By C. Claiborne Ray Q. How do bees find the flowers in the container garden on the fourth-floor deck of my city apartment? A. Foraging bees use the same methods to find nectar and pollen four floors up that they use at ground level. Honeybees routinely fly two miles from their hives in their search for raw material for honey; it doesn’t require much extra energy to fly several stories up. It takes only one scout to report a promising garden to the rest of the hive with a famous waggle dance. The scout relies on its sophisticated eyes, which are tuned to a variety of wavelengths, including ultraviolet color patterns in flowers that are invisible to people. We’re taking you on a journey to help you understand how bees, while hunting for pollen, use all of their senses — taste, touch, smell and more — to decide what to pick up and bring home. When the bees get closer to flowers, smell receptors begin transmitting information. And it has recently been discovered that both bumblebees and honeybees can detect and discriminate among weak electrostatic fields emanating from flowers. The bees accumulate a positive charge, while the flowers have a negative charge. The interaction between the fields is detected by antennae or sensitive hairs on the body. The electrical field helps bees to recognize pollen-rich blooms and perhaps even to transfer the pollen. © 2019 The New York Times Company

Keyword: Animal Migration; Animal Communication
Link ID: 26102 - Posted: 04.02.2019

By Jane E. Brody Attention all consumers seeking to protect brain health: You can save hundreds of dollars a year and enhance the health of your brain and body by ignoring the myriad unproven claims for anti-dementia supplements and instead focusing on a lifestyle long linked to better mental and physical well-being. How many of these purported brain boosters have you already tried — Ginkgo biloba, coenzyme Q10, huperzine A, caprylic acid and coconut oil, coral calcium, among others? The Alzheimer’s Association says that, with the possible exception of omega-3 fatty acids, all that were properly tested thus far have been found wanting. I admit it’s very appealing to think you can maintain your cognitive powers by swallowing a few pills a day instead of adopting a brain-healthy diet, getting regular exercise and adequate sleep, among other health-preserving measures like not smoking. But you’d only be fooling yourself and wasting precious dollars that could be better spent on nutritious foods and a good pair of walking shoes. “No known dietary supplement prevents cognitive decline or dementia,” Dr. Joanna Hellmuth stated emphatically in JAMA in January. “Yet,” she added, “supplements advertised as such are widely available and appear to gain legitimacy when sold by major U.S. retailers.” Dr. Hellmuth, a neurologist at the University of California, San Francisco, Memory and Aging Center, reminds consumers that supplement manufacturers do not have to test their products for effectiveness or safety. Lacking sound scientific backing, most are promoted by testimonials that appeal to people worried about developing dementia. © 2019 The New York Times Company

Keyword: Alzheimers; Learning & Memory
Link ID: 26101 - Posted: 04.01.2019

By Heather Murphy An article this week about Jo Cameron, who has lived for 71 years without experiencing pain or anxiety because she has a rare genetic mutation, prompted questions from New York Times readers. The notion that the same gene could be responsible for the way a person processes physical and psychological pain left many perplexed: Aren’t they totally different? Or does her story hint that sensitivity to one type of pain might be intertwined with sensitivity to another? Childbirth, Ms. Cameron said, felt like “a tickle.” She often relies on her husband to alert her when she is bleeding, bruised or burned because nothing hurts. When someone close to her has died, she said, she has felt sad but “I don’t go to pieces.” She cannot recall ever having been riled by anything — even a recent car crash. On an anxiety disorder questionnaire, she scored zero out of 21. “I drive people mad by being cheerful,” she said. Here’s a bit about what’s known: Do those who live without pain also live without anxiety? No. Before encountering Ms. Cameron, the scientists who studied her case worked with other patients who did not experience pain. “Reduced anxiety has not really been noted before in the other pain insensitivity disorders we work on,” said Dr. James Cox, a senior lecturer from the Molecular Nociception Group at University College London. He also said that given Ms. Cameron had gone more than six decades without realizing just how unusual she was, there could be others like her. A number of such individuals contacted The Times after the article was published. © 2019 The New York Times Company

Keyword: Pain & Touch; Emotions
Link ID: 26100 - Posted: 04.01.2019

By Ilana Marcus Grit alone got Linda Greene through her husband’s muscular dystrophy, her daughter’s traumatic brain injury, and her own mysterious illness that lasted for three years and left her vomiting daily before doctors identified the cause. But eventually, after too many days sitting at her desk at work crying, she went to see her doctor for help. He prescribed an antidepressant and referred her to a psychiatrist. When the first medication didn’t help, the psychiatrist tried another — and another and another — hoping to find one that made her feel better. Instead, Greene felt like a zombie and sometimes she hallucinated and couldn’t sleep. In the worst moment, she found herself contemplating suicide. “It was horrible,” she said. She never had suicidal thoughts before and was terrified. She went back her primary care doctor. In the past, when Jeremy Bruce, Greene’s physician in Cincinnati, treated patients for depression, he followed the same steps for almost everyone: start the patient on one antidepressant and switch to another until something helped. Sometimes, before they found the right treatment, the patient would leave his practice to find a new doctor. “They would usually be very angry,” Bruce said. But about three years ago, Bruce tried a new approach. Linda Greene and her husband. She tried many antidepressants before her doctor suggested genetic testing to find a medicine that worked for her. Doctors increasingly use information about genes to evaluate potential risk for some diseases and to determine the best drug treatment. But using pharmacogenetics to help treat depression remains controversial. (Family Photo) © 1996-2019 The Washington Post

Keyword: Depression; Genes & Behavior
Link ID: 26099 - Posted: 04.01.2019

By Michael C. Reichert Early in my first go at being a father, I was hijacked by ancient impulses. Our family lived in a rowhouse neighborhood in Philadelphia, and right down the street was a small playground where gangs of boys gathered for games of stickball and basketball. My son loved playing sports. But he was unprepared for what developed as his friends grew older. After years together laughing and riding their tricycles and then bikes up and down the block, several of the boys grew angry and mean. Ultimately, they turned on my son, taunting him, leaving him out of their games. He began to trudge home, tail between his legs. And I felt called to action. At first, I tried to bolster his confidence so he would give the playground another go. But one Saturday morning I met him at the front steps and told him he could not come into the house. “You have to figure this out,” I said. “I’ll stay with you as long as you need, but I cannot let you just give up.” He tried to push past me, his humiliation becoming frantic. He melted down, screaming and crying. I kept saying: “You can do it. You don’t have to give up.” A neighbor poked her head out, concerned about what must have sounded like child abuse. Did I do the right thing? Even now I’m not sure. He did go back to the playground, and eventually managed some kind of truce with the other kids. He grew up into a fine man, a teacher, and understands I was trying to help, in my clumsy way. But while teaching him to stand up for himself, was I also passing along the prejudice that a boy should override his pain and never back down from a fight? What happened in my son’s peer group was perfectly predictable. Boyhood immerses boys in violence and the bullying that leads to it. High school boys are more likely than girls to have been in a physical fight in the past year and male children are more likely to have been victims of violence. Three types of male violence — violence against women, violence against other men and violence against themselves — are deeply interwoven. © 2019 The New York Times Company

Keyword: Sexual Behavior; Aggression
Link ID: 26098 - Posted: 04.01.2019

Maria Temming Synthetic opioids outlast current antidotes. A nanoparticle-based alternative could fix that. A newly developed single-dose opioid antidote lasts several days, a study in mice shows. If the results can be duplicated in humans, the treatment may one day help prevent overdoses from deadly drugs like fentanyl. Normally, a dose of the opioid antidote naloxone passes through a person’s body in about 30 minutes — far too quickly to fully counteract the effects of such synthetic opioids as fentanyl and carfentanil (SN Online: 5/1/18). These drugs, tens to thousands of times stronger than morphine, can linger in a person’s system for hours or even days (SN: 6/10/17, p. 22). That requires multiple doses of an antidote to prevent someone from overdosing. So researchers developed a new naloxone-based antidote to outlast synthetic opioids by creating nanoparticles in which naloxone molecules are tangled up with a biodegradable polymer called polylactic acid. Water and enzymes in the body slowly break down these nanosized tangles, gradually releasing naloxone. In mice, the new nanoparticle delivery system counteracted the pain-relieving effects of morphine for up to 96 hours after administering a single dose of the antidote, according to research being presented March 31 at the American Chemical Society meeting in Orlando, Fla. |© Society for Science & the Public 2000 - 2019

Keyword: Drug Abuse
Link ID: 26097 - Posted: 04.01.2019

Alix Spiegel Our thoughts and fears, movements and sensations all arise from the electrical blips of billions of neurons in our brain. Streams of electricity flow through neural circuits to govern these actions of the brain and body, and some scientists think that many neurological and psychiatric disorders may result from dysfunctional circuits. As this understanding has grown, some scientists have asked whether we could locate these faulty circuits, reach deep into the brain and nudge the flow to a more functional state, treating the underlying neurobiological cause of ailments like tremors or depression. The idea of changing the brain for the better with electricity is not new, but deep brain stimulation takes a more targeted approach than the electroconvulsive therapy introduced in the 1930s. DBS seeks to correct a specific dysfunction in the brain by introducing precisely timed electric pulses to specific regions. It works by the action of a very precise electrode that is surgically inserted deep in the brain and typically controlled by a device implanted under the collarbone. Once in place, doctors can externally tailor the pulses to a frequency that they hope will fix the faulty circuit. This week's Invisibilia podcast features the story of a woman with obsessive-compulsive disorder and depression who signed up for a deep brain stimulation trial. The story describes what it's like to be able to adjust her mood by adjusting the settings on her device. Listen to that story here. © 2019 npr

Keyword: Depression; Emotions
Link ID: 26096 - Posted: 03.30.2019

Alix Spiegel We have the story of one woman who is taking part in an experiment on deep brain stimulation. RACHEL MARTIN, HOST: We are about to go deep - deep into your brain. STEVE INSKEEP, HOST: With a story about deep brain stimulation, or DBS, which sounds like a kind of massage, actually. But it means that patients get an implant that delivers small pulses of electricity to their brains. MARTIN: It's often used to treat Parkinson's disease. But for years, researchers have been trying to figure out how to use it to treat psychiatric disorders. INSKEEP: Results and experiments so far have been mixed. Many patients see no benefit. But some with obsessive-compulsive disorder have seen big changes. MARTIN: Like the next woman you're going to meet. For privacy, we are withholding her last name. Alix Spiegel from NPR's INVISIBILIA has her story. ALIX SPIEGEL, BYLINE: During the appointment, Megan didn't have to do that much, just sit in a chair while one of the doctors from the experiment used what looked like an oversized remote control to reprogram her electricity levels. Even after five years of having the implant, getting her electricity adjusted was unpredictable. Sometimes it went fine. But having electrodes in your brain is really complicated. And occasionally, the adjustments didn't go well. UNIDENTIFIED DOCTOR: While you were talking, I slowly ramped it up again. Anything different now? MEGAN: Slightly more aware. UNIDENTIFIED DOCTOR: OK. MEGAN: It's not like in the past, where it was like, oh, I feel good. But it's, like, a different feeling. SPIEGEL: After the doctor turned her up higher, Megan said she felt better. But then he decided to dial it back just a notch. He was worried that too much electricity might make her manic. UNIDENTIFIED DOCTOR: Now, if you notice me turning it down, then maybe I'll change my mind on that. MEGAN: (Crying) I'm sorry; don't do it. UNIDENTIFIED DOCTOR: Did you just feel it? MEGAN: (Crying) I don't feel very good at all right now. © 2019 npr

Keyword: Depression
Link ID: 26095 - Posted: 03.30.2019

Emma Yasinski In the 1970s, scientists discovered that certain neurons in the hippocampus—an area of the brain involved in learned and memory—would fire in response to particular locations. They were called “place cells,” explains Charlotte Boccara, a researcher at the University of Oslo. “They were deemed important for spatial representation . . . a bit like the ‘You Are Here’ signal’ on a map.” But it wasn’t until 2005 that researchers discovered the brain’s grid cells, which they believed function as that map. These cells, found adjacent to the hippocampus in the medial entorhinal cortex (MEC), self-organize into a pattern of hexagons that serve as coordinates to help animals make sense of their surroundings and the signals from our place cells. A pair of studies published today (March 28) in Science suggests that this map may not be as rigid as once thought. The experiments demonstrated that, in rats at least, the cellular activity within these grids changes as the animals learn and remember where they can find food rewards. “These are wonderful studies,” says György Buzsáki, a neuroscientist at New York University who was not involved in either of them. “When ideas converge from multiple, different directions, and they converge and come to the same conclusion, the result is always stronger.” In the first study, Boccara, then a researcher at the Institute of Science and Technology Austria, and her team placed rats one by one in a cheeseboard maze, a flat board drilled full of holes. They hid three food rewards in different holes then scattered food dust over the entire surface so the rats would not be able to sniff their ways to the reward. The rats explored the maze until they found the prizes and repeated the task until they learned to go straight to the food instead of foraging. The next day, the researchers conducted the same experiment but changed the locations of the rewards. © 1986 - 2019 The Scientist.

Keyword: Learning & Memory
Link ID: 26094 - Posted: 03.30.2019

By Simon Makin Neurodegenerative diseases all involve the accumulation of toxic versions of naturally produced proteins in the brain. Multiple proteins are often abnormal in a patient, and the same aberrant protein can be involved in several different conditions. One common culprit is tau, which is abnormal in various conditions: chronic traumatic encephalopathy, a neurodegenerative disorder caused by repeated head trauma; a group of conditions known collectively as frontotemporal dementia; and, most famously, Alzheimer’s disease (AD). Normally, tau stabilizes structures inside neural connections, called microtubules, which facilitate chemical communication between cells. In disease states, tau is chemically altered, becoming misshapen and breaking away from microtubules. These toxic versions accumulate into structures called “neurofibrillary tangles,” which disrupt cells’ ability to communicate and may trigger other forms of damage, such as inflammation. Tau is involved in AD, but abnormalities in a different protein, amyloid-beta, are thought to be the initial trigger for a chain of biological events (including tau pathology) that underlies neurodegeneration. This is why most AD drugs developed to date have targeted amyloid, although tau has received increasing attention as multiple drugs intended to remove amyloid have failed. A new study, published Wednesday in Science Translational Medicine, suggests that an existing drug, lonafarnib, could be repurposed to treat neurodegenerative diseases that involve tau. A team of researchers, led by neuroscientist Kenneth Kosik of the University of California, Santa Barbara, found the drug had beneficial effects on tau-related pathology in mice, if administered early over an extended period. They also found evidence suggesting it works via a previously unknown biological mechanism. “This opens up a previously completely unsuspected pathway for tau degradation,” says Kosik, a longtime tau researcher. “We don’t have all the molecular details, but as a place to look, this is full of new opportunities.” © 2019 Scientific American

Keyword: Alzheimers
Link ID: 26093 - Posted: 03.29.2019

Nell Greenfieldboyce Mosquitoes searching for a meal of blood use a variety of clues to track down humans, including our body heat and the carbon dioxide in our breath. Now, research shows that a certain olfactory receptor in their antennae also serves as a detector of humans, responding to smelly chemicals in our sweat. Targeting this receptor might offer a new way to foil blood-seeking mosquitoes and prevent the transmission of diseases including malaria, Zika virus and dengue, according to the study published Thursday in the journal Current Biology. "We found a receptor for human sweat, and we found that acidic volatiles that come off of us are really key for mosquitoes to find us," says Matthew DeGennaro, a neurogeneticist at Florida International University in Miami. "I think what's exciting about it is that finally we have evidence that there is some sort of pathway, in the sense of smell, that is required for mosquitoes to like us," says Lindy McBride, a scientist at Princeton University who studies mosquito behavior and was not part of the research team. It's long been known that mosquitoes rely on multiple clues to target humans. First, a mosquito will sense exhaled carbon dioxide from a distance that can be more than 30 feet. "After the carbon dioxide," DeGennaro explains, "then it begins to sense human odor." © 2019 npr

Keyword: Chemical Senses (Smell & Taste)
Link ID: 26092 - Posted: 03.29.2019

By James Gallagher Health and science correspondent, BBC News French scientists say they have proof that dogs can pick up the smell of an epileptic seizure. The University of Rennes team hope the findings could lead to ways to predict when people will have a seizure. These could include dogs or "electronic noses" that pick up the precise odour being given off during a seizure. Dogs have previously been shown to be able to sniff out diseases including cancers, Parkinson's, malaria and diabetes. Some people with epilepsy already rely on the animals. One sleeping in a child's bedroom can alert family members of a seizure in the middle of the night. The latest study, in the journal Scientific Reports, trained five dogs from Medical Mutts, in the US, to recognise the smell of sweat taken from a patient having a seizure. They were then given a choice of seven sweat samples taken from other patients while they were either relaxing, exercising or having a seizure. Two of the dogs found the seizure sample about two-thirds of the time and the other three were 100% accurate The report says: "The results are extremely clear and constitute a first step towards identifying a seizure-specific odour." © 2019 BBC

Keyword: Chemical Senses (Smell & Taste); Epilepsy
Link ID: 26091 - Posted: 03.29.2019

Ian Sample Science editor Doctors have identified a new mutation in a woman who is barely able to feel pain or stress after a surgeon who was baffled by her recovery from an operation referred her for genetic testing. Jo Cameron, 71, has a mutation in a previously unknown gene which scientists believe must play a major role in pain signalling, mood and memory. The discovery has boosted hopes of new treatments for chronic pain which affects millions of people globally. Cameron, a former teacher who lives in Inverness, has experienced broken limbs, cuts and burns, childbirth and numerous surgical operations with little or no need for pain relief. She sometimes leans on the Aga and knows about it not from the pain, but the smell. “I’m vegan, so the smell is pretty obvious,” she says. “There’s no other burning flesh going on in the house.” But it is not only an inability to sense pain that makes Cameron stand out: she also never panics. When a van driver ran her off the road two years ago, she climbed out of her car, which was on its roof in a ditch, and went to comfort the shaking young driver who cut across her. She only noticed her bruises later. She is relentlessly upbeat, and in stress and depression tests she scored zero. “I knew that I was happy-go-lucky, but it didn’t dawn on me that I was different,” she says. “I thought it was just me. I didn’t know anything strange was going on until I was 65.” © 2019 Guardian News & Media Limited

Keyword: Pain & Touch; Genes & Behavior
Link ID: 26090 - Posted: 03.28.2019

Amber Dance Robert Sorge was studying pain in mice in 2009, but he was the one who ended up with a headache. At McGill University in Montreal, Canada, Sorge was investigating how animals develop an extreme sensitivity to touch. To test for this response, Sorge poked the paws of mice using fine hairs, ones that wouldn’t ordinarily bother them. The males behaved as the scientific literature said they would: they yanked their paws back from even the finest of threads. But females remained stoic to Sorge’s gentle pokes and prods1. “It just didn’t work in the females,” recalls Sorge, now a behaviourist at the University of Alabama at Birmingham. “We couldn’t figure out why.” Sorge and his adviser at McGill University, pain researcher Jeffrey Mogil, would go on to determine that this kind of pain hypersensitivity results from remarkably different pathways in male and female mice, with distinct immune-cell types contributing to discomfort2. Sorge and Mogil would never have made their discovery if they had followed the conventions of most pain researchers. By including male and female mice, they were going against the crowd. At the time, many pain scientists worried that females’ hormone cycles would complicate results. Others stuck with males because, well, that’s how things were done. Today, inspired in part by Sorge and Mogil’s work and spurred on by funders, pain researchers are opening their eyes to the spectrum of responses across sexes. Results are starting to trickle out, and it’s clear that certain pain pathways vary considerably, with immune cells and hormones having key roles in differing responses. © 2019 Springer Nature Publishing AG

Keyword: Pain & Touch; Hormones & Behavior
Link ID: 26089 - Posted: 03.28.2019

National Institutes of Health scientists studying the progression of inherited and infectious eye diseases that can cause blindness have found that microglia, a type of nervous system cell suspected to cause retinal damage, surprisingly had no damaging role during prion disease in mice. In contrast, the study findings indicated that microglia might delay disease progression. The discovery could apply to studies of inherited photoreceptor degeneration diseases in people, known as retinitis pigmentosa. In retinitis pigmentosa cases, scientists find an influx of microglia near the photoreceptors, which led to the belief that microglia contribute to retina damage. These inherited diseases appear to damage the retina similarly to prion diseases. Prion diseases are slow degenerative diseases of the central nervous system that occur in people and various other mammals. No vaccines or treatments are available, and the diseases are almost always fatal. Prion diseases primarily involve the brain but also can affect the retina and other tissues. Expanding on work published in 2018, scientists at NIH’s National Institute of Allergy and Infectious Diseases (NIAID) used an experimental drug to eliminate microglia in prion-infected mice. They studied prion disease progression in the retina to see if they could discover additional details that might be obscured in the more complex structure of the brain. When the scientists examined their prion-infected study mice, they found that photoreceptor damage still occurred – even somewhat faster – despite the absence of microglia. They also observed early signs of new prion disease in the photoreceptor cells, which may provide clues as to how prions damage photoreceptors. Their work appears in Acta Neuropathologica Communications.

Keyword: Vision; Prions
Link ID: 26088 - Posted: 03.28.2019

By Richard Schiffman The patient, a 48-year-old real estate professional in treatment for anxiety and mild depression, revealed that he had eaten three dozen oysters over the weekend. His psychiatrist, Dr. Drew Ramsey, an assistant clinical professor of psychiatry at Columbia University, was impressed: “You’re the only person I’ve prescribed them to who came back and said he ate 36!” Dr. Ramsey, the author of several books that address food and mental health, is a big fan of oysters. They are rich in vitamin B12, he said, which studies suggest may help to reduce brain shrinkage. They are also well stocked with long chain omega-3 fatty acids, deficiencies of which have been linked to higher risk for suicide and depression. But shellfish are not the only food he is enthusiastic about. Dr. Ramsey is a pioneer in the field of nutritional psychiatry, which attempts to apply what science is learning about the impact of nutrition on the brain and mental health. Dr. Ramsey argues that a poor diet is a major factor contributing to the epidemic of depression, which is the top driver of disability for Americans aged 15 to 44, according to a report by the World Health Organization. Together with Samantha Elkrief, a chef and food coach who sits in on many of his patient sessions, he often counsels patients on how better eating may lead to better mental health. The irony, he says, is that most Americans are overfed in calories yet starved of the vital array of micronutrients that our brains need, many of which are found in common plant foods. A survey published in 2017 by the Centers for Disease Control and Prevention reported that only one in 10 adults meets the minimal daily federal recommendations for fruit and vegetables — at least one-and-a-half to two cups per day of fruit and two to three cups per day of vegetables. © 2019 The New York Times Company

Keyword: Depression
Link ID: 26087 - Posted: 03.28.2019

Jon Hamilton When you're thirsty, a swig of fresh water brings instant relief. But gulp down some salty sea water and you'll still feel parched. That's because your brain is trying to keep the concentration of salt in your body within a very narrow range, says Zachary Knight, an associate professor in physiology at the University of California, San Francisco and an investigator with the Howard Hughes Medical Institute. "If you experience, for example, a 10 percent change, you would be very sick," he says. "A 20 percent change and you could die." Knight and a team of researchers wanted to know how the brain keeps that from happening. They report the results of their search in an article published Wednesday in the journal Nature. "There has to be a mechanism for the brain to track how salty the solutions that you drink are and use that to fine-tune thirst," Knight says. "But the mechanism was unknown." So Knight's team began studying brain cells known as thirst neurons. First, the team piped fresh water directly into the stomachs of some thirsty mice. "Within a minute or two, infusing water into the stomach rapidly turns off these thirst neurons in the brain," says Chris Zimmerman, a graduate student in Knight's lab who conducted the experiment. "And not only that," Zimmerman says, "if we give [the mouse] access to water it doesn't drink at all." © 2019 npr

Keyword: Miscellaneous
Link ID: 26086 - Posted: 03.28.2019

By Nicholas Bakalar Urban air pollution is associated with an increased risk for psychotic experiences in teenagers, researchers report. A study published in JAMA Psychiatry included 2,063 British teenagers whose health had been followed from birth through age 18. Almost a third of them said they had at least one psychotic experience, ranging from a mild feeling of paranoia to a severe psychotic symptom, since age 12. Researchers linked air pollution data to locations where they spent most of their time — at home, school or work. Compared with teenagers who lived where pollution was lowest, those in the most polluted areas were 27 percent to 72 percent more likely to have psychotic experiences, depending on the type of pollutant; exposure to two pollutants, nitrogen dioxide and nitrogen oxides, accounted for 60 percent of the association. The study controlled for family psychiatric history, maternal psychosis, substance use, socioeconomic status, neighborhood social characteristics and other factors, but it is an observational study that does not prove causation. “From this one study, we can’t say that air pollution causes psychosis,” said the lead author, Helen L. Fisher, a research psychologist at King’s College London. “The study only says that these things commonly occur together.” © 2019 The New York Times Company

Keyword: Schizophrenia; Neurotoxins
Link ID: 26085 - Posted: 03.28.2019

Laura Sanders A few months back, a new storefront appeared in my small Oregon town. Its shelves were packed with tinctures, jars of salve, coffee beans, bath bombs — even beard oil. This motley collection shared a single star ingredient: CBD. Produced by the cannabis plant, CBD is the straitlaced cousin of marijuana’s more famous component — the THC that delivers a mind-swirling high. CBD, or cannabidiol, has no such intoxicating effects on the mind. Yet the molecule has captured people’s attention in a profound way, sold as a remedy for pain, anxiety, insomnia and other ailments — all without the high. That neighborhood shop, CBD Scientific, is far from alone in its efforts to sell people on the benefits of CBD, which is found in both marijuana and hemp, two versions of the Cannabis sativa plant. CBD is popping up in products in pet stores, coffee shops and the health and beauty sections of mainstream grocery stores. It’s even being brewed into beer. I left the shop with a $5 bottle of water infused with “5,000,000 nanograms” of CBD. So far, messages of CBD’s purported health benefits come from people trying to sell CBD products — not from scientists, says Margaret Haney, a neurobiologist who directs the Marijuana Research Laboratory at Columbia University. A gaping chasm separates the surging CBD market and the scientific evidence backing it. While there are reasons to be excited about CBD, the science just isn’t there yet, Haney says. |© Society for Science & the Public 2000 - 2019

Keyword: Drug Abuse; Sleep
Link ID: 26084 - Posted: 03.27.2019

Laura Sanders SAN FRANCISCO — Seizures during sleep can scramble memories — a preliminary finding that may help explain why people with epilepsy sometimes have trouble remembering. The sleeping brain normally rehashes newly learned material, a nocturnal rehearsal that strengthens those memories. Neuroscientist Jessica Creery and her colleagues forced this rehearsal by playing certain sounds while nine people with epilepsy learned where on a screen certain pictures of common objects were located. Then, while the subjects later slept, the researchers played the sounds to call up some of the associated memories. This sneaky method of strengthening memories, called targeted memory reactivation, worked as expected for five people who didn’t have seizures during the process. When these people woke up, they remembered the picture locations reactivated by a tone better than those that weren’t reactivated during sleep, said Creery, of Northwestern University in Evanston, Ill. She presented the research March 25 at the annual meeting of the Cognitive Neuroscience Society. The opposite was true, however, for four people who had mild seizures, detected only by electrodes implanted deep in the brain, while they slept. For these people, memory reactivation during sleep actually worsened memories, making the reactivated memories weaker than the memories that weren’t reactivated during sleep. The combination of seizures and memory reactivation “seems like it’s actually scrambling the memory,” Creery says, a finding that suggest that seizures somehow accelerate forgetting. |© Society for Science & the Public 2000 - 2019

Keyword: Sleep; Epilepsy
Link ID: 26083 - Posted: 03.27.2019