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By Linda Searing The precise cause, or causes, of dementias such as Alzheimer’s disease remain unclear, but one theory points to molecules called free radicals that can damage nerve cells. This damage, called oxidative stress, may lead to changes in the brain over time that result in dementia. Might antioxidant supplements prevent this? The study involved 7,540 men 60 and older (average age, 67) with no indications of dementia and no history of serious head injury, substance abuse or neurological conditions that affect cognition. They were randomly assigned to take vitamin E (an antioxidant, 400 International Units daily), selenium (also an antioxidant, 200 micrograms daily), both vitamin E and selenium or a placebo. The men also had their memory assessed periodically. In just over five years, 325 of the men (about 4 percent) developed dementia, with essentially no difference in the rate of occurrence between those who took one or both supplements and those who took the placebo. The researchers concluded that the antioxidant supplements “did not forestall dementia and are not recommended as preventive agents.” Who may be affected? Older men. The risk for dementia increases with advanced age and is most common among the very elderly. Memory loss is the most well-known symptom, but people with dementia may also have problems thinking, speaking, controlling emotions and doing daily activities such as getting dressed and eating. Alzheimer’s disease is the most common type of dementia, affecting more than 5.5 million Americans, including more than 10 percent of those 65 and older and more women than men. Caveats Participants took the supplements for a relatively short time. Whether the findings would apply to women was not tested. The study did not prove that the dementia developed by the study participants was caused by oxidative stress. © 1996-2017 The Washington Post
Link ID: 23403 - Posted: 03.25.2017
By Anil Ananthaswamy People who have chronic pain are more likely to experience mood disorders, but it’s not clear how this happens. Now a study in mice has found that chronic pain can induce genetic changes in brain regions that are linked to depression and anxiety, a finding that may lead to new treatments for pain. “At least 40 per cent of patients who suffer from severe forms of chronic pain also develop depression at some point, along with other cognitive problems,” says Venetia Zachariou of the Icahn School of Medicine at Mount Sinai in New York. To see if there might be a genetic link between these conditions, Zachariou and her team studied mice with damage to their peripheral nervous system. These mice show symptoms similar to chronic pain in people – they become hypersensitive to harmless touch, and avoid other situations that might also cause them pain. Until now, pain behaviour in mice had only been studied for at most a week at a time, says Zachariou, whose team monitored their mice for 10 weeks. “At the beginning, we saw only sensory deficits and pain-like symptoms. But several weeks later, the animals developed anxiety and depression-like behaviours.” The team then examined gene activity in three regions in the mouse brains we know are associated with depression and anxiety. Analysing the nucleus accumbens, medial prefrontal cortex, and periaqueductal gray, they found nearly 40 genes where activity was significantly higher or lower than in mice without the nervous system damage. © Copyright Reed Business Information Ltd.
By Jason G. Goldman In the summer of 2015 University of Oxford zoologists Antone Martinho III and Alex Kacelnik began quite the cute experiment—one involving ducklings and blindfolds. They wanted to see how the baby birds imprinted on their mothers depending on which eye was available. Why? Because birds lack a part of the brain humans take for granted. Suspended between the left and right hemispheres of our brains sits the corpus callosum, a thick bundle of nerves. It acts as an information bridge, allowing the left and right sides to rapidly communicate and act as a coherent whole. Although the hemispheres of a bird's brain are not entirely separated, the animals do not enjoy the benefits of this pathway. This quirk of avian neuroanatomy sets up a natural experiment. “I was in St. James's Park in London, and I saw some ducklings with their parents in the lake,” Martinho says. “It occurred to me that we could look at the instantaneous transfer of information through imprinting.” The researchers covered one eye of each of 64 ducklings and then presented a fake red or blue adult duck. This colored duck became “Mom,” and the ducklings followed it around. But when some of the ducklings' blindfolds were swapped so they could see out of only the other eye, they did not seem to recognize their “parent” anymore. Instead the ducklings in this situation showed equal affinity for both the red and blue ducks. It took three hours before any preferences began to emerge. Meanwhile ducklings with eyes that were each imprinted to a different duck did not show any parental preferences when allowed to use both eyes at once. The study was recently published in the journal Animal Behaviour. © 2017 Scientific American
If your parrot is feeling glum, it might be tweetable. Wild keas spontaneously burst into playful behaviour when exposed to the parrot equivalent of canned laughter – the first birds known to respond to laughter-like sounds. The parrots soared after one another in aerobatic loops, exchanged foot-kicking high fives in mid-air and tossed objects to each other, in what seems to be emotionally contagious behaviour. And when the recording stops, so does the party, and the birds go back to whatever they had been doing. We already knew that these half-metre-tall parrots engage in playful behaviour, especially when young. What’s new is that a special warbling call they make has been shown to trigger behaviour that seems to be an equivalent of spontaneous, contagious laughter in humans. Moreover, it’s not just the young ones that respond, adults of both sexes join in the fun too. Raoul Schwing of the University of Veterinary Medicine in Vienna, Austria, and his team played 5-minute recordings to gatherings of between two and a dozen wild keas on a mountainside of New Zealand’s Arthur’s Pass National Park, on the southern island. The group played recordings of the warble sound, or other sounds, including two other frequent kea sounds – a screech and a whistle – plus the alarm call of a local robin species and a bland tone. © Copyright Reed Business Information Lt
By DENISE GRADY Dr. Lewis P. Rowland, a neurologist who made fundamental discoveries in nerve and muscle diseases and clashed with government investigators during the McCarthy era, died on March 16 in Manhattan. He was 91. The cause was a stroke, his son Steven said. Dr. Rowland, the chairman of Columbia University’s neurology department for 25 years, died at NewYork-Presbyterian/Columbia University Medical Center. Dr. Rowland was a prolific researcher and writer, with nearly 500 published scientific articles that focused on devastating neuromuscular diseases, including muscular dystrophy, myasthenia gravis and many rare syndromes. He took a special interest in amyotrophic lateral sclerosis, or A.L.S., also called Lou Gehrig’s disease, which causes degeneration of nerves in the brain and spinal cord, leading to weakness, paralysis and death. Dr. Rowland led research teams that delineated a number of uncommon diseases that had been poorly understood. They also found that in a subgroup of A.L.S. patients, the disease was linked to lymphoma, a cancer of the immune system. Other studies led to the discovery that a gene defect causes an unusual form of dementia in some patients with A.L.S. In myasthenia gravis, Dr. Rowland and his colleagues documented its high death rate and helped identify treatments that prolonged survival. In the 1970s, long before the tools existed to study DNA’s role in neurological diseases like A.L.S., Alzheimer’s and Parkinson’s, Dr. Rowland predicted correctly that genetics would be the key to understanding them. One of his accomplishments at Columbia was the expansion in 1982 of an intensive care unit that added beds for patients who were severely ill with neurological disorders. Before then, it was often difficult to find I.C.U. space for them. © 2017 The New York Times Company
by Laura Sanders Many babies born early spend extra time in the hospital, receiving the care of dedicated teams of doctors and nurses. For these babies, the hospital is their first home. And early experiences there, from lights to sounds to touches, may influence how babies develop. Touches early in life in the NICU, both pleasant and not, may shape how a baby’s brain responds to gentle touches later, a new study suggests. The results, published online March 16 in Current Biology, draw attention to the importance of touch, both in type and number. Young babies can’t see that well. But the sense of touch develops early, making it a prime way to get messages to fuzzy-eyed, pre-verbal babies. “We focused on touch because it really is some of the basis for communication between parents and child,” says study coauthor Nathalie Maitre, a neonatologist and neuroscientist at Nationwide Children’s Hospital in Columbus, Ohio. Maitre and her colleagues studied how babies’ brains responded to a light puff of air on the palms of their hands — a “very gentle and very weak touch,” she says. They measured these responses by putting adorable, tiny electroencephalogram, or EEG, caps on the babies. The researchers puffed babies’ hands shortly before they were sent home. Sixty-one of the babies were born early, from 24 to 36 weeks gestation. At the time of the puff experiment, they had already spent a median of 28 days in the hospital. Another group of 55 babies, born full-term, was tested in the three days after birth. |© Society for Science & the Public 2000 - 2017
/ By Katie Rose Quandt One afternoon in 2013, after swimming and playing outside, 9-year-old Taylor Johnson, from outside Atlanta, began sneezing incessantly. The fit lasted days before stopping abruptly, only to return months later. For a year, her violent sneezing fits came and went, to the bewilderment of a series of doctors. For families, the diagnosis can seem like an answer to their prayers. But there’s a catch: Most doctors won’t treat the diseases — and many don’t believe they even exist. “She was making this noise with her mouth at times 140 to 150 times a minute,” said her mother, Lori Johnson. “She was frantic, she couldn’t eat, she couldn’t sleep.” And “when she wasn’t sneezing, she was very depressed… She lost all interest in anything. Her whole personality just dissolved into nothing.” Then an otolaryngologist (an ear, nose, and throat doctor) realized Taylor wasn’t sneezing at all — the behavior was a repetitive, sneeze-like tic. That prompted a round of visits to neurologists, psychologists, and other specialists, until an allergist finally suggested a set of diagnoses unfamiliar to the Johnsons: PANS and PANDAS. These disorders, a specialist told them, can arise in certain predisposed children when the immune system responds to an infection like strep throat by attacking the brain. The resulting inflammation can lead to violent body tics and OCD-like symptoms. Copyright 2017 Undark
A study in Neurology suggests that analyzing levels of the protein p75ECD in urine samples from people with amyotrophic lateral sclerosis (ALS) may help monitor disease progression as well as determine the effectiveness of therapies. The study was supported by National Institute of Neurological Disorders and Stroke (NINDS) and National Center for Advancing Translational Sciences (NCATS), both part of the National Institutes of Health. Mary-Louise Rogers, Ph.D., senior research fellow at Flinders University in Adelaide, Australia, and Michael Benatar, M.D., Ph.D, professor of neurology at the University of Miami, and their teams, discovered that levels of urinary p75 ECD increased gradually in patients with ALS as their disease progressed over a 2-year study period. “It was encouraging to see changes in p75ECD over the course of the study, because it suggests an objective new method for tracking the progression of this aggressive disease,” said Amelie Gubitz, Ph.D., program director at NINDS. “In addition, it indicates the possibility of assessing whether levels of that protein decrease while patients try future treatments, to tell us whether the therapies are having any beneficial effects.” Further analysis of the samples from 54 patients revealed that those who began the study with lower levels of urinary p75ECD survived longer than did patients who had higher levels of the protein initially, suggesting that it could be a prognostic marker of the disease and may inform patients about their illness. Dr. Benatar and his team noted that this may be useful in selecting participants for clinical trials and in improving study design.
Keyword: ALS-Lou Gehrig's Disease
Link ID: 23396 - Posted: 03.23.2017
By Jia Naqvi A drug frequently prescribed for pain is no more effective than a placebo at controlling sciatica, a common source of pain in the lower back and leg, according to a study published Wednesday in the New England Journal of Medicine. The researchers at the George Institute for Global Health in Australia followed 209 sciatica patients in Sydney who were randomly assigned to receive either the drug pregabalin, more commonly known as Lyrica, or a placebo. The results showed no significant differences in leg pain intensity between the group on the placebo and that on Lyrica after eight weeks taking the drug or during the rest of the year on follow-up exams. Similarly, there were no differences for other outcomes such as back pain, quality of life and degree of disability. After Lyrica was approved in 2004, it has become the most commonly prescribed medicine for neuropathic pain, which is caused by damage to the nervous system. The drug was ranked as the 19th-highest-earning pharmaceutical in 2015, with worldwide sales rising annually at a rate of 9 percent and sale revenue of more than $3 billion in 2015 in the United States. “We have seen a huge rise in the amount of prescriptions being written each year for patients suffering from sciatica. It’s an incredibly painful and disabling condition, so it’s no wonder people are desperate for relief and medicines such as pregabalin have been widely prescribed,” Christine Lin, one of the authors of the study and an associate professor at the George Institute for Global Health, said in a news release. © 1996-2017 The Washington Post
Keyword: Pain & Touch
Link ID: 23395 - Posted: 03.23.2017
By Sam Wong It takes brains to choose a good partner. In one of the first experiments to look at the cognitive demands of choosing a mate, female guppies with big brains showed a preference for more colourful males, while those with smaller brains showed no preference. In guppies, like most animals, females are choosy about who to mate with, since they invest more in their offspring than males, which don’t help care for them. They tend to prefer males with striking colour patterns and big tails, traits that have been linked to good foraging ability and health. By choosing a male with these qualities, female guppies give their offspring a good chance of inheriting the same useful traits. Despite this, females often go on to make different choices. Alberto Corral López and colleagues at Stockholm University wanted to find out if brain size could account for this. Corral López and his team tested 36 females bred to have large brains, 36 bred to have small brains, and 16 females similar to guppies found in the wild. Previous studies have shown that large-brained guppies perform better in cognitive tests, suggesting that they are smarter. Each female was given the opportunity to associate with two males, one more colourful than the other. Females are known to spend more time close to males they would prefer to mate with, so the team timed how long they spent with each male. © Copyright Reed Business Information Ltd
By Daisy Yuhas, Spectrum on March 22, 2017 In children with a deletion on chromosome 22, having autism does not boost the risk of developing schizophrenia later in life, according to a new study1. The children in the study have 22q11.2 deletion syndrome, which is linked to a 25-fold increase in the risk of developing a psychotic condition such as schizophrenia. A deletion in the region is also associated with an increased risk of autism. Some researchers have suggested that the relatively high autism prevalence in this population is the result of misdiagnoses of early signs of schizophrenia. The new findings, published 21 January in Schizophrenia Research, support an alternate theory: Autism and schizophrenia are independent outcomes of the same genetic syndrome. If there is a relationship between the two conditions, “that can only be a very small, probably negligible effect,” says lead investigator Jacob Vorstman, assistant professor of child psychiatry and genetics at the University Medical Center Utrecht in the Netherlands. The new findings could help guide clinical care, says Opal Ousley, assistant professor of psychiatry at the Emory Autism Center in Atlanta. If prenatal testing picks up the 22q11.2 deletion, for instance, clinicians could discuss the risk of both autism and schizophrenia with parents. © 2017 Scientific American
By David Wiegand I just did something great for my brain and you can do the same, when the documentary “My Love Affair With the Brain: The Life and Science of Dr. Marian Diamond” airs on KQED on Wednesday, March 22. According to the UC Berkeley professor emerita, the five things that contribute to the continued development of the brain at any age are: diet, exercise, newness, challenge and love. You can check off three of those elements for the day by watching the film by Catherine Ryan and Gary Weimberg. No matter how smart you are, even about anatomy and neuroscience, you will find newness in the information about the miraculous human brain, how it works, and how it keeps on working no matter how old you are. That’s one of the fundamentals of modern neuroscience, of which Diamond is one of the founders. You will also be challenged to consider your own brain, to consider how Diamond’s favorite expression — “use it or lose it” — applies to your brain and your life. You will be challenged to consider what Diamond means when she says brain plasticity (its ability to keep developing by forming new connections between its cells) makes us “the masters of our own minds. We literally create our own masterpiece.” Before Diamond and her colleagues proved otherwise, the prevailing thought was that brains developed according to a genetically determined pattern, hit a high point and then essentially began to deteriorate. Bushwa: A brain can grow — i.e., learn — at any age, and you can teach an old dog new tricks. © 2017 Hearst Corporation
Keyword: Learning & Memory
Link ID: 23392 - Posted: 03.23.2017
By Mo Costandi This map of London shows how many other streets are connected to each street, with blue representing simple streets with few connecting streets and red representing complex streets with many connecting streets. Credit: Joao Pinelo Silva The brain contains a built-in GPS that relies on memories of past navigation experiences to simulate future ones. But how does it represent new environments in order to determine how to navigate them successfully? And what happens in the brain when we enter a new space, or use satellite navigation (SatNav) technology to help us find our way around? Research published Tuesday in Nature Communications reveals two distinct brain regions that cooperate to simulate the topology of one’s environment and plan future paths through it when one is actively navigating. In addition, the research suggests both regions become inactive when people follow SatNav instructions instead of using their spatial memories. In a previous study researchers at University College London took participants on a guided tour through the streets of London’s Soho district and then used functional magnetic resonance imaging (fMRI) to scan their brains as they watched 10 different simulations of navigating those streets. Some of the movies required them to decide at intersections which way would be the shortest path to a predetermined destination; others came with instructions about which way to go at each junction. © 2017 Scientific American,
Keyword: Learning & Memory
Link ID: 23391 - Posted: 03.22.2017
Hannah Devlin Scientists have developed a new genetic test for Alzheimer’s risk that can be used to predict the age at which a person will develop the disease. A high score on the test, which is based on 31 genetic markers, can translate to being diagnosed many years earlier than those with a low-risk genetic profile, the study found. Those ranked in the top 10% in terms of risk were more than three times as likely to develop Alzheimer’s during the course of the study, and did so more than a decade before those who ranked in the lowest 10%. Strobe lighting provides a flicker of hope in the fight against Alzheimer’s Read more Rahul Desikan, of the University of California – who led the international effort, said the test could be used to calculate any individual’s risk of developing Alzheimer’s that year. “That is, if you don’t already have dementia, what is your yearly risk for AD onset, based on your age and genetic information,” he said. The so-called polygenic hazard score test was developed using genetic data from more than 70,000 individuals, including patients with Alzheimer’s disease and healthy elderly people. It is already known that genetics plays a powerful role in Alzheimer’s. Around a quarter of patients have a strong family history of the disease, and scientists have shown this is partly explained by a gene called ApoE, which comes in three versions, and is known to have a powerful influence on the risk of getting the most common late-onset type of Alzheimer’s. One version of ApoE appears to reduce risk by up to 40%, while those with two copies (one from each parent) of the high-risk version can increase risk by 12 times.
Link ID: 23390 - Posted: 03.22.2017
By KIM SEVERSON SONOMA, Calif. — The first thing Paula Wolfert wants to make a guest is coffee blended with butter from grass-fed cows and something called brain octane oil. She waves a greasy plastic bottle of the oil around her jumble of a kitchen like a preacher who has taken up a serpent. Never mind that this is the woman who introduced tagines, Aleppo pepper and cassoulet to American kitchens, wrote nine cookbooks and once possessed a palate the food writer Ruth Reichl declared the best she’d ever encountered. Ms. Wolfert, 78, has dementia. She can’t cook much, even if she wanted to. Which, by the way, she doesn’t. She learned she probably had Alzheimer’s disease in 2013, but she suspected something wasn’t right long before. Words on a page sometimes made no sense. Complex questions started to baffle her. Since she has always been an audacious and kinetic conversationalist with a touch of hypochondria, friends didn’t notice anything was wrong. Doctors spoke of “senior moments.” But she knew. One day, Ms. Wolfert went to make an omelet for her husband, the crime novelist William Bayer. She had to ask him how. The woman who once marched up to the French chef Jean-Louis Palladin and told him a dish didn’t have enough salt can no longer taste the difference between a walnut and a pecan, or smell whether the mushrooms are burning. The list of eight languages she once understood has been reduced to English. Maybe 40 percent of the words she knew have evaporated. “What am I going to do, cry about it?” Ms. Wolfert said in an interview at her home this month, the slap of her Brooklyn accent still sharp. After all, she points out, her first husband left her in Morocco with two small children and $2,000: “I cried for 20 minutes and I thought, ‘This isn’t going to do any good.’” © 2017 The New York Times Company
Link ID: 23389 - Posted: 03.22.2017
By NICHOLAS BAKALAR Some research has suggested that vitamin E and selenium supplements might lower the risk for Alzheimer’s disease, but a new long-term trial has found no evidence that they will. The study began as a randomized clinical trial in 2002 testing the supplements for the prevention of prostate cancer. When that study was stopped in 2009 because no effect was found, 3,786 of the original 7,540 men participated in a continuing study to test the antioxidants as a preventive for Alzheimer’s. The study, in JAMA Neurology, randomly assigned the men, whose average age was 67 at the start, to take either vitamin E, selenium, both supplements, or a placebo. By 2015, 4.4 percent of the men had dementia, but there was no difference between the groups. Neither selenium, vitamin E, nor both in combination were any more effective than a placebo. The study controlled for age, family history of Alzheimer’s disease, education, race, diabetes and other factors. The lead author, Richard J. Kryscio, a professor of statistics at the University of Kentucky, said that it is possible that different dosages or different types of selenium or vitamin E might show an effect. “We could have picked the wrong version or the wrong dose,” he said. “But there’s really no evidence that these supplements will make a difference down the road in preventing dementia.” © 2017 The New York Times Company
Link ID: 23388 - Posted: 03.22.2017
By Jill Serjeant NEW YORK (Reuters) - Long-running children's television show "Sesame Street" is welcoming a new kid to the block - a Muppet with autism called Julia. A redhead who loves to sing and remembers the words to lots of songs, Julia will debut on the show for preschoolers on April 10 after a five-year outreach effort to families and experts on autism, Sesame Workshop said on Monday. "For years, families of children with autism have asked us to address the issue," Dr. Jeanette Betancourt, senior vice president of U.S. social impact at the nonprofit Sesame Workshop, said in a statement. One in 68 American children is currently diagnosed with autism, according to the Centers for Disease Control and Prevention, an increase of some 119 percent since 2000. Autism is a developmental disorder present from early childhood, characterized by difficulty in communicating and forming relationships with other people and in using language and abstract concepts Stacey Gordon, the puppeteer who will perform the role of Julia, and Christine Ferraro who wrote her part, both have family members who are on the autism spectrum. "It's important for kids without autism to see what autism can look like," Gordon told the CBS show "60 Minutes" in a preview on Sunday. "Had my son's friends been exposed to his behaviors through something that they had seen on TV before they experienced them in the classroom, they might not have been frightened. They might not have been worried when he cried. They would have known that he plays in a different way and that that's okay," she added. © 2017 Scientific American
Link ID: 23387 - Posted: 03.22.2017
by Helen Thompson Aside from being adorable, sea otters and Indo-Pacific bottlenose dolphins share an ecological feat: Both species use tools. Otters crack open snails with rocks, and dolphins carry cone-shaped sponges to protect their snouts while scavenging for rock dwelling fish. Researchers have linked tool use in dolphins to a set of differences in mitochondrial DNA — which passes from mother to offspring — suggesting that tool-use behavior may be inherited. Biologist Katherine Ralls of the Smithsonian Institution in Washington, D.C., and her colleagues looked for a similar pattern in otters off the California coast. The team tracked diet (primarily abalone, crab, mussels, clams, urchins or snails) and tool use in the wild and analyzed DNA from 197 individual otters. Otters that ate lots of hard-shelled snails — and used tools most frequently — rarely shared a common pattern in mitochondrial DNA, nor were they more closely related to other tool-users than any other otter in the population. Unlike dolphins, sea otters may all be predisposed to using tools because their ancestors probably lived off mollusks, which required cracking open. However, modern otters only take up tools when their diet requires them, the researchers report March 21 in Biology Letters. |© Society for Science & the Public 2000 - 2017.
Link ID: 23386 - Posted: 03.22.2017
Laura Sanders Not too long ago, the internet was stationary. Most often, we’d browse the Web from a desktop computer in our living room or office. If we were feeling really adventurous, maybe we’d cart our laptop to a coffee shop. Looking back, those days seem quaint. Today, the internet moves through our lives with us. We hunt Pokémon as we shuffle down the sidewalk. We text at red lights. We tweet from the bathroom. We sleep with a smartphone within arm’s reach, using the device as both lullaby and alarm clock. Sometimes we put our phones down while we eat, but usually faceup, just in case something important happens. Our iPhones, Androids and other smartphones have led us to effortlessly adjust our behavior. Portable technology has overhauled our driving habits, our dating styles and even our posture. Despite the occasional headlines claiming that digital technology is rotting our brains, not to mention what it’s doing to our children, we’ve welcomed this alluring life partner with open arms and swiping thumbs. Scientists suspect that these near-constant interactions with digital technology influence our brains. Small studies are turning up hints that our devices may change how we remember, how we navigate and how we create happiness — or not. Somewhat limited, occasionally contradictory findings illustrate how science has struggled to pin down this slippery, fast-moving phenomenon. Laboratory studies hint that technology, and its constant interruptions, may change our thinking strategies. Like our husbands and wives, our devices have become “memory partners,” allowing us to dump information there and forget about it — an off-loading that comes with benefits and drawbacks. Navigational strategies may be shifting in the GPS era, a change that might be reflected in how the brain maps its place in the world. Constant interactions with technology may even raise anxiety in certain settings. |© Society for Science & the Public 2000 - 2017
Ian Sample Science editor Doctors have stumbled on an unlikely source for a drug to ward off brain damage caused by strokes: the venom of one of the deadliest spiders in the world. A bite from an Australian funnel web spider can kill a human in 15 minutes, but a harmless ingredient found in the venom can protect brain cells from being destroyed by a stroke, even when given hours after the event, scientists say. If the compound fares well in human trials, it could become the first drug that doctors have to protect against the devastating loss of neurons that strokes can cause. Researchers discovered the protective molecule by chance as they sequenced the DNA of toxins in the venom of the Darling Downs funnel web spider (Hadronyche infensa) that lives in Queensland and New South Wales. Venom from three spiders was gathered for the study after scientists trapped and “milked exhaustively” three spiders on Orchid beach, about 400km north of Brisbane. The molecule, called Hi1a, stood out because it looked like two copies of another brain cell-protecting chemical stitched together. It was so intriguing that scientists decided to synthesise the compound and test its powers. “It proved to be even more potent,” said Glenn King at the University of Queensland’s centre for pain research. Strokes occur when blood flow to the brain is interrupted and the brain is starved of oxygen. About 85% of strokes are caused by blockages in blood vessels in the brain, with the rest due to bleeds when vessels rupture. Approximately six million people a year die from stroke, making it the second largest cause of death worldwide after heart attacks. © 2017 Guardian News and Media Limited