astronomer Edith Alice Muller, who counted eleven of the seventeen planar groups in the adornments of the palace (more have been counted since). All seventeen space groups can also be found in the periodic patterns of Japanese wallpaper. Without conscious intent or explicit knowledge, the creations of artists across cultures at different times nevertheless had to conform to the constraints of periodicity in two dimensional Euclidean space, and were thus subject to mathematically precise theory. Does the same apply to the “endless forms most beautiful,” created by the biological evolutionary process? Are there theoretical principles, ideally ones which may be formulated in mathematical terms, underlying the bewildering complexity of biological phenomema? Without the guidance of such principles, we are only generating ever larger digital butterfly collections with ever better tools. In a recent article, Krakauer and colleagues argue that by marginalizing ethology, the study of adaptive behaviors of animals in their natural settings, modern neuroscience has lost a key theoretical framework. The conceptual framework of ethology contains in it the seeds of a future mathematical theory that might unify neurobiological complexity as Fedorov’s theory of wallpaper groups unified the patterns of the Alhambra. © 2017 Scientific American
Link ID: 23482 - Posted: 04.12.2017
By ANAHAD O’CONNOR About a year and a half ago, Robin Collier and her husband, Wayne, were like millions of other Americans: overweight and living with Type 2 diabetes. Despite multiple diets, the couple could not seem to lose much weight. Then Ms. Collier’s doctor told her she was going to need daily insulin shots to control her diabetes. That was the motivation she needed. “I made up my mind right then and there,” said Ms. Collier, 62, an administrator at an accounting firm in Lafayette, Ind. “I said to myself, ‘I’m not going on insulin. I’m too young to have this disease.’” Instead, Ms. Collier and her husband entered a study sponsored by a company called Virta Health, one of a new crop of high-tech companies that have designed programs aimed at helping people prevent or even reverse their diabetes. On the program, patients video-chat with a remote Virta doctor, who consults with their primary care doctor, reviews their blood tests and medical history, and makes diet and drug recommendations. While studies show that a variety of different diets can benefit people with Type 2 diabetes, Virta, based in San Francisco, takes a low-carbohydrate approach, training patients to swap foods like pastries, pasta and sugary snacks for veggie omelets, almonds and salads with grilled chicken and beef. Every day, patients use an app to upload their blood sugar levels, blood pressure, body weight and other measurements. A health coach, usually a registered dietitian, monitors their data and checks in by phone, text or email to discuss any problems or just to provide daily encouragement. Today, Ms. Collier has lost 75 pounds and has avoided taking insulin. Her husband has lost 45 pounds and was able to stop two diabetes medications. Both are still in the program, which she called “life changing,” as part of an ongoing clinical trial. © 2017 The New York Times Company
Link ID: 23481 - Posted: 04.12.2017
Consider two children who have childhood absence epilepsy (CAE), the most common form of pediatric epilepsy. They both take the same drug — one child sees an improvement in their seizures, but the other does not. A new study in the Annals of Neurology identified the genes that may underlie this difference in treatment outcomes, suggesting there may be potential for using a precision medicine approach to help predict which drugs will be most effective to help children with CAE. The study was funded by the National Institute of Neurological Disorders and Stroke (NINDS) and the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), both part of the National Institutes of Health. “A better understanding of genetic factors underlying a disease and the way that people respond to treatments may help healthcare providers select the best therapies for children with CAE,” said Vicky Whittemore, Ph.D., program director at NINDS. A team led by Tracy A. Glauser, M.D., director of the Comprehensive Epilepsy Center at Cincinnati Children’s Hospital Medical Center and professor of pediatrics in the University of Cincinnati College of Medicine, investigated whether there may be a genetic basis for different responses to three drugs used for CAE (ethosuximide, valproic acid, and lamotrigine). The experiments focused on three genes that code for T-type calcium channels that are involved in CAE and one gene that codes for a transporter that shuttles the drugs out of the brain. T-type calcium channels help control the firing rate of brain cells. The current study is part of a 32-center, randomized, controlled clinical trial that compared the effects of the three most commonly used drugs in 446 children who were recently diagnosed with CAE.
Laura Sanders Soon after systems biologist Juergen Hahn published a paper describing a way to predict whether a child has autism from a blood sample, the notes from parents began arriving. “I have a bunch of parents writing me now who want to test their kids,” says Hahn, of Rensselaer Polytechnic Institute in Troy, N.Y. “I can’t do that.” That’s because despite their promise, his group’s results, reported March 16 in PLOS Computational Biology, are preliminary — nowhere close to a debut in a clinical setting. The test will need to be confirmed and repeated in different children before it can be used to help diagnose autism. Still, the work of Hahn and colleagues, along with other recent papers, illustrates how the hunt for a concrete biological signature of autism, a biomarker, is gaining speed. Currently, pediatricians, child psychologists and therapists rely on behavioral observations and questionnaires, measures with limitations. Barring genetic tests for a handful of rare mutations, there are no blood draws, brain scans or other biological tests that can reveal whether a child has — or will get — autism. Objective tests would be incredibly useful, helping provide an early diagnosis that could lead to therapy in the first year of life, when the brain is the most malleable. A reliable biomarker might also help distinguish various types of autism, divisions that could reveal who would benefit from certain therapies. And some biomarkers may reveal a deeper understanding of how the brain normally develops. |© Society for Science & the Public 2000 - 2017
By Michael Price Do the anatomical differences between men and women—sex organs, facial hair, and the like—extend to our brains? The question has been as difficult to answer as it has been controversial. Now, the largest brain-imaging study of its kind indeed finds some sex-specific patterns, but overall more similarities than differences. The work raises new questions about how brain differences between the sexes may influence intelligence and behavior. For decades, brain scientists have noticed that on average, male brains tend to have slightly higher total brain volume than female ones, even when corrected for males’ larger average body size. But it has proved notoriously tricky to pin down exactly which substructures within the brain are more or less voluminous. Most studies have looked at relatively small sample sizes—typically fewer than 100 brains—making large-scale conclusions impossible. In the new study, a team of researchers led by psychologist Stuart Ritchie, a postdoctoral fellow at the University of Edinburgh, turned to data from UK Biobank, an ongoing, long-term biomedical study of people living in the United Kingdom with 500,000 enrollees. A subset of those enrolled in the study underwent brain scans using MRI. In 2750 women and 2466 men aged 44–77, Ritchie and his colleagues examined the volumes of 68 regions within the brain, as well as the thickness of the cerebral cortex, the brain’s wrinkly outer layer thought to be important in consciousness, language, memory, perception, and other functions. © 2017 American Association for the Advancement of Science
By Andy Coghlan “PRENATAL exposure to progesterone affects sexual orientation in humans”. A bold and unequivocal-sounding title for a scientific paper. And certainly important if true. But is it? The study claimed to show that women given extra progesterone during pregnancy, routinely prescribed to prevent miscarriage, bleeding or premature delivery, have children who are “29 per cent more likely” to later identify as bisexual. It would be a landmark finding, allowing us to also ground in biology the established social science contention that sexuality has more dimensions than straight and gay. We suspected that exposing a fetus to strong hormones can shape sexual orientation. But there are no animal models of sexual orientation, and doing this kind of experiment in humans would be deeply unethical. The next best thing would be a retrospective analysis looking at a birth cohort exposed to a specific hormone “in the wild”. And that’s what this study did. June Reinisch of the Kinsey Institute in Indiana and her colleagues trawled a public database containing records of more than 9000 pregnancies in Denmark between 1959 and 1961. They identified women who were given a progesterone-mimicking hormone by the trade name lutocyclin to prevent miscarriage. Lutocyclin did seem to have mild effects on sexual orientation: later in life, exposed individuals were five times more likely to self-identify as non-heterosexual, and were more likely to report relationships with the same sex, than unexposed controls. © Copyright Reed Business Information Ltd.
Keyword: Sexual Behavior
Link ID: 23477 - Posted: 04.11.2017
Nicola Davis Scientists have unpicked the regions of the brain involved in dreaming, in a study with significant implications for our understanding of the purpose of dreams and of consciousness itself. What’s more, changes in brain activity have been found to offer clues as to what the dream is about. Dreaming had long been thought to occur largely during rapid eye-movement (REM) sleep, a period of slumber involving fast brain activity similar to that when awake, but dreams have also been reported to occur during non-REM sleep, leaving scientists scratching their heads as to the hallmark of dreaming. “It seemed a mystery that you can have both dreaming and the absence of dreaming in these two different types of stages,” said Francesca Siclari, co-author of the research from the University of Wisconsin-Madison in the US. Now it seems the puzzle has been solved. In addition the team found that dreaming about faces was linked to increased high-frequency activity in the region of the brain involved in face recognition, with dreams involving spatial perception, movement and thinking similarly linked to regions of the brain that handle such tasks when awake. “[It is] a proof for the fact that dreaming really is an experience that occurs during sleep, because many researchers up until now have suggested that it is just something you invent when you wake up,” said Siclari.
Link ID: 23476 - Posted: 04.11.2017
By Knvul Sheikh For the past five decades pharmaceutical drugs like levodopa have been the gold standard for treating Parkinson’s disease. These medications alleviate motor symptoms of the disease, but none of them can cure it. Patients with Parkinson’s continue to lose dopamine neurons critical to the motor control centers of the brain. Eventually the drugs become ineffective and patients’ tremors get worse. They experience a loss of balance and a debilitating stiffness takes over their legs. To replace the lost dopamine neurons, scientists have begun investigating stem cell therapy as a potential treatment or even a cure. But embryonic cells and adult stem cells have proved difficult to harness and transplant into the brain. Now a study from the Karolinska Institute in Stockholm shows it is possible to coax the brain’s own astrocytes—cells that typically support and nurture neurons—into producing a new generation of dopamine neurons. The reprogrammed cells display several of the properties and functions of native dopamine neurons and could alter the course of Parkinson’s, according to the researchers. “You can directly reprogram a cell that is already inside the brain and change the function in such a way that you can improve neurological symptoms,” says senior author Ernest Arenas, a professor of medical biochemistry at Karolinska. Previously, scientists had to nudge specialized cells like neurons into becoming pluripotent cells before they could develop a different kind of specialized cell, he says. It was like having to erase all the written instructions for how a cell should develop and what job it should do and then rewriting them all over again. But Arenas and his team found a way to convert the instructions into a different set of commands without erasing them. © 2017 Scientific American