By John Horgan In my freshman humanities class, I make students ponder the pros and cons of knowledge. We talk about Plato’s parable, in which people imprisoned in a cave mistake shadows projected on a wall for reality. I ask, Assuming we’re in the cave, how many of you want to escape? Most students dutifully raise their hands, because of course truth is good and ignorance is bad. Then I ask, What if the cave is comfy and the outside world nasty? I bring up The Matrix, in which humans live in a computer simulation, called the Matrix, constructed by evil machines. A band of rebels who have escaped this digital cave is trying to liberate other humans. A rebel named Cypher gives Agent Smith, nasty sentient software created by the machines, information to help him capture the rebels. Agent Smith asks Cypher what he wants for betraying his comrades, and Cypher says he doesn't want to live in reality any more. It’s ugly and stressful, and he hates being bossed around by the rebel leader. Cypher asks for a happy simulated life in the Matrix. Here is an excerpt from his dialogue with Agent Smith, which takes place in a virtual restaurant: Cypher: You know, I know this steak doesn't exist. I know that when I put it in my mouth, the Matrix is telling my brain that it is juicy and delicious. After nine years, you know what I realize? Ignorance is bliss. Agent Smith: Then we have a deal? Cypher: I don't want to remember nothing. Nothing. You understand? And I want to be rich. You know, someone important, like an actor. Agent Smith: Whatever you want.

Keyword: Alzheimers; Consciousness
Link ID: 25885 - Posted: 01.21.2019

Jonathan Lambert Pain is a complicated experience. Our skin and muscles sense it, just like they sense softness or warmth. But unlike other sensations, the experience of pain is distinctly unpleasant. Pain has to hurt for us to pay attention to it, and avoid hurting ourselves further. But for people in chronic pain, the pain has largely lost its purpose. It just hurts. While it has long been understood how nerves signal pain to the brain, scientists haven't known how the brain adds a layer of unpleasantness. Findings of a study published Thursday in Science offer an answer. A research team from Stanford University pinpointed the neurons in mouse brains that make pain hurt and were able to alter these neurons in a way that reduced the unpleasantness of pain without eliminating the sensation. The study lays the groundwork for future research into more targeted pain treatments. "This study is a major advance," says Irene Tracey, a pain neuroscientist at Oxford University who wasn't involved in the study. "It was a tour de force and a welcome addition to understanding this complex and major problem." Stanford neuroscientist Grégory Scherrer, who co-led the study, started the search for pain neurons in the amygdala — the slim, almond-shaped region scientists know regulates many emotions. The challenge for Scherrer was to sift through the tangle of neurons there and identify the ones associated with pain. © 2019 npr

Keyword: Pain & Touch
Link ID: 25884 - Posted: 01.19.2019

By David Blum Many of us have personally experienced or witnessed the impact of Parkinson’s disease (PD), a movement disorder that affects nearly 10 million people worldwide. This chronic, progressive neurodegenerative disorder leads to disability from motor impairments, such as tremors, rigidity, absence or slowness of movement and impaired balance, as well as from non-motor symptoms including sleep disruption, gastrointestinal issues, sexual dysfunction or loss of sense of smell or taste, to name a few. The ideal outcome of PD clinical research would be to find a cure. But researchers are also looking at novel ways to administer proven Parkinson’s medicines in order to help people living with the disease better control their symptoms and maintain their regular, daily activities. The brain cells that die from PD are responsible for producing dopamine, a neurotransmitter involved in complex behaviors including motor coordination, addiction and motivation. As a result, treatment typically includes the use of levodopa—a medication that is converted into dopamine in the brain and relieves PD symptoms. For the first few years after diagnosis, many individuals’ symptoms are well controlled by levodopa. The average age of onset is 60, but some people are diagnosed at 40 or even younger, potentially requiring treatment for decades. Over time, a patient’s response to levodopa changes, and the therapeutic window, or period when levodopa is effective, narrows, often leading to the prescription of additional levodopa or more frequent dosing of levodopa to manage symptoms. © 2019 Scientific American

Keyword: Parkinsons
Link ID: 25883 - Posted: 01.19.2019

Aimee Cunningham As public health officials tackle opioid addiction and overdoses, another class of prescription drugs has been contributing to a growing number of deaths across the United States. Benzodiazepines, such as Valium and Xanax, are commonly prescribed for anxiety and insomnia. The drugs are also highly addictive and can be fatal, especially when combined with alcohol or opioids. In the latest sign of the drug’s impact, the number of overdose deaths involving “benzos” rose from 0.54 per 100,000 in 1999 to 5.02 per 100,000 in 2017 among women aged 30 to 64, researchers report January 11 in the Morbidity and Mortality Weekly Report. That’s a spike of 830 percent, surpassed only by increases seen in overdose deaths involving synthetic opioids or heroin. Overall, there were 10,684 overdose deaths involving benzodiazepines in the United States in 2016, according to the National Institute on Drug Abuse. In 1999, the total was 1,135. Benzodiazepines have a sedating effect, and are particularly dangerous when used with other drugs that slow breathing, such as opioids and alcohol. In combination, the substances can “cause people to fall asleep and essentially never wake up again,” says Anna Lembke, an addiction psychiatrist at Stanford University School of Medicine. Benzos and opioids are often prescribed together, and opioids contribute to 75 percent of overdose deaths involving benzos. The rising number of deaths involving benzos hasn’t stopped the flow of prescriptions. The number of U.S. adults who filled a prescription for benzos rose from 8.1 million in 1996 to 13.5 million in 2013, a jump of 67 percent, a study in the American Journal of Public Health in 2016 found. The quantity of benzos acquired more than tripled over the same time. |© Society for Science & the Public 2000 - 2019.

Keyword: Drug Abuse; Stress
Link ID: 25882 - Posted: 01.19.2019

By Abby Goodnough WASHINGTON — A new study offers some of the strongest evidence yet of the connection between the marketing of opioids to doctors and the nation’s addiction epidemic. It found that counties where opioid manufacturers offered a large number of gifts and payments to doctors had more overdose deaths involving the drugs than counties where direct-to-physician marketing was less aggressive. The study, published Friday in JAMA Network Open, said the industry spent about $40 million promoting opioid medications to nearly 68,000 doctors from 2013 through 2015, including by paying for meals, trips and consulting fees. And it found that for every three additional payments that companies made to doctors per 100,000 people in a county, overdose deaths involving prescription opioids there a year later were 18 percent higher. Even as the opioid epidemic was killing more and more Americans, such marketing practices remained widespread. From 2013 through 2015, roughly 1 in 12 doctors received opioid-related marketing, according to the study, including 1 in 5 family practice doctors. The authors, from Boston Medical Center and New York University School of Medicine, found that counties where doctors received more industry marketing subsequently saw an increase in both the number of opioids prescribed and opioid-related overdose deaths. In response to the study, Dr. John Cullen, president of the American Academy of Family Physicians, said, “A limitation of the study, as acknowledged by the authors, is the many unknown variables that prevent drawing a direct causal link between pharmaceutical marketing and opioid-related deaths.” He added, “We’re very much aware of the critical and devastating impact of the opioid epidemic and work every day, with every patient interaction, to fight it. At the same time, we must protect the physician’s ability to provide adequate pain management.” © 2019 The New York Times Company

Keyword: Drug Abuse
Link ID: 25881 - Posted: 01.19.2019

By Diana Kwon o For the longest time the cerebellum, a dense, fist-size formation located at the base of the brain, never got much respect from neuroscientists. For about two centuries the scientific community believed the cerebellum (Latin for “little brain”), which contains approximately half of the brain’s neurons, was dedicated solely to the control of movement. In recent decades, however, the tide has started to turn, as researchers have revealed details of the structure’s role in cognition, emotional processing and social behavior. The longstanding interest in the cerebellum can be seen in the work of French physiologist Marie Jean Pierre Flourens—(1794–1867). Flourens removed the cerebella of pigeons and found the birds became unbalanced, although they could still move. Based on these observations, he concluded the cerebellum was responsible for coordinating movements. “[This] set the dogma that the cerebellum was involved in motor coordination,” says Kamran Khodakhah, a neuroscientist at Albert Einstein College of Medicine, adding: “For many years, we ignored the signs that suggested it was involved in other things.” One of the strongest pieces of evidence for the cerebellum’s broader repertoire emerged around two decades ago, when Jeremy Schmahmann, a neurologist at Massachusetts General Hospital, described cerebellar cognitive affective syndrome after discovering behavioral changes such as impairments in abstract reasoning and regulating emotion in individuals whose cerebella had been damaged. Since then this line of study has expanded. There has been human neuroimaging work showing the cerebellum is involved in cognitive processing and emotional control—and investigations in animals have revealed, among other things, that the structure is important for the normal development of social and cognitive capacities. Researchers have also linked altered cerebellar function to addiction, autism and schizophrenia.

Keyword: Drug Abuse; Emotions
Link ID: 25880 - Posted: 01.19.2019

Rachel Zamzow Patterns of brain activity in people with autism are unusually consistent over seconds—and even years, two new studies suggest. One study shows that patterns of connectivity remain stable in autistic adolescents, whereas they tend to change and specialize in controls. The other study found that connections remain fixed longer in people with autism than in controls. Both focused on so-called “functional connectivity,” the extent to which the activity of pairs of brain areas is synchronized. Together, the studies may help untangle seemingly contradictory findings on connectivity in autism: reports of both underconnectivity and overconnectivity in the brain. “Maybe the primary abnormality isn’t just that things are too weakly or strongly connected, that it has more to do with the timing of brain connections,” says Jeff Anderson, professor of radiology at the University of Utah, who led the second study. The studies also highlight the importance of measuring brain activity over varying time periods and at different ages. Researchers who home in on a single age may overlook differences that appear over time, says Mirella Dapretto, professor of psychiatry and biobehavioral sciences at the University of California, Los Angeles, and lead researcher on the adolescent study. “You miss some of the bigger picture.” Studying brain activity over time provides a rare window into the development of connectivity. © 1986 - 2019 The Scientist

Keyword: Autism; Development of the Brain
Link ID: 25879 - Posted: 01.19.2019

Laura Sanders Using laser light, ballooning tissue and innovative genetic tricks, scientists are starting to force brains to give up their secrets. By mixing and matching powerful advances in microscopy and cell biology, researchers have imaged intricate details of individual nerve cells in fruit flies and mice, and even controlled small groups of nerve cells in living mice. The techniques, published in two new studies, represent big steps forward for understanding how the brain operates, says molecular neuroscientist Hongkui Zeng of the Allen Institute for Brain Science in Seattle. “Without this kind of technology, we were only able to look at the soup level,” in which diverse nerve cells, or neurons, are grouped and analyzed together, she says. But the new studies show that nerve cells can be studied individually. That zoomed-in approach will begin to uncover the tremendous diversity that’s known to exist among cells, says Zeng, who was not involved in the research. “That is where the field is going. It’s very exciting to see that technologies are now enabling us to do that,” she says. These novel abilities came from multiple tools. At Howard Hughes Medical Institute’s Janelia Research Campus in Ashburn, Va., physicist Eric Betzig and his colleagues had developed a powerful microscope that can quickly peer deep into layers of brain tissue. Called a lattice light sheet microscope, the rig sweeps a thin sheet of laser light down through the brain, revealing cells’ structures. But like any microscope, it hits a wall when structures get really small, unable to resolve the most minute aspects of the scene. |© Society for Science & the Public 2000 - 2019.

Keyword: Brain imaging
Link ID: 25878 - Posted: 01.18.2019

By: Brenna Hassinger-Das, Ph.D., and Kathryn Hirsh-Pasek, Ph.D. In 1954, Walt Disney was the first to envision a new form of entertainment that melded traditional fun and education—a form that he dubbed “edutainment.” By the latter part of the 20th century, this form had morphed into educational toys and games, a multi-billion-dollar industry that is projected to capture a full 36 percent of the global toy market share by 2022. Nowhere is this trend more apparent than in the explosion of digital apps: of the 2.2 million apps available in the Apple Store, roughly 176,000—8.5 percent—are loosely designated as “ educational. ” Their growth continues, with annual increases of 10 percent expected through 2021. Whether called edutainment, educational toys, or the digital learning revolution, this trend shares the implicit philosophy that mixing fun and learning will offer a kind of “brain training” that will enhance children’s thinking and amplify their learning potential. But there are many questions before us. What do manufacturers and marketers mean when they designate a product “ educational? ” What relevant research in the science of learning has been done? Is there a standard definition of educational value that guides the field? Indeed, a framework we use highlights when toys might sculpt mental muscle and when products are likely to be total imposters. This framework helps us elucidate which educational and digital toys are likely to confer benefits for children.

Keyword: Learning & Memory; Development of the Brain
Link ID: 25877 - Posted: 01.18.2019

A new study in rodents has shown that the brain’s cerebellum—known to play a role in motor coordination—also helps control the brain’s reward circuitry. Researchers found a direct neural connection from the cerebellum to the ventral tegmental area (VTA) of the brain, which is an area long known to been involved in reward processing and encoding. These findings, published in Science, demonstrate for the first time that the brain’s cerebellum plays a role in controlling reward and social preference behavior, and sheds new light on the brain circuits critical to the affective and social dysfunction seen across multiple psychiatric disorders. The research was funded by the National Institute of Mental Health (NIMH), part of the National Institutes of Health. “This type of research is fundamental to deepening our understanding of how brain circuit activity relates to mental illnesses,” said Joshua A. Gordon, M.D., Ph.D., director of NIMH. “Findings like the ones described in this paper help us learn more about how the brain works, a key first step on the path towards developing new treatments.” The cerebellum plays a well-recognized role in the coordination and regulation of motor activity. However, research has also suggested that this brain area contributes to a host of non-motor functions. For example, abnormalities in the cerebellum have been linked to autism, schizophrenia, and substance use disorders, and brain activation in the cerebellum has been linked to motivation, social and emotional behaviors, and reward learning, each of which can be disrupted in psychiatric disorders.

Keyword: Drug Abuse; Emotions
Link ID: 25876 - Posted: 01.18.2019

By Benedict Carey Nearly a century after the film “Reefer Madness” alarmed the nation, some policymakers and doctors are again becoming concerned about the dangers of marijuana, although the reefers are long gone. Experts now distinguish between the “new cannabis” — legal, highly potent, available in tabs, edibles and vapes — and the old version, a far milder weed passed around in joints. Levels of T.H.C., the chemical that produces marijuana’s high, have been rising for at least three decades, and it’s now possible in some states to buy vape cartridges containing little but the active ingredient. The concern is focused largely on the link between heavy usage and psychosis in young people. Doctors first suspected a link some 70 years ago, and the evidence has only accumulated since then. In a forthcoming book, “Tell Your Children,” Alex Berenson, a former Times reporter, argues that legalization is putting a generation at higher risk of schizophrenia and other psychotic syndromes. Critics, including leading researchers, have called the argument overblown, and unfaithful to the science. Can cannabis use cause psychosis? Yes, but so can overuse of caffeine, nicotine, alcohol, stimulants and hallucinogens. Psychosis is a symptom: a temporary disorientation that resembles a waking dream, with odd, imagined sights and sounds, often accompanied by paranoia or an ominous sensation. The vast majority of people who have this kind of psychotic experience do not go on to develop a persistent condition such as schizophrenia, which is characterized by episodes of psychosis that recur for years, as well as cognitive problems and social withdrawal. © 2019 The New York Times Company

Keyword: Drug Abuse; Schizophrenia
Link ID: 25875 - Posted: 01.18.2019

By Elie Dolgin The compound eyes of the common fruit fly are normally brick red. But in neurologist Tom Lloyd's lab at Johns Hopkins University School of Medicine in Baltimore, Maryland, many of the fly eyes are pocked with white and black specks, a sign that neurons in each of their 800-odd eye units are shriveling away and dying. Those flies have the genetic equivalent of amyotrophic lateral sclerosis (ALS), the debilitating neurodegenerative disorder also known as Lou Gehrig's disease, and their eyes offer a window into the soul of the disease process. By measuring the extent of damage to each insect's eyes, researchers can quickly gauge whether a drug, genetic modification, or some other therapeutic intervention helps stop neuronal loss. Those eyes have also offered an answer to the central mystery of ALS: just what kills neurons—and, ultimately, the patient. The flies carry a mutation found in about 40% of ALS patients who have a family history of the disease, and in about 10% of sporadic cases. The mutation, in a gene called C9orf72, consists of hundreds or thousands of extra copies of a short DNA sequence, just six bases long. They lead to unusually large strands of RNA that glom onto hundreds of proteins in the cell nucleus, putting them out of action. Some of those RNA-ensnared proteins, Lloyd and his Hopkins colleague Jeffrey Rothstein hypothesized, might hold the key to ALS. © 2018 American Association for the Advancement of Science

Keyword: ALS-Lou Gehrig's Disease
Link ID: 25874 - Posted: 01.17.2019

Using a novel patient-specific stem cell-based therapy, researchers at the National Eye Institute (NEI) prevented blindness in animal models of geographic atrophy, the advanced "dry" form of age-related macular degeneration (AMD), which is a leading cause of vision loss among people age 65 and older. The protocols established by the animal study, published January 16 in Science Translational Medicine (STM), set the stage for a first-in-human clinical trial testing the therapy in people with geographic atrophy, for which there is currently no treatment. "If the clinical trial moves forward, it would be the first ever to test a stem cell-based therapy derived from induced pluripotent stem cells (iPSC) for treating a disease," said Kapil Bharti, Ph.D., a Stadtman Investigator and head of the NEI Unit on Ocular and Stem Cell Translational Research. Bharti was the lead investigator for the animal-model study published in STM. The NEI is part of the National Institutes of Health. The therapy involves taking a patient’s blood cells and, in a lab, converting them into iPS cells, which can become any type of cell in the body. The iPS cells are programmed to become retinal pigment epithelial cells, the type of cell that dies early in the geographic atrophy stage of macular degeneration. RPE cells nurture photoreceptors, the light-sensing cells in the retina. In geographic atrophy, once RPE cells die, photoreceptors eventually also die, resulting in blindness. The therapy is an attempt to shore up the health of remaining photoreceptors by replacing dying RPE with iPSC-derived RPE.

Keyword: Vision
Link ID: 25873 - Posted: 01.17.2019

Nicola Davis Moving more might help to keep people’s brains sharp as they age – even in the face of dementia, researchers have said. Scientists have found older adults fared better when it came to cognitive tasks if they clocked up higher levels of daily activity on a wrist-based tracker – something the researchers said picked up everything from exercising to mundane tasks like chopping onions. What’s more, the benefits of movement remained even when the team took into account the level of tell-tale signs of Alzheimer’s and other dementia-related diseases in the brain. Co-author of the Rush University study, Dr Aron Buchman, said the results showed that “even though we don’t have a treatment for Alzheimer’s disease pathology, and we know people are accumulating it, you can mitigate the deleterious effects … by having more activity.” But it’s not only moving more which is linked to better scores for traits like thinking, comprehension and and memory: the team found better motor abilities, as measured through tasks like the strength in gripping items or speed of turning on the spot, also seemed to offer protection when it comes to cognitive prowess. The team say previous work has shown that moving more is linked to a lower risk of dementia, and slows the decline in thinking and memory skills in older adults as they age – but the latest research goes further. © 2019 Guardian News and Media Limited

Keyword: Alzheimers
Link ID: 25872 - Posted: 01.17.2019

By Nicholas Bakalar Sleeping less than six hours a night, and sleeping poorly, are associated with hardening of the arteries, a new study has found. Researchers used accelerometers attached to the waists of 3,974 healthy men and women, average age 46, to monitor the duration and quality of their sleep over seven nights. All underwent physical exams and three-dimensional ultrasound, an imaging system that evaluates blood flow through the blood vessels. The study is in the Journal of the American College of Cardiology. After controlling for smoking, diabetes, fasting glucose, cholesterol and many other factors, they found that compared with people who slept seven to eight hours a night, those who slept less than six hours were 27 percent more likely to be in the highest one-third for the amount of plaque in their arteries. The scientists also found that various blood markers of inflammation were higher in those who got the least sleep. The people who moved the most during sleep also had higher accumulations of plaque than those who slept soundly. “We’re detecting disease in its earliest stages in apparently healthy young people,” said a co-author, Dr. Valentin Fuster, director of the Mount Sinai Heart Center. “This is something that was done only at autopsy until now. This is an alarm system, telling you that there is another cardiovascular risk factor you should pay attention to.” © 2019 The New York Times Company

Keyword: Sleep
Link ID: 25871 - Posted: 01.17.2019

By Kelly Servick In multiple sclerosis (MS), a disease that strips away the sheaths that insulate nerve cells, the body’s immune cells come to see the nervous system as an enemy. Some drugs try to slow the disease by keeping immune cells in check, or by keeping them away from the brain. But for decades, some researchers have been exploring an alternative: wiping out those immune cells and starting over. The approach, called hematopoietic stem cell transplantation (HSCT), has long been part of certain cancer treatments. A round of chemotherapy knocks out the immune system and an infusion of stem cells—either from a patient’s own blood or, in some cases, that of a donor—rebuilds it. The procedure is already in use for MS and other autoimmune diseases at several clinical centers around the world, but it has serious risks and is far from routine. Now, new results from a randomized clinical trial suggest it can be more effective than some currently approved MS drugs. “A side-by-side comparison of this magnitude had never been done,” says Paolo Muraro, a neurologist at Imperial College London who has also studied HSCT for MS. “It illustrates really the power of this treatment—the level of efficacy—in a way that’s very eloquent.” Nearly 30 years ago, when hematologist Richard Burt saw how HSCT worked in patients with leukemia and lymphoma, he was struck by a curious effect: After those patients rebuilt their immune systems, their childhood vaccines no longer protected them, recalls Burt, now at Northwestern University’s Feinberg School of Medicine in Evanston, Illinois. Without a new vaccination, the new immune cells wouldn’t recognize viruses such as measles and mumps and launch a prompt counterattack. That suggested that in the case of an autoimmune disease, reseeding the immune system might help the body “forget” that its own cells were the enemy. © 2018 American Association for the Advancement of Science

Keyword: Multiple Sclerosis
Link ID: 25870 - Posted: 01.16.2019

By Catherine L. Caldwell-Harris, Ph.D. Does the language you speak influence how you think? This is the question behind the famous linguistic relativity hypothesis, that the grammar or vocabulary of a language imposes on its speakers a particular way of thinking about the world. The strongest form of the hypothesis is that language determines thought. This version has been rejected by most scholars. A weak form is now thought to be obviously true, which is that if one language has a specific vocabulary item for a concept but another language does not, then speaking about the concept may happen more frequently or more easily. For example, if someone explained to you, an English speaker, the meaning for the German term Schadenfreude, you could recognize the concept, but you may not have used the concept as regularly as a comparable German speaker. Scholars are now interested in whether having a vocabulary item for a concept influences thought in domains far from language, such as visual perception. Consider the case of the "Russian blues." While English has a single word for blue, Russian has two words, goluboy for light blue and siniy for dark blue. These are considered "basic level" terms, like green and purple, since no adjective is needed to distinguish them. Lera Boroditsky and her colleagues displayed two shades of blue on a computer screen and asked Russian speakers to determine, as quickly as possible, whether the two blue colors were different from each other or the same as each other. The fastest discriminations were when the displayed colors were goluboy and siniy, rather than two shades of goluboy or two shades of siniy. The reaction time advantage for lexically distinct blue colors was strongest when the blue hues were perceptually similar.

Keyword: Language; Vision
Link ID: 25869 - Posted: 01.16.2019

By Gretchen Reynolds A hormone that is released during exercise may improve brain health and lessen the damage and memory loss that occur during dementia, a new study finds. The study, which was published this month in Nature Medicine, involved mice, but its findings could help to explain how, at a molecular level, exercise protects our brains and possibly preserves memory and thinking skills, even in people whose pasts are fading. Considerable scientific evidence already demonstrates that exercise remodels brains and affects thinking. Researchers have shown in rats and mice that running ramps up the creation of new brain cells in the hippocampus, a portion of the brain devoted to memory formation and storage. Exercise also can improve the health and function of the synapses between neurons there, allowing brain cells to better communicate. In people, epidemiological research indicates that being physically active reduces the risk for Alzheimer’s disease and other dementias and may also slow disease progression. But many questions remain about just how exercise alters the inner workings of the brain and whether the effects are a result of changes elsewhere in the body that also happen to be good for the brain or whether the changes actually occur within the brain itself. Those issues attracted the attention of an international consortium of scientists, some neuroscientists, others cell biologists, all of whom were focused on preventing, treating and understanding Alzheimer’s disease. Those concerns had brought a hormone called irisin into their sphere of interest. Irisin, first identified in 2012 and named for Iris, the gods’ messenger in Greek mythology, is produced by muscles during exercise. The hormone jump-starts multiple biochemical reactions throughout the body, most of them related to energy metabolism. © 2019 The New York Times Company

Keyword: Alzheimers; Hormones & Behavior
Link ID: 25868 - Posted: 01.16.2019

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