By Laura Sanders Call it a comeback — maybe. After being shelved earlier this year for lackluster preliminary results, a drug designed to slow Alzheimer’s progression is showing new signs of life. A more in-depth look at the data from two clinical trials suggests that patients on the biggest doses of the drug, called aducanumab, may indeed benefit, the company reported December 5. People who took the highest amounts of the drug declined about 30 percent less, as measured by a commonly used Alzheimer’s scale, than people who took a placebo, Samantha Haeberlein of the biotechnology company Biogen reported at the Clinical Trials on Alzheimer’s Disease meeting in San Diego. With these encouraging results in hand, Biogen, based in Cambridge, Mass., plans to seek drug approval from the U.S. Food and Drug Administration in early 2020. The results are “exhilarating, not just to the scientific community but our patients as well,” Sharon Cohen, a behavioral neurologist at the Toronto Memory Program, said during a panel discussion at the meeting. Cohen participated in the clinical trials and has received funding from Biogen. The presentation marks “an important moment for the Alzheimer’s field,” says Rebecca Edelmayer, director of scientific engagement for the Alzheimer’s Association in Chicago. Alzheimer’s disease slowly kills cells in the brain, gradually erasing people’s abilities to remember, navigate and think clearly. Current Alzheimer’s medicines can hold off symptoms temporarily, but don’t fight the underlying brain destruction. A treatment that could actually slow or even stop the damage would have a “huge impact for patients and their caregivers,” she says. © Society for Science & the Public 2000–2019

Keyword: Alzheimers
Link ID: 26879 - Posted: 12.06.2019

By Kelly Servick When Samantha Budd Haeberlein, Biogen’s head of clinical development, took the stage in San Diego, California, before a room full of Alzheimer’s disease researchers and physicians this morning, she knew she had some explaining to do. In October, the pharmaceutical company, based in Cambridge, Massachusetts, unexpectedly revived an experimental Alzheimer’s drug that it had declared a failure 7 months earlier. Ever since, scientists and industry analysts have been hungry for more detail about two large clinical trials meant to prove that Biogen’s drug, an antibody called aducanumab, slows down cognitive decline in the early stages of disease. At the Clinical Trials on Alzheimer’s Disease congress today, Budd Haeberlein tried to clarify what has emboldened the company to apply to the U.S. Food and Drug Administration (FDA) for market approval for aducanumab early next year. After analyzing more patient data than were available at the time of a discouraging preliminary analysis, she explained, the company found evidence that the higher of two tested doses led to 22% less cognitive decline after 78 weeks than a placebo in one trial. However, the other trial failed to show any benefit, leaving some researchers with a grim outlook on the drug. “I surely don’t think that it should be given market approval on the basis of these data,” says Robert Howard, a psychiatrist at University College London who has run clinical trials of potential Alzheimer’s treatments. More positive results from a subset of patients that weren’t preselected at the trial’s launch are not convincing, he says. “[Biogen has] broken all the rules, really, about how you analyze data and report it.” © 2019 American Association for the Advancement of Science.

Keyword: Alzheimers
Link ID: 26878 - Posted: 12.06.2019

By Anisha Kalidindi The room is pitch black. Every light, from the power button on the computer to the box controlling the microscope, is covered with electrical tape. I feel a gush of air as the high-powered AC kicks on, offsetting the heat emitted from the microscope’s lasers. I take my mouse out of its cage and get ready to image its brain. I’m wearing a red headlamp so I can see, but it is still quite dim. I peer closely at my lab notebook and note the two positions: –1, +2. I recite them repeatedly in a hushed tone, so I don’t forget; it is 1 A.M., after all. I hook the mouse up to the stage of the microscope and then use my handy toothpick to make sure its head position is correct. While there are many unsung heroes of science—veterinarians, lab technicians, graduate students (I might be a bit biased with this one!)—these aren’t the ones I’m talking about. I’m talking about a toothpick that played a significant role in my research project. Advertisement I am lucky enough to have access to a cutting-edge microscope and several other pieces of expensive equipment in my lab. But can also find things you might never guess were used in science: red-light headlamps, black electrical tape, and toothpicks. Using the microscope, I can take a picture of a mouse’s living, working brain through a literal window: a piece of glass that replaces a small piece of the animal’s skull. To image the mouse, we affix a plastic bar on the front of its head and then secure the bar to a head-mounting device on the stage under the microscope lens. Using this mount, we can precisely position the head up and down and right to left. This is where our problem starts. © 2019 Scientific American

Keyword: Learning & Memory
Link ID: 26877 - Posted: 12.06.2019

Richard Harris Scientists know that if they transfuse blood from a young mouse to an old one, then they can stave off or even reverse some signs of aging. But they don't know what in the blood is responsible for this remarkable effect. Researchers now report that they've identified hundreds of proteins in human blood that wax and wane in surprising ways as we age. The findings could provide important clues about which substances in the blood can slow aging. The scientists studied nearly 3,000 proteins in blood plasma that was drawn from more than 4,000 people with a span of ages from 18 to 95. The project focused on proteins that change in both men and women. "When we went into this, we assumed you aged gradually, so we would see these changes taking place relatively steadily as individuals get older," said Tony Wyss-Coray, a professor of neurology at Stanford University. Instead, Wyss-Coray and his colleagues report in Nature Medicine on Thursday that these proteins change in three distinct waves, the first of which happens "very surprisingly" during our 30s, peaking around age 34. "Then we found a second wave around 60, and then we found a third one, the most prominent one, really around 80 years of age," Wyss-Coray said. (An earlier version of their paper is freely available on the bioRxiv preprint server.) This observation raises a host of questions about the biology of aging. What age-related transition is occurring in our 30s? And what do the changes in the blood actually mean? "Most of the proteins in the blood are actually from other tissue sources," he said. "So we can start to ask where ... these proteins come from and if they change with age," he said. For example, in proteins traced back to the liver, "that would tell us that the liver is aging." © 2019 npr

Keyword: Alzheimers
Link ID: 26876 - Posted: 12.06.2019

By Viorica Marian Psycholinguistics is a field at the intersection of psychology and linguistics, and one if its recent discoveries is that the languages we speak influence our eye movements. For example, English speakers who hear candle often look at a candy because the two words share their first syllable. Research with speakers of different languages revealed that bilingual speakers not only look at words that share sounds in one language but also at words that share sounds across their two languages. When Russian-English bilinguals hear the English word marker, they also look at a stamp, because the Russian word for stamp is marka. Even more stunning, speakers of different languages differ in their patterns of eye movements when no language is used at all. In a simple visual search task in which people had to find a previously seen object among other objects, their eyes moved differently depending on what languages they knew. For example, when looking for a clock, English speakers also looked at a cloud. Spanish speakers, on the other hand, when looking for the same clock, looked at a present, because the Spanish names for clock and present—reloj and regalo—overlap at their onset. The story doesn’t end there. Not only do the words we hear activate other, similar-sounding words—and not only do we look at objects whose names share sounds or letters even when no language is heard—but the translations of those names in other languages become activated as well in speakers of more than one language. For example, when Spanish-English bilinguals hear the word duck in English, they also look at a shovel, because the translations of duck and shovel—pato and pala, respectively—overlap in Spanish. © 2019 Scientific American

Keyword: Language; Attention
Link ID: 26875 - Posted: 12.06.2019

By Aimee Cunningham Socially isolated and faced with a persistently white polar landscape, a long-term crew of an Antarctic research station saw a portion of their brains shrink during their stay, a small study finds. “It’s very exciting to see the white desert at the beginning,” says physiologist Alexander Stahn, who began the research while at Charité-Universitätsmedizin Berlin. “But then it’s always the same.” The crew of eight scientists and researchers and a cook lived and worked at the German research station Neumayer III for 14 months. Although joined by other scientists during the summer, the crew alone endured the long darkness of the polar winter, when temperatures can plummet as low as –50° Celsius and evacuation is impossible. That social isolation and monotonous environment is the closest thing on Earth to what a space explorer on a long mission may experience, says Stahn, who is interested in researching what effect such travel would have on the brain. Animal studies have revealed that similar conditions can harm the hippocampus, a brain area crucial for memory and navigation (SN: 11/6/18). For example, rats are better at learning when the animals are housed with companions or in an enriched environment than when alone or in a bare cage, Stahn says. But whether this is true for a person’s brain is unknown. Stahn, now at the Perelman School of Medicine at the University of Pennsylvania, and his colleagues used magnetic resonance imaging to capture views of the team members’ brains before their polar stay and after their return. On average, an area of the hippocampus in the crew’s brains shrank by 7 percent over the course of the expedition, compared with healthy people matched for age and gender who didn’t stay at the station, the researchers report online December 4 in the New England Journal of Medicine. © Society for Science & the Public 2000–2019

Keyword: Learning & Memory; Biological Rhythms
Link ID: 26874 - Posted: 12.05.2019

By Jade Wu What do the sounds of whispering, crinkling paper, and tapping fingernails have in common? What about the sight of soft paint brushes on skin, soap being gently cut to pieces, and hand movements like turning the pages of a book? Well, if you are someone who experiences the autonomous sensory meridian response—or ASMR, for short—you may recognize these seemingly ordinary sounds and sights as “triggers” for the ASMR experience. No idea what I’m talking about? Don’t worry, you’re actually in the majority. Most people, myself included, aren’t affected by these triggers. But what happens to those who are? What is the ASMR experience? It’s described as a pleasantly warm and tingling sensation that starts on the scalp and moves down the neck and spine. ASMR burst onto the Internet scene in 2007, according to Wikipedia, when a woman with the username “okaywhatever” described her experience of ASMR sensations in an online health discussion forum. At the time, there was no name for this weird phenomenon. But by 2010, someone called Jennifer Allen had named the experience, and from there, ASMR became an Internet sensation. Today, there are hundreds of ASMR YouTubers who collectively post over 200 videos of ASMR triggers per day, as reported by a New York Times article in April, 2019. Some ASMR YouTubers have become bona fide celebrities with ballooning bank accounts, millions of fans, and enough fame to be stopped on the street for selfies. There’s been some controversy. Some people doubt whether this ASMR experience is “real,” or just the result of recreational drugs or imagined sensations. Some have chalked the phenomenon up to a symptom of loneliness among Generation Z, who get their dose of intimacy from watching strangers pretend to do their makeup without having to interact with real people. Some people are even actively put off by ASMR triggers. One of my listeners, Katie, said that most ASMR videos just make her feel agitated. But another listener, Candace, shared that she has been unknowingly chasing ASMR since she was a child watching BBC. © 2019 Scientific American

Keyword: Hearing; Emotions
Link ID: 26873 - Posted: 12.05.2019

Ian Sample Science editor Scientists have created artificial neurons that could potentially be implanted into patients to overcome paralysis, restore failing brain circuits, and even connect their minds to machines. The bionic neurons can receive electrical signals from healthy nerve cells, and process them in a natural way, before sending fresh signals on to other neurons, or to muscles and organs elsewhere in the body. One of the first applications may be a treatment for a form of heart failure that develops when a particular neural circuit at the base of the brain deteriorates through age or disease and fails to send the right signals to make the heart pump properly. Rather than implanting directly into the brain, the artificial neurons are built into ultra-low power microchips a few millimetres wide. The chips form the basis for devices that would plug straight into the nervous system, for example by intercepting signals that pass between the brain and leg muscles. “Any area where you have some degenerative disease, such as Alzheimer’s, or where the neurons stop firing properly because of age, disease, or injury, then in theory you could replace the faulty biocircuit with a synthetic circuit,” said Alain Nogaret, a physicist who led the project at the University of Bath. The breakthrough came when researchers found they could model live neurons in a computer program and then recreate their firing patterns in silicon chips with more than 94% accuracy. The program allows the scientists to mimic the full variety of neurons found in the nervous system. © 2019 Guardian News & Media Limited

Keyword: Robotics; Learning & Memory
Link ID: 26872 - Posted: 12.04.2019

By Gaby Maimon What is the biological basis of thought? How do brains store memories? Questions like these have intrigued humanity for millennia, but the answers still remain largely elusive. You might think that the humble fruit fly, Drosophila melanogaster, has little to add here, but since the 1970s, scientists have actually been studying the neural basis of higher brain functions, like memory, in these insects. Classic work––performed by several labs, including those of Martin Heisenberg and Seymour Benzer––focused on studying the behavior of wild-type and genetically mutated Drosophila in simple learning and memory tasks, ultimately leading to the discovery of several key molecules and other underlying mechanisms. However, because one could not peer into the brain of behaving flies to eavesdrop on neurons in action, this field, in its original form, could only go so far in helping to explain the mechanisms of cognition. In 2010, when I was a postdoctoral researcher in the lab of Michael Dickinson, we developed the first method for measuring electrical activity of neurons in behaving Drosophila. A similar method was developed in parallel by Johannes Seelig and Vivek Jayaraman. In these approaches, one glues a fly to a custom plate that allows one to carefully remove the cuticle over the brain and measure neural activity via electrodes or fluorescence microscopy. Even though the fly is glued in place, the animal can still flap her wings in tethered flight or walk on an air-cushioned ball, which acts like a spherical treadmill beneath her legs. These technical achievements attracted the attention of the Drosophila neurobiology community, but should anyone really care about seeing a fly brain in action beyond this small, venerable, group of arthropod-loving nerds (of which I'm honored to be a member)? In other words, will these methods help to reveal anything of general relevance beyond flies? Increasingly, the answer looks to be yes. © 2019 Scientific American

Keyword: Learning & Memory
Link ID: 26871 - Posted: 12.04.2019

There are three treatment options commonly used by doctors in the emergency room to treat patients with refractory status epilepticus, severe seizures that continue even after benzodiazepine medications, which are effective in controlling seizures in more than two-thirds of patients. New findings published in the New England Journal of Medicine reveal that the three drugs, levetiracetam, fosphenytoin, and valproate, are equally safe and effective in treating patients with this condition. The study was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “Doctors can be confident that the particular treatment they choose for their patients with status epilepticus is safe and effective and may help them avoid the need to intubate the patient as well as stays in the intensive care unit,” said Robin Conwit, M.D., NINDS program director and an author of the study. “This was a truly collaborative, multidisciplinary study that involved pediatricians, emergency medicine doctors, neurologists, pharmacologists, and biostatisticians all contributing their expertise.” In the Established Status Epilepticus Treatment Trial (ESETT), led by Robert Silbergleit, M.D., professor at the University of Michigan, Ann Arbor; Jordan Elm, Ph.D., professor at Medical University of South Carolina; James Chamberlain, M.D., professor at George Washington University; and Jaideep Kapur, M.B., B.S., Ph.D., professor at the University of Virginia, more than 380 children and adults were randomized to receive levetiracetam, fosphenytoin, or valproate when they came to the emergency room experiencing a seizure. The researchers were trying to determine which of the anticonvulsant drugs was most effective in stopping seizures and improving a patient’s level of responsiveness within 60 minutes of administering treatment.

Keyword: Epilepsy
Link ID: 26870 - Posted: 12.04.2019

By David Brooks This has been a golden age for brain research. We now have amazing brain scans that show which networks in the brain ramp up during different activities. But this emphasis on the brain has subtly fed the illusion that thinking happens only from the neck up. It’s fed the illusion that the advanced parts of our thinking are the “rational” parts up top that try to control the more “primitive” parts down below. So it’s interesting how many scientists are now focusing on the thinking that happens not in your brain but in your gut. You have neurons spread through your innards, and there’s increasing attention on the vagus nerve, which emerges from the brain stem and wanders across the heart, lungs, kidney and gut. The vagus nerve is one of the pathways through which the body and brain talk to each other in an unconscious conversation. Much of this conversation is about how we are relating to others. Human thinking is not primarily about individual calculation, but about social engagement and cooperation. One of the leaders in this field is Stephen W. Porges of Indiana University. When you enter a new situation, Porges argues, your body reacts. Your heart rate may go up. Your blood pressure may change. Signals go up to the brain, which records the “autonomic state” you are in. Maybe you walk into a social situation that feels welcoming. Green light. Your brain and body get prepared for a friendly conversation. But maybe the person in front of you feels threatening. Yellow light. You go into fight-or-flight mode. Your body instantly changes. Your ear, for example, adjusts to hear high and low frequencies — a scream or a growl — rather than midrange frequencies, human speech. Or maybe the threat feels like a matter of life and death. Red light. Your brain and body begin to shut down. According to Porges’s “Polyvagal Theory,” the concept of safety is fundamental to our mental state. People who have experienced trauma have bodies that are highly reactive to perceived threat. They don’t like public places with loud noises. They live in fight-or-flight mode, stressed and anxious. Or, if they feel trapped and constrained, they go numb. Their voice and tone go flat. Physical reactions shape our way of seeing and being. © 2019 The New York Times Company

Keyword: Emotions
Link ID: 26869 - Posted: 12.04.2019

Shawna Williams In September of this year, pharmaceutical companies Biogen and Eisai announced that they were halting Phase 3 clinical trials of a drug, elenbecestat, aimed at thwarting amyloid-β buildup in Alzheimer’s disease. Although the drug had seemed so promising that the companies elected to test it in two Phase 3 trials simultaneously, preliminary analyses determined that elenbecestat’s risks outweighed its benefits, and the drug shouldn’t be moved to market. The cancellation “amounts to a further step in the unwinding of Biogen’s expensive, painful, and ultimately fruitless investment in Alzheimer’s disease (AD) drug development,” analyst Geoffrey Porges told Reuters at the time. Biogen’s misfortune is just the latest in a slew of late-stage Alzheimer’s drug failures. Six months earlier, the company had halted another set of parallel Phase 3 trials due to lack of efficacy of a different drug candidate, aducanumab (though after further data analysis, Biogen announced that it will seek approval for aducanumab after all). And between 2013 and 2018, Pfizer, Eli Lilly, Merck, and Johnson & Johnson all terminated Phase 3 or Phase 2/3 trials due to poor early results. Yet some Alzheimer’s researchers say they think they’ve spotted a silver lining in this cloud of bad news—a hint in the data from these studies about how future work might meet with more success. In some of these trials, Alzheimer’s patients who were at earlier stages of the disease did better than those with more advanced cognitive decline, says Colin Masters, a neuroscientist at Florey Institute of Neuroscience and Mental Health in Australia who was not involved in the trials. This indicates that the key to finding an effective treatment might be to catch subjects before their condition advances too far, he adds. © 1986–2019 The Scientist

Keyword: Alzheimers
Link ID: 26868 - Posted: 12.04.2019

By Claudia Wallis For more than 25 years one idea has dominated scientific thinking about Alzheimer's disease: the amyloid cascade hypothesis. It holds that the disorder, which afflicts about one in 10 Americans age 65 or older, is caused by a buildup in the brain of abnormal amyloid-beta protein, which eventually destroys neurons and synapses, producing the tragic symptoms of dementia. There's plenty of evidence for this. First, the presence of sticky clumps or “plaques” containing amyloid is a classic hallmark of the disease (along with tangles of a protein called tau). It was what Alois Alzheimer saw in the autopsied brain of patient zero in 1906. Second, families with inherited defects in amyloid precursor protein (APP) or in genes encoding proteins that process APP are plagued by early-onset Alzheimer's. Third, mice genetically engineered to churn out excess amyloid tend to develop memory problems and do better when the amyloid pileup is stopped. This evidence and more has led grant makers and drug companies to pour billions of dollars into amyloid-targeting therapies. More than a dozen have been tested, and one by one they have flopped. One of the biggest heartbreaks came last March, when a promising antibody to amyloid, called aducanumab, performed no better than placebo in patients with very early Alzheimer's. Meanwhile researchers pursuing nonamyloid approaches were often left out in the cold, struggling to get grants and to have their work published. Science journalist Sharon Begley spent more than a year reporting on the lost opportunities in an article for the Web site Stat entitled “The Maddening Saga of How an Alzheimer's ‘Cabal’ Thwarted Progress toward a Cure for Decades.” Begley notes that the amyloid crowd was “neither organized nor nefarious,” but its outsized influence stifled other avenues of investigation. © 2019 Scientific American

Keyword: Alzheimers
Link ID: 26867 - Posted: 12.04.2019

By Virginia Morell Say “sit!” to your dog, and—if he’s a good boy—he’ll likely plant his rump on the floor. But would he respond correctly if the word were spoken by a stranger, or someone with a thick accent? A new study shows he will, suggesting dogs perceive spoken words in a sophisticated way long thought unique to humans. “It’s a very solid and interesting finding,” says Tecumseh Fitch, an expert on vertebrate communication at the University of Vienna who was not involved in the research. The way we pronounce words changes depending on our sex, age, and even social rank. Some as-yet-unknown neural mechanism enables us to filter out differences in accent and pronunciation, helping us understand spoken words regardless of the speaker. Animals like zebra finches, chinchillas, and macaques can be trained to do this, but until now only humans were shown to do this spontaneously. In the new study, Holly Root-Gutteridge, a cognitive biologist at the University of Sussex in Brighton, U.K., and her colleagues ran a test that others have used to show dogs can recognize other dogs from their barks. The researchers filmed 42 dogs of different breeds as they sat with their owners near an audio speaker that played six monosyllabic, noncommand words with similar sounds, such as “had,” “hid,” and “who’d.” The words were spoken—not by the dog’s owner—but by several strangers, men and women of different ages and with different accents. © 2019 American Association for the Advancement of Science.

Keyword: Language; Evolution
Link ID: 26866 - Posted: 12.04.2019

By Austin Frakt Some days I’m grumpy; other times, my head hurts or my feet or my arms do. Yet when I play the trumpet, my mood improves and the pain disappears. Why? Alternative medicine — including music therapy — is full of pain-relief claims. Although some are simply too good to be true, the oddities of pain can explain why others hold up, as well as why my trumpet playing helps. One thing we tend to believe about pain, but is wrong, is that it always stems from a single, fixable source. Another is that pain is communicated from that source to our brains by “pain nerves.” That’s so wrong it’s called “the naïve view” by neuroscientists. In truth, pain is in our brain. Or as the author and University of California, San Diego, neuroscientist V. S. Ramachandran put it, “Pain is an opinion.” We feel it because of how our brain interprets input transmitted to it from all our senses, not necessarily because of the inherent properties of the input itself. There are no nerves dedicated to sensing and transmitting pain. Anyone who has willed themselves to not feel a tickle as ticklish can appreciate the difference between stimulation and our perception of it. Pain can be experienced and relieved in phantom limbs. Discomfort and swelling increase when people believe a painful hand or knee is larger. They decrease when it seems smaller, for example in a distorted image or based on virtual reality technology. Injections are less painful when we don’t watch them. Using our brains, we can exert some control over it. © 2019 The New York Times Company

Keyword: Pain & Touch; Emotions
Link ID: 26865 - Posted: 12.02.2019

By Laura Sanders “Does the pill cause depression?” the news headline asked. Prompted by a recent study that described a link between taking birth control pills as a teenager and depression in adulthood, the news got some doctors hopping mad. Early research hints that there are reasons to look more closely at hormonal birth control’s side effects. But so far, the link is less than certain. “This is a premature connection,” says pediatrician Cora Breuner of Seattle Children’s Hospital. Putting too much stock in preliminary evidence may lead to fewer teenagers getting birth control and, in turn, more unwanted pregnancies among teens — a situation that can upend young lives, Breuner says. Headlines that frighten teens, their families and doctors are “yet another barrier in place for accessing a completely effective way to prevent unplanned pregnancies.” Ob-gyn and contraception researcher Katharine O’Connell White agrees. “Birth control gets all of the worry and concern,” says White, of Boston University School of Medicine. “But we know that other things are much more dangerous.” Teen pregnancy, for instance. Access to effective birth control is vital for sexually active teenagers, the doctors say. “I don’t think the evidence is there right now to say that this is a threat,” adds epidemiologist and public health researcher Sarah McKetta of Columbia University, who has studied birth control use in teens. Still, she sees value in more research on the issue. “Women deserve good medication … that’s not giving them problems.” If there are risks that come with the pill, then scientists ought to get a handle on them. © Society for Science & the Public 2000–2019

Keyword: Depression; Hormones & Behavior
Link ID: 26864 - Posted: 12.02.2019

Davide Castelvecchi The group of nerve agents known as Novichoks are to be added to the Chemical Weapons Convention’s list of controlled substances, in one of the first major changes to the treaty since it was agreed in the 1990s. The compounds, developed by the Soviet Union during the cold war, came to prominence after they were used in a high-profile assassination attempt on a former Russian military officer, Sergei Skripal, in Salisbury, UK, in March last year. The Organisation for the Prohibition of Chemical Weapons (OPCW), which is tasked with enforcing the treaty, announced the decision to explicitly ban Novichoks on 27 November as representatives from the 193 member states met in The Hague this week for a periodic review of the convention. The member states agreed unanimously to classify Novichoks as chemical weapons, the OPCW said. The update to the treaty, which will come into effect in 180 days, was initially proposed by the United States, Canada and the Netherlands. “There is a recognition that we all win with this agreement,” says Alastair Hay, an environmental toxicologist at the University of Leeds, UK, who was at the meeting. “The decision means that OPCW can now keep tabs on these chemicals.” The OPCW has the power to send inspectors to any signatory country to search for evidence of production of banned chemicals. It also can send experts to help countries to investigate crime scenes where chemical agents may have been used. © 2019 Springer Nature Limited

Keyword: Neurotoxins
Link ID: 26863 - Posted: 12.02.2019

By Anna Schaverien and Allison McCann LONDON — Homeless drug users in Scotland will be allowed to inject pharmaceutical-grade heroin twice a day under the supervision of medical officials as part of a new program intended to reduce drug deaths and H.I.V. infection. From 9 a.m. to 5 p.m. seven days a week, a $1.5 million facility in Glasgow that opened on Tuesday will allow a handful of drug users to receive doses of the drug alongside other treatment for their physical and psychological health, according to Glasgow City Council. The pilot project, known as heroin-assisted treatment, is the first such licensed operation in Scotland, a country that has been called the “drug death capital of the world.” It has struggled to cope with high rates of fatal drug overdoses and its worst H.I.V. outbreak in decades. The program will target those with the “most severe, longstanding and complex addiction issues,” the City Council said. It aims to reduce the risk of overdoses and the spread of viruses such as H.I.V. by prescribing diamorphine — the clinical name for pharmaceutical-grade heroin — for patients to inject in a secure clinical room under the supervision of trained medics. The clinic opened in Glasgow, Scotland’s largest city, after Britain’s Home Office granted it a license, and follows a similar initiative that began in Middlesbrough, England, last month. © 2019 The New York Times Company

Keyword: Drug Abuse
Link ID: 26862 - Posted: 12.02.2019

Nicola Davis Dolphins, like humans, have a dominant right-hand side, according to research. About 90% of humans are right-handed but we are not the only animals that show such preferences: gorillas tend to be right-handed, kangaroos are generally southpaws, and even cats have preferences for a particular side – although which is favoured appears to depend on their sex. Now researchers have found common bottlenose dolphins appear to have an even stronger right-side bias than humans. “I didn’t expect to find it in that particular behaviour, and I didn’t expect to find such a strong example,” said Dr Daisy Kaplan, co-author of the study from the Dolphin Communication Project, a non-profit organisation in the US. Researchers studying common bottlenose dolphins in the Bahamas say the preference shows up in crater feeding, whereby dolphins swim close to the ocean floor, echolocating for prey, before shoving their beaks into the sand to snaffle a meal. Writing in the journal Royal Society Open Science, Kaplan and colleagues say the animals make a sharp and sudden turn before digging in with their beaks. Crucially, however, they found this turn is almost always to the left, with the same direction taken in more than 99% of the 709 turns recorded between 2012 and 2018. The researchers say the findings indicate a right-side bias, since a left turn keeps a dolphin’s right eye and right side close to the ocean floor. The team found only four turns were made to the right and all of these were made by the same dolphin, which had an oddly shaped right pectoral fin. However the Kaplan said it was unlikely this fin was behind the right turns: two other dolphins had an abnormal or missing right fin yet still turned left.

Keyword: Laterality; Evolution
Link ID: 26861 - Posted: 12.02.2019

By Denise Grady A lifelong swimmer leapt into deep water near his lakeside home, and was horrified to find himself completely unable to swim. Had his wife not rescued him, he might have drowned. He had recently received an electronic brain implant to control tremors and other symptoms of Parkinson’s disease, and somehow the signals from the device had knocked out his ability to coordinate his arms and legs for swimming. He was one of nine patients, all good swimmers despite having Parkinson’s, who had the same strange, dangerous side effect from deep brain stimulators. Three of them tried turning off the stimulators, and immediately could swim again, according to an article in the journal Neurology by a medical team from the University of Zurich. At first, doctors thought the case of the man in the lake was an isolated event, Dr. Christian R. Baumann, an author of the paper, said in an interview. But when the same thing happened to another patient, one who had been a competitive swimmer, Dr. Baumann and his colleagues began to ask other patients about swimming. They found seven more cases among about 250 patients. About 150,000 people worldwide have brain implants made by Medtronic, the leading manufacturer, the company said. Most had the implants for relief of Parkinson’s symptoms. The swimming problem is not that common Dr. Baumann said, adding: “I think it’s a minority of patients. We find many who are still wonderfully able to swim and we don’t know why. We have no clue. They are treated in the same region of the brain. But this is life-threatening, and we need to pay more attention in the future.” Now, Dr. Baumann warns all patients with stimulators never to go into deep water alone. © 2019 The New York Times Company

Keyword: Parkinsons
Link ID: 26860 - Posted: 11.29.2019