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By Emily Baumgaertner The brain-eating monsters are real enough — they lurk in freshwater ponds in much of the United States. Now scientists may have discovered a new way to kill them. Minuscule silver particles coated with anti-seizure drugs one day may be adapted to halt Naegleria fowleri, an exceptionally lethal microbe that invades through the sinuses and feeds on human brain tissue. The research, published in the journal Chemical Neuroscience, showed that repurposing seizure medicines and binding them to silver might kill the amoebae while sparing human cells. Scientists hope the findings will lay an early foundation for a quick cure. “Here is a nasty, often devastating infection that we don’t have great treatments for,” said Dr. Edward T. Ryan, the director of the global infectious diseases division of Massachusetts General Hospital, who was not involved in the research. “This work is clearly in the early stages, but it’s an interesting take.” Infections with brain-eating amoebae are rare but almost always deadly. Since 1962, only four of 143 known victims in the United States have survived, according to the Centers for Disease Control and Prevention. More than half of all cases have occurred in Texas and Florida, where the microscopic organisms thrive in warm pond water. “The classic case is a 10-year-old boy who goes swimming in the South in the summer and starts to get a headache a few days later,” Dr. Ryan said. The amoebae’s feeding causes meningoencephalitis — or swelling of the brain and nearby tissues — and is often misdiagnosed. “When it comes to treatment, doctors often end up throwing in the kitchen sink,” he added. Patients typically are given antimicrobial drugs in extremely high doses in order to break through the body’s protective blood-brain barrier. Many suffer severe side effects. © 2019 The New York Times Company

Keyword: Miscellaneous
Link ID: 25867 - Posted: 01.15.2019

Marise Parent Of course you know that eating is vital to your survival, but have you ever thought about how your brain controls how much you eat, when you eat and what you eat? This is not a trivial question, because two-thirds of Americans are either overweight or obese and overeating is a major cause of this epidemic. To date, the scientific effort to understand how the brain controls eating has focused primarily on brain areas involved in hunger, fullness and pleasure. To be better armed in the fight against obesity, neuroscientists, including me, are starting to expand our investigation to other parts of the brain associated with different functions. My lab’s recent research focuses on one that’s been relatively overlooked: memory. For many people, decisions about whether to eat now, what to eat and how much to eat are often influenced by memories of what they ate recently. For instance, in addition to my scale and tight clothes, my memory of overeating pizza yesterday played a pivotal role in my decision to eat salad for lunch today. Memories of recently eaten foods can serve as a powerful mechanism for controlling eating behavior because they provide you with a record of your recent intake that likely outlasts most of the hormonal and brain signals generated by your meal. But surprisingly, the brain regions that allow memory to control future eating behavior are largely unknown. Studies done in people support the idea that meal-related memory can control future eating behavior. © 2010–2019, The Conversation US, Inc.

Keyword: Obesity; Learning & Memory
Link ID: 25866 - Posted: 01.15.2019

By Bryan Clark You slide the key into the door and hear a clunk as the tumblers engage. You rotate the key, twist the doorknob and walk inside. The house is familiar, but the contents foreign. At your left, there’s a map of Minnesota, dangling precariously from the wall. You’re certain it wasn’t there this morning. Below it, you find a plush M&M candy. To the right, a dog, a shiba inu you’ve never seen before. In its mouth, a pair of your expensive socks. And then it comes to you, 323-3607, a phone number. If none of this makes sense, stick with us; by the end of this piece you’ll be using the same techniques to memorize just about anything you’ve ever wanted to remember. The “memory athlete” Munkhshur Narmandakh once employed a similar combination of mnemonics to commit more than 6,000 binary digits to memory in just 30 minutes. Alex Mullen, a three-time World Memory Champion, used them to memorize the order of a deck of cards in just 15 seconds, a record at the time. It was later broken by Shijir-Erdene Bat-Enkh, who did it in 12. We’re going to aim lower, applying these strategies to real-world scenarios, like remembering the things we often forget at dinner parties or work-related mixers. At the start of this piece, we employed two mnemonic strategies to remember the seven digits of a phone number. The first, called the “Major System,” was developed in 1648 by historian Johann Winkelmann. In his book “Moonwalking With Einstein,” the author Joshua Foer described this system as a simple cipher that transforms numbers to letters or phonetic sounds. From there we can craft words and, ultimately, images. Some will, no doubt, be crude or enigmatic. Others may contain misspellings and factual errors. It doesn’t matter. This system is designed to create rich imagery, not accurate representations. © 2019 The New York Times Company

Keyword: Learning & Memory
Link ID: 25865 - Posted: 01.15.2019

Emily Chung · CBC News · Could the pain you feel in your body be all in your head? At least some of it might be — if you're a man (or a male mouse), a new study has found. Male humans and male mice — but not females of either species — both became hypersensitive to pain when put in an environment where they had previous had a painful experience, reports a new Canadian-led study published last week in the journal Current Biology. "The sex difference was completely unexpected," said Loren Martin, the University of Toronto Mississauga assistant professor of psychology who led the study. While there was no reason to believe males and females would respond differently, if they did, he would have expected females, not males, to develop pain hypersensitivity, since they're generally more sensitive to pain and more prone to chronic pain. Martin originally ran an experiment on mice while he was a postdoctoral researcher in the lab of McGill University professor Jeffrey Mogil, who holds two research chairs related to pain. They wanted to to see how the mice would react if brought back to a place where they had had a painful experience — a 30-minute tummy ache cause by dilute vinegar in their stomachs — and whether they could be conditioned to be hypersensitive to pain. The reason they were interested is because there is growing evidence that chronic pain is linked to biochemical "rewiring" in nerves similar to what happens with the formation of memories in the brain, and may itself be akin to or linked to memory, Martin said. If that's the case, chronic pain could potentially be treated by de-rewiring the nerves back to their normal state. ©2018 CBC/Radio-Canada

Keyword: Pain & Touch; Sexual Behavior
Link ID: 25864 - Posted: 01.15.2019

By Carolyn Y. Johnson For years, public health experts have been arguing that where people live matters crucially to their health and life span, even though factors such as genetics or access to health insurance typically get more attention. Health systems and governments have embarked on massive projects to decode people’s DNA, in the hopes that the information will lead to a new era of tailored treatments and personalized prevention. It’s the next chapter in the nature-nurture debate: To keep people healthy, is it better to focus on people’s Zip codes or their genetic codes? A new study in Nature Genetics examined 56,000 pairs of twins from a database of 45 million people insured through Aetna to try to answer the question, and found — as might be expected — a mixed picture. Of 560 diseases and conditions studied, 40 percent had some genetic contribution, while a quarter were influenced by shared environment. Cognitive conditions such as attention-deficit/hyperactivity disorder had the strongest genetic influence, while eye disorders and respiratory diseases such as sinusitis or hyperventilation were more influenced by the environment. The relative influence of Zip code or genetic code “is incredibly nuanced. It depends on what disease you’re interested in,” said Chirag Patel, a data scientist at Harvard Medical School who oversaw the work that was led by Chirag Lakhani, a postdoctoral researcher. © 1996-2019 The Washington Post

Keyword: Genes & Behavior; Development of the Brain
Link ID: 25863 - Posted: 01.15.2019

Nobel Prize-winning American scientist James Watson has been stripped of his honorary titles after repeating comments about race and intelligence. In a TV programme, the pioneer in DNA studies made a reference to a view that genes cause a difference on average between blacks and whites on IQ tests. Cold Spring Harbor Laboratory said the 90-year-old scientist's remarks were "unsubstantiated and reckless". Dr Watson had made similar claims in 2007 and subsequently apologised. He shared the Nobel in 1962 with Maurice Wilkins and Francis Crick for their 1953 discovery of the DNA's double helix structure. Dr Watson sold his gold medal in 2014, saying he had been ostracised by the scientific community after his remarks about race. He is currently in a nursing home recovering from a car accident and is said to have "very minimal" awareness of his surroundings. In 2007, the scientist, who once worked at the University of Cambridge's Cavendish Laboratory, told the Times newspaper that he was "inherently gloomy about the prospect of Africa" because "all our social policies are based on the fact that their intelligence is the same as ours - whereas all the testing says not really". While his hope was that everybody was equal, he added, "people who have to deal with black employees find this is not true". After those remarks, Dr Watson lost his job as chancellor at the laboratory and was removed from all his administrative duties. He wrote an apology and retained his honorary titles of chancellor emeritus, Oliver R Grace professor emeritus and honorary trustee. © 2019 BBC

Keyword: Intelligence; Genes & Behavior
Link ID: 25862 - Posted: 01.14.2019

Abby Olena In the never-ending search for ways to help people eat healthy, scientists have been looking into brain stimulation, specifically, sending a weak electrical current to the brain through two scalp electrodes—a technique called transcranial direct current stimulation. It has previously shown promise in limiting both food cravings and consumption in people, but in a study published yesterday (January 9) in Royal Society Open Science, researchers didn’t find any effects of tDCS on food-related behavior, indicating that the technique’s use needs another look. “The good things about the study are the large sample size and the fact that it’s fairly rigorous,” says Mark George, a psychiatrist and neurologist at the Medical University of South Carolina who did not participate in the study. “The problem [is] interpreting studies where there’s a failure to find. All you can say is that it didn’t work . . . with this group.” During tDCS, one to two milliamps of electricity—enough to feel tingles or pins and needles, but far less than the 800 or so milliamps used for electroconvulsive therapy—are delivered to the brain. Over the last two decades, scientists have reported targeting the technique to the dorsolateral prefrontal cortex, a brain area that’s been shown to be involved in food-related behavior. They’ve found it has helped people crave less and, to a lesser extent, eat fewer sweets and other tempting foods. Yet these experiments have generally included groups of 20 or fewer people, and other studies have failed to replicate their effects. © 1986 - 2019 The Scientist.

Keyword: Obesity
Link ID: 25861 - Posted: 01.14.2019

By Aaron E. Carroll Are we underestimating the harms of legalizing marijuana? Those who hold this view have been in the news recently, saying that research shows we are moving too far too fast without understanding the damage. America is in the midst of a sea change in policies on pot, and we should all be a bit nervous about unintended consequences. Vigilance is required. But it should be reasoned and thoughtful. To tackle recent claims, we should use the best methods and evidence as a starting point. Does Marijuana Increase Crime? Crime has gone up in Colorado and Washington since those states legalized marijuana. It’s reasonable to wonder about the connection, but it’s also reasonable to be skeptical about causation. The best method to investigate this may be synthetic controls. Researchers can use a weighted combination of similar groups (states that are like Colorado and Washington in a number of ways) to create a model of how those states might have been expected to perform with respect to crime without any changes in marijuana laws. Benjamin Hansen, a professor of economics at the University of Oregon, used this methodology to create a comparison group that most closely resembled the homicide trends and levels from 2000-12. “I picked those years because they were after the tremendous crime drop in the early ’90s and most predictive of crime today,” he said. “I ended in 2012 because that’s when Colorado and Washington voted to legalize marijuana.” This model showed that we might have predicted more of an increase in Colorado or Washington just based on trends seen in comparable states, even without legalization. When he compared the two states with the synthetic control, Colorado and Washington actually had lower rates after legalization than you’d expect given trends. © 2019 The New York Times Company

Keyword: Drug Abuse
Link ID: 25860 - Posted: 01.14.2019

Ian Stewart For the first time in U.S. history, a leading cause of deaths, vehicle crashes, has been surpassed in likelihood by opioid overdoses, according to a new report on preventable deaths from the National Safety Council. Americans now have a 1 in 96 chance of dying from an opioid overdose, according to the council's analysis of 2017 data on accidental death. The probability of dying in a motor vehicle crash is 1 in 103. "The nation's opioid crisis is fueling the Council's grim probabilities, and that crisis is worsening with an influx of illicit fentanyl," the council said in a statement released Monday. Fentanyl is now the drug most often responsible for drug overdose deaths, the Centers for Disease Control and Prevention reported in December. And that may only be a partial view of the problem: Opioid-related overdoses have also been under-counted by as much as 35 percent, according to a study published last year in the journal Addiction. The council has recommended tackling the epidemic by increasing pain management training for opioid prescribers, making the potentially-lifesaving drug naloxone more widely available and expanding access to addiction treatment. While the leading causes of death in the U.S. are heart disease (1 in 6 chance) and cancer (1 in 7), the rising overdose numbers are part of distressing trend the non-profit has tracked: The lifetime odds of an American dying from a preventable, unintentional injury have gone up over the past 15 years. © 2019 npr

Keyword: Drug Abuse
Link ID: 25859 - Posted: 01.14.2019

Maria Temming A new smartphone app may help people who shoot up alone get medical treatment if they accidentally overdose. The app, dubbed Second Chance, monitors its user for breathing problems that foreshadow an opioid overdose (SN: 3/31/18, p. 18). In an emergency, the app could call 911 or send an SOS to friends or family who could provide opioid-counteracting medication. “Being able to track an overdose when a person may be by themselves could significantly improve the ability to save lives,” says psychiatrist Nora Volkow, director of the National Institute on Drug Abuse in Bethesda, Md., who was not involved in developing the app. More than 115 people die from an opioid overdose every day in the United States, according to the NIDA, and many victims are alone or with people who are either untrained or too impaired to help. Second Chance, described online January 9 in Science Translational Medicine, converts a smartphone’s speaker and microphone into a sonar system that works within about a meter of a user’s body. When the app is running, the phone continuously emits sound waves at frequencies too high to hear, which bounce off a user’s chest. Tracking when these echoes reach the phone allows the app to detect two possible signs of an impending overdose: slow breathing or no breathing at all. Phone a friend (or EMS) If the Second Chance app judges that a user is likely succumbing to opioids, it could call emergency contacts or medical personnel to deliver the drug naloxone, used to counteract an overdose. |© Society for Science & the Public 2000 - 2018

Keyword: Drug Abuse
Link ID: 25858 - Posted: 01.11.2019

By Elizabeth Pennisi TAMPA, FLORIDA—Swimming through the oceans, voraciously consuming plankton and other small creatures—and occasionally startling a swimmer—the beautiful gelatinous masses known as comb jellies won’t be joining Mensa anytime soon. But these fragile creatures have nerve cells—and they offer insights about the evolutionary origins of all nervous systems, including our own. Inspired by studies of a glue-secreting cell unique to these plankton predators, researchers have now proposed that neurons emerged in the last common ancestor of today’s animals—and that their progenitors were secretory cells, whose primary function was to release chemicals into the environment. Joseph Ryan, a computational evolutionary biologist the University of Florida Whitney Laboratory for Marine Bioscience in St. Augustine, suggested that scenario last year after tracing the development of nerve cells in embryos of comb jellies, among the most ancient animals. Earlier this week at the annual meeting of the Society for Integrative and Comparative Biology (SICB) here, he marshaled evidence from developmental studies of other animals, all pointing to common origins for some neuron and secretory cells. “What Ryan is proposing is novel and important,” says David Plachetzki, an evolutionary biologist at the University of New Hampshire in Durham. Among other mysteries, it could resolve a long debate about whether the nervous system evolved twice early in animal life. © 2018 American Association for the Advancement of Science

Keyword: Evolution
Link ID: 25857 - Posted: 01.11.2019

Laura Sanders Young nerve cells derived from people with autism are precocious, growing bigger and developing sooner than cells taken from people without autism, a new study shows. The results, described January 7 in Nature Neuroscience, hint that in some cases nerve cells veer off course early in brain development to ultimately cause the disorder. As a proxy of brain growth, researchers led by Simon Schafer of the Salk Institute in La Jolla, Calif., transformed skin cells from people with and without autism into stem cells that then developed into nerve cells in the lab. Along the way, the scientists monitored the cells’ growth and the behavior of their genes. Compared with cells derived from five people without autism, cells from eight people with autism grew bigger, with longer and more elaborate branches, the researchers found. Three-dimensional balls called organoids made of the autism-derived cells were bulkier, too. In addition to this physical development, a group of genes important for brain development switched on sooner. Trouble in the autism-derived cells, however, actually began a bit earlier, just as the cells were on the cusp of becoming nerve cells. At the neural stem cell stage, certain spots of these cells’ chromatin — tightly packed genetic material — were more open and accessible than they should have been, an unfolding that can lead to abnormally active genes. The results show that open chromatin “can have major effects on neuronal development,” says neuroscientist David Amaral of the University of California, Davis. |© Society for Science & the Public 2000 - 2018.

Keyword: Autism
Link ID: 25856 - Posted: 01.11.2019

Bruce Bower An ancient hominid skeleton dubbed Little Foot possessed a brain largely similar to that of modern chimpanzees and an inner ear with a mix of apelike and humanlike features, two studies suggest. These findings, along with other analyses of the adult female’s 3.67-million-year-old skeleton, point to the piecemeal evolution of humanlike traits in close relatives of our species, scientists say. The research is part of the first formal analyses of Little Foot’s skeleton, which was discovered more than 20 years ago in a South African cave but was recently removed from its rocky encasing. Other analyses of trunk and limb bones indicate that Little Foot, who lived perhaps a million years before the emergence of the human genus, Homo, already walked upright about as well as people today do (SN: 1/19/19, p.13). Although Little Foot consists of a nearly complete skeleton, her evolutionary identity is controversial. Paleoanthropologist Ronald Clarke of the University of the Witwatersrand in Johannesburg — Little Foot’s discoverer and a coauthor of the two new studies — assigns the find to Australopithecus prometheus, an early extinct hominid species that many scientists don’t regard as valid. Other researchers regard Little Foot as an early member of Australopithecus africanus, a species previously known from fossils discovered at several South African sites (SN: 1/19/19, p. 13). |© Society for Science & the Public 2000 - 2018

Keyword: Evolution
Link ID: 25855 - Posted: 01.10.2019

By Perri Klass, M.D. Pain control in infants and children has come a long way over the past few decades. Experts know how to provide appropriate anesthesia when children need surgery and understand the ways that even very young children express distress when they’re hurting afterward. There is a lot of evidence about reducing the pain and anxiety that can accompany immunizations and blood draws, and there is increasing expertise about helping children who struggle with chronic pain. But today’s parents may be shocked to learn that was not always the case. As recently as the early 1980s, the pain of children and infants was thought to be different from that of adults and was sometimes treated differently, or sometimes not treated at all. Change doesn’t always come easily in medicine, so there’s a certain onus on parents to make sure that their children get state-of-the-art pain management around procedures, large and small. That means preparation before any planned surgery, ideally with a child life specialist, and it means careful attention to the child’s pain afterward, with parents well backed up by medical specialists. Let me start in the bad old days: About 30 years ago, when I was doing my residency, my 4-year-old son fractured his femur. After surgery, he found himself on the orthopedic ward of my very own hospital, and in a fair amount of pain (the femur is the biggest bone in the body, and there was a lot of tissue damage). As his busybody on-call pediatric resident mother, I discovered that the pain control ordered by the surgeons was “IM MSO4 PRN.” That meant he could have an intramuscular dose of morphine whenever the pain from the fracture was so bad that it overcame a 4-year-old’s fear of shots. To get pain relief, he would have to request the needle. © 2019 The New York Times Company

Keyword: Pain & Touch; Development of the Brain
Link ID: 25854 - Posted: 01.10.2019

Diana Kwon When Adriano Aguzzi, a neuropathologist at the University of Zurich, learned that the application to renew his lab’s license for mouse experiments was rejected in December, he was stunned. Aguzzi uses rodents to investigate prions—misfolded proteins that cause fatal neurodegenerative disorders such as Creutzfeldt-Jakob Disease—and for the last two decades, he has successfully received authorization to conduct studies that involve inoculating animals with prions and monitoring their vital signs as they develop disease. The latest license request was “the same application that has been renewed every three years,” he tells The Scientist. Aguzzi is one of several scientists who say it has become increasingly difficult to get licenses for animal experiments in recent years. Switzerland has some of the strictest animal protection laws in the world, and as a result, the quantity of animals used in research has steadily declined over the years. Between 2008 and 2017, for example, the number dropped by more than 100,000 per year. “What I’ve seen over the past 20 years is that regulations have tightened quite a lot. It requires much more work to write a license application and to get it approved,” says Isabelle Mansuy, a neuroepigeneticist at the University of Zurich and ETH Zurich. “Most of the additional requirements are good, because they have optimized the research in terms of animal numbers and forced us to better plan and document our experiments—but some changes are not necessary and have complicated our work.” © 1986 - 2019 The Scientist

Keyword: Animal Rights
Link ID: 25853 - Posted: 01.10.2019

By Elizabeth Pennisi American Kennel Club descriptions of dog breeds can read like online dating profiles: The border collie is a workaholic; the German shepherd will put its life on the line for loved ones. Now, in the most comprehensive study of its kind to date, scientists have shown that such distinct breed traits are actually rooted in a dog’s genes. The findings may shed light on human behaviors as well. “It’s a huge advance,” says Elaine Ostrander, a mammalian geneticist at the National Human Genome Research Institute in Bethesda, Maryland, who was not involved with the work. “It’s a finite number of genes, and a lot of them do make sense.” When the dog genome was sequenced in 2005, scientists thought they would quickly be able to pin down the genes that give every breed its hallmark personality. But they found so much variation even within a breed that they could never study enough dogs to get meaningful results. So in the new study, Evan MacLean, a comparative psychologist at the University of Arizona in Tucson, and colleagues began by looking at behavioral data for about 14,000 dogs from 101 breeds. The analyses come from the Canine Behavioral Assessment & Research Questionnaire (C-BARQ), a sort of pet personality quiz developed by James Serpell, an ethologist at the University of Pennsylvania. C-BARQ asks questions like, “What does your dog do when a stranger comes to the door?” to allow owners to objectively characterize 14 aspects of their pet’s personalities, including trainability, attachment, and aggression. Since the survey was developed in 2003, more than 50,000 owners have participated. © 2018 American Association for the Advancement of Science

Keyword: Genes & Behavior; Emotions
Link ID: 25852 - Posted: 01.09.2019

Elizabeth Preston A little blue-and-black fish swims up to a mirror. It maneuvers its body vertically to reflect its belly, along with a brown mark that researchers have placed on its throat. The fish then pivots and dives to strike its throat against the sandy bottom of its tank with a glancing blow. Then it returns to the mirror. Depending on which scientists you ask, this moment represents either a revolution or a red herring. Alex Jordan, an evolutionary biologist at the Max Planck Institute for Ornithology in Germany, thinks this fish — a cleaner wrasse — has just passed a classic test of self-recognition. Scientists have long thought that being able to recognize oneself in a mirror reveals some sort of self-awareness, and perhaps an awareness of others’ perspectives, too. For almost 50 years, they have been using mirrors to test animals for that capacity. After letting an animal get familiar with a mirror, they put a mark someplace on the animal’s body that it can see only in its reflection. If the animal looks in the mirror and then touches or examines the mark on its body, it passes the test. Humans don’t usually reach this milestone until we’re toddlers. Very few other species ever pass the test; those that do are mostly or entirely big-brained mammals such as chimpanzees. And yet as reported in a study that appeared on bioRxiv.org earlier this year and that is due for imminent publication in PLOS Biology, Jordan and his co-authors observed this seemingly self-aware behavior in a tiny fish. Jordan’s findings have consequently inspired strong feelings in the field. “There are researchers who, it seems, do not want fish to be included in this secret club,” he said. “Because then that means that the [primates] are not so special anymore.” All Rights Reserved © 2019

Keyword: Consciousness; Evolution
Link ID: 25851 - Posted: 01.09.2019

By Karen Weintraub Sometimes a whale just wants to change its tune. That’s one of the things researchers have learned recently by eavesdropping on whales in several parts of the world and listening for changes in their pattern and pitch. Together, the new studies suggest that whales are not just whistling in the water, but constantly evolving a form of communication that we are only beginning to understand. Most whales and dolphins vocalize, but dolphins and toothed whales mostly make clicking and whistling sounds. Humpbacks, and possibly bowheads, sing complex songs with repeated patterns, said Michael Noad, an associate professor in the Cetacean Ecology and Acoustics Laboratory at the University of Queensland in Australia. Birds may broadcast their social hierarchy among song-sharing populations by allowing the dominant bird to pick the playlist and patterns. But how and why whales pass song fragments across hundreds of miles, and to thousands of animals, is far more mysterious. The biggest question is why whales sing at all. “The thing that always gets me out of bed in the morning is the function of the song,” Dr. Noad said. “I find humpback song fascinating from the point of view of how it’s evolved.” The leading hypothesis is that male humpbacks — only the males sing — are trying to attract females. But they may also switch tunes when another male is nearby, apparently to assess a rival’s size and fitness, said Dr. Noad, who was the senior author of one of four new papers on whale songs. © 2019 The New York Times Company

Keyword: Animal Communication; Sexual Behavior
Link ID: 25850 - Posted: 01.09.2019

By Karen Weintraub Research on Alzheimer’s has mainly focused on Caucasians. New findings, however, suggest the disease process that leads to dementia may differ in African–Americans. According to a study published Monday in JAMA Neurology, the brains of African–Americans diagnosed with Alzheimer’s have less buildup of a protein called tau—one of the two hallmark proteins that characterize the disease. It is not clear why African–Americans would have less tau while still suffering from Alzheimer’s, says neurologist John Morris, who led the research. But the finding is significant because it means the medical community needs to exercise caution when defining Alzheimer’s by measures of tau buildup alone. The study also suggests race might affect other aspects of the disease’s pathology, says Morris, who directs the Knight Alzheimer Disease Research Center at Washington University in Saint Louis. “The study of Alzheimer’s disease, which really began formally in the United States in the mid-1980s, has largely been of white people,” he notes. “The U.S. in general and the older adult portion of the U.S. population is increasingly diverse, so we really do need to study all populations to try to understand the disease and its forms.” For the moment, the differences detected in the disease’s pathology will not change existing treatment protocols, which do not yet look at certain aberrant proteins to make a diagnosis. Physicians today diagnose Alzheimer’s largely based on a patient’s neuropsychological characteristics. But once researchers have developed a more practical way to measure levels of key proteins involved in the disease, such differences could be crucial for accurate diagnoses, Morris says. Brain scans can detect tau as well as amyloid beta—another protein that builds up in the brains of Alzheimer’s sufferers—but the scans are expensive and not widely available. © 2019 Scientific American,

Keyword: Alzheimers
Link ID: 25849 - Posted: 01.09.2019

By Malcolm Gladwell A few years ago, the National Academy of Medicine convened a panel of sixteen leading medical experts to analyze the scientific literature on cannabis. The report they prepared, which came out in January of 2017, runs to four hundred and sixty-eight pages. It contains no bombshells or surprises, which perhaps explains why it went largely unnoticed. It simply stated, over and over again, that a drug North Americans have become enthusiastic about remains a mystery. For example, smoking pot is widely supposed to diminish the nausea associated with chemotherapy. But, the panel pointed out, “there are no good-quality randomized trials investigating this option.” We have evidence for marijuana as a treatment for pain, but “very little is known about the efficacy, dose, routes of administration, or side effects of commonly used and commercially available cannabis products in the United States.” The caveats continue. Is it good for epilepsy? “Insufficient evidence.” Tourette’s syndrome? Limited evidence. A.L.S., Huntington’s, and Parkinson’s? Insufficient evidence. Irritable-bowel syndrome? Insufficient evidence. Dementia and glaucoma? Probably not. Anxiety? Maybe. Depression? Probably not. Then come Chapters 5 through 13, the heart of the report, which concern marijuana’s potential risks. The haze of uncertainty continues. Does the use of cannabis increase the likelihood of fatal car accidents? Yes. By how much? Unclear. Does it affect motivation and cognition? Hard to say, but probably. Does it affect employment prospects? Probably. Will it impair academic achievement? Limited evidence. This goes on for pages. © 2019 Condé Nast.

Keyword: Drug Abuse
Link ID: 25848 - Posted: 01.08.2019