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Hannah Devlin Science correspondent The death in 2002 of the former England and West Bromwich Albion striker Jeff Astle from degenerative brain disease placed the spotlight firmly on the possibility of a link between heading footballs and the risk of dementia. The coroner at the inquest ruled that Astle, 59, died from an “industrial disease” brought on by the repeated trauma of headers, and a later examination of Astle’s brain appeared to bear out this conclusion. At that time there was sparse scientific data on the issue, but since then the balance of evidence has steadily tipped further in favour of a link. It has been shown that even single episodes of concussion can have lifelong consequences. Children in Scotland could be banned from heading footballs over dementia link Read more A 2016 study based on health records of more than 100,000 people in Sweden found that after a single diagnosed concussion people were more likely to have mental health problems and less likely to graduate from high school and college. Other research has shown that people in prison or homeless are more likely to have had a past experience of concussion. In 2017, researchers from University College London examined postmortem the brains of six former footballers who had developed dementia. They found signs of brain injury called chronic traumatic encephalopathy (CTE) in four cases. Last year a study by a team at Glasgow University found that former professional footballers were three and a half times more likely to die from dementia and other serious neurological diseases. The study was the largest ever, based on the health records of 7,676 ex-players and 23,000 members of the public, and was possibly the trigger for the Scottish FA’s plan to follow US soccer in banning heading the ball for young players. © 2020 Guardian News & Media Limited

Keyword: Brain Injury/Concussion
Link ID: 26969 - Posted: 01.17.2020

By Betsy Mason Despite weighing less than half an ounce, mountain chickadees are able to survive harsh winters complete with subzero temperatures, howling winds and heavy snowfall. How do they do it? By spending the fall hiding as many as 80,000 individual seeds, which they then retrieve — by memory — during the winter. Their astounding ability to keep track of that many locations puts their memory among the most impressive in the animal kingdom. It also makes chickadees an intriguing subject for animal behavior researchers. Cognitive ecologist Vladimir Pravosudov of the University of Nevada, Reno, has dedicated his career to studying this tough little bird’s amazing memory. Writing in 2013 on the cognitive ecology of food caching in the Annual Review of Ecology, Evolution, and Systematics, he and coauthor Timothy Roth argued that answers to big questions about the evolution of cognition may lie in the brains of these little birds. In July, at a meeting of the Animal Behavior Society in Chicago, Pravosudov presented his group’s latest research on the wild chickadees that live in the Sierra Nevada mountains. He and his graduate students were able to show for the first time that an individual bird’s spatial memory has a direct impact on its survival. The team did this by building an experimental contraption that uses radio-frequency identification (RFID) technology and electronic leg bands to test individual birds’ memory in the wild and then track their longevity. The researchers found that the birds with the best memory were most likely to survive the winter. What are some of the big ideas driving your work on chickadees? If some species are smart, or not smart, the question is: Why? Cognitive ecologists like me are specifically trying to figure out which ecological factors may have shaped the evolution of these differences in cognition. In other words, the idea is to understand the ecological and evolutionary reasons for variation in cognition. © 2020 Annual Reviews, Inc

Keyword: Learning & Memory
Link ID: 26968 - Posted: 01.17.2020

By Karen Weintraub Alzheimer's disease has long been characterized by the buildup of two distinct proteins in the brain: first beta-amyloid, which accumulates in clumps, or plaques, and then tau, which forms toxic tangles that lead to cell death. But how beta-amyloid leads to the devastation of tau has never been precisely clear. Now a new study at the University of Alabama at Birmingham appears to describe that missing mechanism. The study details a cascade of events. Buildup of beta-amyloid activates a receptor that responds to a brain chemical called norepinephrine, which is commonly known for mobilizing the brain and body for action. Activation of this receptor by both beta-amyloid and norepinephrine boosts the activity of an enzyme that activates tau and increases the vulnerability of brain cells to it, according to the study, published in Science Translational Medicine. Essentially, beta-amyloid hijacks the norepinephrine pathway to trigger a toxic buildup of tau, says Qin Wang, the study’s senior author and a professor of neuropharmacology in the department of cell, developmental and integrative biology at the University of Alabama at Birmingham. “We really show that this norepinephrine is a missing piece of this whole Alzheimer’s disease puzzle,” she says. This cascade explains why so many previous Alzheimer’s treatments have failed, Wang says. Most of the drugs developed in recent decades have targeted the elimination of beta-amyloid. But the new research suggests that norepinephrine amplifies the damage wrought by that protein. © 2020 Scientific American

Keyword: Alzheimers
Link ID: 26967 - Posted: 01.17.2020

Ashley Yeager About four years ago, pathologist Matthew Anderson was examining slices of postmortem brain tissue from an individual with autism under a microscope when he noticed something extremely odd: T cells swarming around a narrow space between blood vessels and neural tissue. The cells were somehow getting through the blood-brain barrier, a wall of cells that separates circulating blood from extracellular fluid, neurons, and other cell types in the central nervous system, explains Anderson, who works at Beth Israel Deaconess Medical Center in Boston. “I just have seen so many brains that I know that this is not normal.” He soon identified more T-cell swarms, called lymphocytic cuffs, in a few other postmortem brains of people who had been diagnosed with autism. Not long after that, he started to detect another oddity in the brain tissue—tiny bubbles, or blebs. “I’d never seen them in any other brain tissue that I’ve looked at for many, many different diseases,” he says. Anderson began to wonder whether the neurological features he was observing were specific to autism. To test the idea, he and his colleagues examined postmortem brain tissue samples from 25 people with autism spectrum disorder (ASD) and 30 developmentally normal controls. While the lymphocytic cuffs only sporadically turned up in the brains of neurotypical individuals, the cuffs were abundant in a majority of the brains from individuals who had had ASD. Those same samples also had blebs that appeared in the same spots as the cuffs. Staining the brain tissue revealed that the cuffs were filled with an array of different types of T cells, while the blebs contained fragments of astrocytes, non-neuronal cells that support the physical structure of the brain and help to maintain the blood-brain barrier. © 1986–2020 The Scientist

Keyword: Autism; Neuroimmunology
Link ID: 26966 - Posted: 01.17.2020

Merrit Kennedy Smoking can be an easy habit to pick up and a hard one to quit. Here's the good news — there are decades of research on how to drop the habit. And we heard from hundreds of former smokers about how they did it. If you've tried to quit before, and it didn't work out, don't let that discourage you from trying again. It's common for quitting to take multiple attempts. "It's not a one time event. It is a process," says Gary Tedeschi, the clinical director at the California Smokers' Helpline. "And if I could say nothing else, I would say never ever stop trying to quit." We heard about a wide range of methods that helped people quit—and the truth is that no one method will work for everyone. But it's clear that having a roadmap for how you want to quit is going to boost your chances of succeeding. 1. You need a plan "A lot of smokers, when they are thinking about quitting, they sort of dive in without a plan," says Yvonne Prutzman, a scientist from the National Cancer Institute's Tobacco Control Research Branch. "And maybe the plan is to rely on willpower — but that makes it a lot harder for them," she adds. Your plan might be pretty personal. People quit many different ways — and reach the conclusion that they need to quit for very different reasons. For example, for Stacey Moore from Georgia, a serious health scare prompted her decision. "Just a couple of weeks ago I woke up with what I thought was a cancerous lump in my throat," she tells NPR. "It turned out to just be tonsillitis but it scared me enough that I knew I just had to stop, I just can't play this roulette game anymore." Others, like Greg Moulton from South Carolina, spent months or even years preparing to quit, slowly reducing the amount of nicotine they were taking in every day. "You slay the beast slowly and let it bleed to death on its own," he says. © 2020 npr

Keyword: Drug Abuse
Link ID: 26965 - Posted: 01.17.2020

Hannah Devlin Science correspondent A groundbreaking brain-scanning technique has uncovered evidence that suggests schizophrenia is linked to a loss of connections between brain cells. Scientists had previously suspected a breakdown in the connections between neurons played a role in the condition, based on postmortem studies. The latest research, the first to find evidence for this in the brains of living people, could pave the way for new and better treatment. Prof Oliver Howes from the MRC London Institute of Medical Sciences, Imperial College London and King’s College London, who led the study, said: “Our current treatments for schizophrenia target only one aspect of the disease: the psychotic symptoms. “But the debilitating cognitive symptoms, such as loss of abilities to plan and remember, often cause much more long-term disability and there’s no treatment for them at the moment.” Howes believes the loss of connections, known as synapses, between brain cells, could be responsible for this broader array of symptoms. The study, published in Nature Communications, focused on measuring a protein found in synapses called SV2A, which has been shown to be a good marker of the overall density of connections in the brain. They used a tracer that binds to the protein and which emits a signal that can be picked up by a PET brain scan, which provided an indirect measure of the density of connections. The team scanned 18 adults with schizophrenia and compared them with 18 people without the condition. They found that levels of SV2A were significantly lower in the front of the brain – the region involved in planning – in people with schizophrenia. © 2020 Guardian News & Media Limited

Keyword: Schizophrenia
Link ID: 26964 - Posted: 01.15.2020

By Laura Sanders A parasite common in cats can eliminate infected mice’s fear of felines — a brain hijack that leads to a potentially fatal attraction. But this cat-related boldness (SN: 9/18/13) isn’t the whole story. Once in the brain, the single-celled parasite Toxoplasma gondii makes mice reckless in all sorts of dangerous scenarios, researchers write January 14 in Cell Reports. Infected mice spent more time in areas that were out in the open, exposed places that uninfected mice usually avoid. Infected mice also prodded an experimenter’s hand inside a cage — an intrusion that drove uninfected mice to the other side of the cage. T. gondii–infected mice were even unfazed by an anesthetized rat, a mouse predator, the researchers from the University of Geneva and colleagues found. And infected mice spent more time than uninfected mice exploring the scents of foxes and relatively harmless guinea pigs. The extent of mice’s infections, measured by the load of parasite cysts in the brain, seemed to track with the behavior changes, the researchers report. Toxoplasma gondiiToxoplasma gondii, tweaked to glow green, was isolated from the brain of an infected mouse.Pierre-Mehdi Hammoudi, Damien Jacot The parasite needs to get into the guts of cats to sexually reproduce. Other animals can become infected by ingesting T. gondii through direct or indirect contact with cat feces. The parasite can then spread throughout the body and ultimately form cysts in the brain. People can become infected with T. gondii, though usually not as severely as mice. Some studies have hinted, however, at links between the parasite and human behaviors such as inattention and suicide, as well as mental disorders such as schizophrenia. © Society for Science & the Public 2000–2020

Keyword: Emotions
Link ID: 26963 - Posted: 01.15.2020

By Tom Siegfried Long before Apple watches, grandfather clocks or even sundials, nature provided living things with a way to tell time. Life evolved on a rotating world that delivered alternating light and darkness on a 24-hour cycle. Over time, cellular chemistry tuned itself to that rhythm. Today, circadian rhythms — governed by a master timekeeper in the brain — guide sleeping schedules and mealtimes and influence everything from diet to depression to the risk of cancer. While an Apple watch can monitor a few vital functions such as your heart rate, your body’s natural clock controls or affects nearly all of them. Lately, research by Takahashi and others has suggested strategies for manipulating the body’s clock to correct circadian-controlled chemistry when it goes awry. Such circadian interventions could lead to relief for shift workers, antidotes for jet lag, and novel treatments for mood disorders and obesity, not to mention the prospect of counteracting aging. Prime weapons for the assault on clock-related maladies, Takahashi believes, can be recruited from an arsenal of small molecules, including some existing medical drugs. “Researchers are increasingly interested in developing small molecules to target the circadian system directly for therapeutic gains,” Takahashi and coauthors Zheng Chen and Seung-Hee Yoo wrote in the 2018 Annual Review of Pharmacology and Toxicology. In sophisticated life-forms (such as mammals), central control of the body’s clock resides in a small cluster of nerve cells within the brain’s hypothalamus. That cluster, called the suprachiasmatic nucleus — SCN for short — is tuned to the day-night signal by light transmitted via the eyes and the optic nerve. But the SCN does not do the job alone. It’s the master clock, for sure, but satellite timekeepers operate in all kinds of cells and body tissues. © 2020 Annual Reviews, Inc

Keyword: Biological Rhythms
Link ID: 26962 - Posted: 01.15.2020

Matthew Schafer and Daniela Schiller How do animals, from rats to humans, intuit shortcuts when moving from one place to another? Scientists have discovered mental maps in the brain that help animals picture the best routes from an internalized model of their environments. Physical space is not all that is tracked by the brain's mapmaking capacities. Cognitive models of the environment may be vital to mental processes, including memory, imagination, making inferences and engaging in abstract reasoning. Most intriguing is the emerging evidence that maps may be involved in tracking the dynamics of social relationships: how distant or close individuals are to one another and where they reside within group hierarchies. We are often told that there are no shortcuts in life. But the brain—even the brain of a rat—is wired in a way that completely ignores this kind of advice. The organ, in fact, epitomizes a shortcut-finding machine. The first indication that the brain has a knack for finding alternative routes was described in 1948 by Edward Tolman of the University of California, Berkeley. Tolman performed a curious experiment in which a hungry rat ran across an unpainted circular table into a dark, narrow corridor. The rat turned left, then right, and then took another right and scurried to the far end of a well-lit narrow strip, where, finally, a cup of food awaited. There were no choices to be made. The rat had to follow the one available winding path, and so it did, time and time again, for four days. On the fifth day, as the rat once again ran straight across the table into the corridor, it hit a wall—the path was blocked. The animal went back to the table and started looking for alternatives. Overnight, the circular table had turned into a sunburst arena. Instead of one track, there were now 18 radial paths to explore, all branching off from the sides of the table. After venturing out a few inches on a few different paths, the rat finally chose to run all the way down path number six, the one leading directly to the food. © 2020 Scientific American,

Keyword: Attention
Link ID: 26961 - Posted: 01.15.2020

By Eryn Brown On March 30, 1981, 25-year-old John W. Hinckley Jr. shot President Ronald Reagan and three other people. The following year, he went on trial for his crimes. Defense attorneys argued that Hinckley was insane, and they pointed to a trove of evidence to back their claim. Their client had a history of behavioral problems. He was obsessed with the actress Jodie Foster, and devised a plan to assassinate a president to impress her. He hounded Jimmy Carter. Then he targeted Reagan. In a controversial courtroom twist, Hinckley’s defense team also introduced scientific evidence: a computerized axial tomography (CAT) scan that suggested their client had a “shrunken,” or atrophied, brain. Initially, the judge didn’t want to allow it. The scan didn’t prove that Hinckley had schizophrenia, experts said — but this sort of brain atrophy was more common among schizophrenics than among the general population. It helped convince the jury to find Hinckley not responsible by reason of insanity. Nearly 40 years later, the neuroscience that influenced Hinckley’s trial has advanced by leaps and bounds — particularly because of improvements in magnetic resonance imaging (MRI) and the invention of functional magnetic resonance imaging (fMRI), which lets scientists look at blood flows and oxygenation in the brain without hurting it. Today neuroscientists can see what happens in the brain when a subject recognizes a loved one, experiences failure, or feels pain. Despite this explosion in neuroscience knowledge, and notwithstanding Hinckley’s successful defense, “neurolaw” hasn’t had a tremendous impact on the courts — yet. But it is coming. Attorneys working civil cases introduce brain imaging ever more routinely to argue that a client has or has not been injured. Criminal attorneys, too, sometimes argue that a brain condition mitigates a client’s responsibility. Lawyers and judges are participating in continuing education programs to learn about brain anatomy and what MRIs and EEGs and all those other brain tests actually show.

Keyword: Brain imaging; Aggression
Link ID: 26960 - Posted: 01.15.2020

By Gareth Cook One of science’s most challenging problems is a question that can be stated easily: Where does consciousness come from? In his new book Galileo’s Error: Foundations for a New Science of Consciousness, philosopher Philip Goff considers a radical perspective: What if consciousness is not something special that the brain does but is instead a quality inherent to all matter? It is a theory known as “panpsychism,” and Goff guides readers through the history of the idea, answers common objections (such as “That’s just crazy!”) and explains why he believes panpsychism represents the best path forward. He answered questions from Mind Matters editor Gareth Cook. Can you explain, in simple terms, what you mean by panpsychism? In our standard view of things, consciousness exists only in the brains of highly evolved organisms, and hence consciousness exists only in a tiny part of the universe and only in very recent history. According to panpsychism, in contrast, consciousness pervades the universe and is a fundamental feature of it. This doesn’t mean that literally everything is conscious. The basic commitment is that the fundamental constituents of reality—perhaps electrons and quarks—have incredibly simple forms of experience. And the very complex experience of the human or animal brain is somehow derived from the experience of the brain’s most basic parts. It might be important to clarify what I mean by “consciousness,” as that word is actually quite ambiguous. Some people use it to mean something quite sophisticated, such as self-awareness or the capacity to reflect on one’s own existence. This is something we might be reluctant to ascribe to many nonhuman animals, never mind fundamental particles. But when I use the word consciousness, I simply mean experience: pleasure, pain, visual or auditory experience, et cetera. © 2020 Scientific American,

Keyword: Consciousness
Link ID: 26959 - Posted: 01.15.2020

By Joseph Stern, M.D. The bullet hole in the teenager’s forehead was so small, it belied the damage already done to his brain. The injury was fatal. We knew this the moment he arrived in the emergency room. Days later, his body was being kept alive in the intensive care unit despite an exam showing that he was brain-dead and no blood was flowing to his brain. Eventually, all his organs failed and his heart stopped beating. But the nurses continued to care for the boy and his family, knowing he was already dead but trying to help the family members with the agonizing process of accepting his death. This scenario occurs all too frequently in the neurosurgical I.C.U. Doctors often delay the withdrawal of life-sustaining supports such as ventilators and IV drips, and nurses continue these treatments — adhering to protocols, yet feeling internal conflict. A lack of consensus or communication among doctors, nurses and families often makes these situations more difficult for all involved. Brain death is stark and final. When the patient’s brain function has ceased, bodily death inevitably follows, no matter what we do. Continued interventions, painful as they may be, are necessarily of limited duration. We can keep a brain-dead patient’s body alive for a few days at the most before his heart stops for good. Trickier and much more common is the middle ground of a neurologically devastating injury without brain death. Here, decisions can be more difficult, and electing to continue or to withdraw treatment much more problematic. Inconsistent communication and support between medical staff members and families plays a role. A new field, neuropalliative care, seeks to focus “on outcomes important to patients and families” and “to guide and support patients and families through complex choices involving immense uncertainty and intensely important outcomes of mind and body.” © 2020 The New York Times Company

Keyword: Consciousness
Link ID: 26958 - Posted: 01.14.2020

By Brooke N. Dulka Glutamate, arguably the most important chemical in your nervous system, is older than the brain itself. From a single cell bacterium, to mushrooms and plants, to you—every living thing on this planet relies on this tiny molecule for cellular communication. It is absolutely critical for everything we do. “The function of most, if not all, of the trillions of cells in the brain are regulated by glutamate,” neuroscientist David Baker explains to me. On November 1, 2019, neuroscientists gathered at the Harley-Davidson Museum in Milwaukee, WI to share their science. The chrome-laden motorcycle in the corner of the room was hard to ignore, but it was the presentation of Baker, a professor at Marquette University, that really caught my attention. Baker has dedicated his career to understanding how glutamate can treat disorders of the brain. Specifically, his hopes for targeting glutamate lie in a mechanism called system xc-. Glutamate is often called the “major excitatory neurotransmitter” within the brain. It is the brain’s “go” signal. Baker notes that glutamate receptors are found in every kind of brain cell, which means it is doing more than regulating the activity of neurons, it is regulating the brain’s support cells too. Glutamate is that widespread and important! But being almost everywhere increases the chances that something, somewhere, could go wrong. Thus, most disorders of the brain involve some degree of glutamate dysfunction. This includes disorders such as schizophrenia, depression, obsessive-compulsive disorder, Alzheimer’s disease and more. While one might think that this awareness provides neuroscientists with critical insights into treating disorders of the brain, actually the opposite has occurred. In fact, most psychiatric drugs weren’t even discovered through systematic drug development, as one might expect. More often than not, the drugs we commonly use today were serendipitous findings or accidental discoveries. Baker notes that almost none of the most commonly prescribed drugs for psychiatric disorders target glutamate. Given the importance of glutamate to nearly every brain function, there is a genuine, and well-reasoned, concern among both neuroscientists and psychiatrists that glutamatergic therapeutics will produce widespread impairments in the brain. © 2020 Scientific American

Keyword: Schizophrenia
Link ID: 26957 - Posted: 01.14.2020

Katarina Zimmer As early as the 1990s, researchers proposed that a very common type of herpes virus—then known as human herpesvirus 6 (HHV6)—could be somehow involved in the development of multiple sclerosis, a neurodegenerative disease characterized by autoimmune reactions against the protective myelin coating of the central nervous system. However, the association between HHV6 and the disease soon became fraught with controversy as further studies produced discordant results. Complicating matters further, HHV6 turned out to be two related, but distinct variants—HHV6A and HHV6B. Because the two viruses are similar, for a while no method existed to tell whether a patient had been infected with one or the other, or both—making it difficult to draw a definitive association between either of the viruses and the disease. Now, a collaboration of European researchers has developed a technique capable of distinguishing antibodies against one variant from the other. Using that method in a Swedish cohort of more than 8,700 multiple sclerosis patients and more than 7,200 controls, they found that patients were much more likely to carry higher levels of anti-HHV6A antibodies than healthy people, while they were likelier to carry fewer antibodies against HHV6B. The findings, published last November in Frontiers in Immunology, hint that previous contradictory results may at least be partially explained by the fact that researchers couldn’t distinguish between the two viruses. “This article now makes a pretty convincing case that it is HHV6A that correlates with multiple sclerosis, and not HHV6B,” remarks Margot Mayer-Pröschel, a neuroscientist at the University of Rochester Medical Center who wasn’t involved in the study. “Researchers can now focus on one of these viruses rather than looking at [both] of them together.” © 1986–2020 The Scientist.

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 26956 - Posted: 01.14.2020

By Matt Richtel The number of women drinking dangerous amounts of alcohol is rising sharply in the United States. That finding was among several troubling conclusions in an analysis of death certificates published Friday by the National Institute on Alcohol Abuse and Alcoholism. The analysis looked at deaths nationwide each year from 1999 through 2017 that were reported as being caused at least partly by alcohol, including acute overdose, its chronic use, or in combination with other drugs. The death rate tied to alcohol rose 51 percent overall in that time period, taking into account population growth. Most noteworthy to researchers was that the rate of deaths among women rose much more sharply, up 85 percent. In sheer numbers, 18,072 women died from alcohol in 2017, according to death certificates, compared with 7,662 in 1999. “More women are drinking and they are drinking more,” said Patricia Powell, deputy director of the alcohol institute, which is a division of the National Institutes of Health. Still, far more men than women die from alcohol-related illnesses, the study showed. In 2017, alcohol played a role in the deaths of 72,558 men, compared to 35,914 in 1999, a 35 percent increase when population growth is factored in. Like much research of its kind, the findings do not alone offer the reasons behind the increase in alcohol deaths. In fact, the data is confounding in some respects, notably because teenage drinking overall has been dropping for years, a shift that researchers have heralded as a sign that alcohol has been successfully demonized as a serious health risk. Experts said that the new findings could partly reflect the fact that baby boomers are aging and the health effects of chronic alcohol use have become more apparent. The increase in deaths might also reflect the increase in opioid-related deaths, which in many cases can involve alcohol as well, and that would be reflected on death certificates. © 2020 The New York Times Company

Keyword: Drug Abuse; Sexual Behavior
Link ID: 26955 - Posted: 01.13.2020

There are differences in the way English and Italian speakers are affected by dementia-related language problems, a small study suggests. While English speakers had trouble pronouncing words, Italian speakers came out with shorter, simpler sentences. The findings could help ensure accurate diagnoses for people from different cultures, the researchers said. Diagnostic criteria are often based on English-speaking patients. In the University of California study of 20 English-speaking patients and 18 Italian-speaking patients, all had primary progressive aphasia - a neuro-degenerative disease which affects areas of the brain linked to language. It is a feature of Alzheimer's disease and other dementia disorders. Brain scans and tests showed similar levels of cognitive function in people in both language groups. But when the researchers asked participants to complete a number of linguistic tests, they picked up obvious differences between the two groups in the challenges they faced. 'Easier to pronounce' "We think this is specifically because the consonant clusters that are so common in English pose a challenge for a degenerating speech-planning system," said study author Maria Luisa Gorno-Tempini, professor of neurology and psychiatry. "In contrast, Italian is easier to pronounce, but has much more complex grammar, and this is how Italian speakers with [primary progressive aphasia] tend to run into trouble." As a result, the English speakers tended to speak less while the Italian speakers had fewer pronunciation problems, but simplified what they did say. English is a Germanic language while Italian is a Romance language, derived from Latin along with French, Spanish and Portuguese. The researchers, writing in Neurology, are concerned that many non-native English speakers may not be getting the right diagnosis "because their symptoms don't match what is described in clinical manuals based on studies of native English speakers". The San Francisco research team says it now wants to repeat the research in larger groups of patients, and look for differences between speakers of other languages, such as Chinese and Arabic. © 2020 BBC

Keyword: Alzheimers; Language
Link ID: 26954 - Posted: 01.13.2020

By John Horgan Last month I participated in a symposium hosted by the Center for Theory & Research at Esalen, a retreat center in Big Sur, California. Fifteen men and women representing physics, psychology and other fields attempted to make sense of mystical and paranormal experiences, which are generally ignored by conventional, materialist science. The organizers invited me because of my criticism of hard-core materialism and interest in mysticism, but in a recent column I pushed back against ideas advanced at the meeting. Below other attendees push back against me. My fellow speaker Bjorn Ekeberg, whose response is below, took the photos of Esalen, including the one of me beside a stream (I'm the guy on the right). -- John Horgan Jeffrey Kripal, philosopher of religion at Rice University and author, most recently, of The Flip: Epiphanies of Mind and the Future of Knowledge (see our online chats here and here): Thank you, John, for reporting on your week with us all. As one of the moderators of “Physics, Experience and Metaphysics,” let me try to reply, briefly (and too simplistically), to your various points. First, let me begin with something that was left out of your generous summary: the key role of the imagination in so many exceptional or anomalous experiences. As you yourself pointed out with respect to your own psychedelic opening, this is no ordinary or banal “imagination.” This is a kind of “super-imagination” that projects fantastic visionary displays that none of us could possibly come up with in ordinary states: this is a flying caped Superman to our bespectacled Clark Kent. None of this, of course, implies that anything seen in these super-imagined states is literally true (like astral travel or ghosts) or non-human, but it does tell us something important about why the near-death or psychedelic experiencers commonly report that these visionary events are “more real” than ordinary reality (which is also, please note, partially imagined, if our contemporary neuroscience of perception is correct). Put in terms of a common metaphor that goes back to Plato, the fictional movies on the screen can ALL be different and, yes, of course, humanly and historically constructed, but the Light projecting them can be quite Real and the Same. Fiction and reality are in no way exclusive of one another in these paradoxical states. © 2020 Scientific American

Keyword: Consciousness
Link ID: 26953 - Posted: 01.13.2020

By Daniel J. Levitin I’m 62 years old as I write this. Like many of my friends, I forget names that I used to be able to conjure up effortlessly. When packing my suitcase for a trip, I walk to the hall closet and by the time I get there, I don’t remember what I came for. And yet my long-term memories are fully intact. I remember the names of my third-grade classmates, the first record album I bought, my wedding day. This is widely understood to be a classic problem of aging. But as a neuroscientist, I know that the problem is not necessarily age-related. Short-term memory contains the contents of your thoughts right now, including what you intend to do in the next few seconds. It’s doing some mental arithmetic, thinking about what you’ll say next in a conversation or walking to the hall closet with the intention of getting a pair of gloves. Short-term memory is easily disturbed or disrupted. It depends on your actively paying attention to the items that are in the “next thing to do” file in your mind. You do this by thinking about them, perhaps repeating them over and over again (“I’m going to the closet to get gloves”). But any distraction — a new thought, someone asking you a question, the telephone ringing — can disrupt short-term memory. Our ability to automatically restore the contents of the short-term memory declines slightly with every decade after 30. But age is not the major factor so commonly assumed. I’ve been teaching undergraduates for my entire career and I can attest that even 20-year-olds make short-term memory errors — loads of them. They walk into the wrong classroom; they show up to exams without the requisite No. 2 pencil; they forget something I just said two minutes before. These are similar to the kinds of things 70-year-olds do. © 2020 The New York Times Company

Keyword: Learning & Memory; Alzheimers
Link ID: 26952 - Posted: 01.13.2020

Lesley McClurg Americans know the dangers of drugs such as morphine and heroin. But what about a supplement that acts in the brain a bit like an opiate and is available in many places to kids — even from vending machines. Kratom, an herb that's abundant, legal in most states and potentially dangerous, is the subject of an ongoing debate over its risks and benefits. Usually, the leaf, which comes from a tropical Southeast Asian tree, is chewed, brewed or crushed into a bitter green powder. The chemicals in the herb interact with different types of receptors in the brain — some that respond to opioids, and others to stimulants. Often sold in the U.S. in a processed form — as pills, capsules or extracts — a small amount of kratom can perk you up, while a large dose has a sedative effect. Some people who have struggled with an opioid addiction and switched to kratom swear the substance salvaged their health, livelihood and relationships. But the federal Food and Drug Administration and the Drug Enforcement Administration worry that kratom carries the risk of physical and psychological dependency and, in some people, addiction. The FDA warns consumers not to use kratom, and the DEA threatened to prohibit kratom's sale and use in the U.S. (outside of research) in 2016; advocates and lawmakers subsequently pushed back, and the stricter scheduling of kratom that would have prompted that sort of ban never occurred. These days, the DEA lists it as a drug of concern. © 2020 npr

Keyword: Drug Abuse
Link ID: 26951 - Posted: 01.13.2020

By Benedict Carey Soldiers with deep wounds sometimes feel no pain at all for hours, while people without any detectable injury live in chronic physical anguish. How to explain that? Over drinks in a Boston-area bar, Ronald Melzack, a psychologist, and Dr. Patrick Wall, a physiologist, sketched out a diagram on a cocktail napkin that might help explain this and other puzzles of pain perception. The result, once their idea was fully formed, was an electrifying theory that would become the founding document for the field of modern pain studies and establish the career of Dr. Melzack, whose subsequent work deepened medicine’s understanding of pain and how it is best measured and treated. Dr. Melzack died on Dec. 22 in a hospital near his home in Montreal, where he lived, his daughter, Lauren Melzack, said. He was 90, and had spent most of his professional life as a professor of psychology at McGill University. When Dr. Melzack and Dr. Wall, then at the Massachusetts Institute of Technology, met that day in 1959 or 1960 (accounts of their encounter vary), pain perception was thought to work something like a voltmeter, in which nerves send signals up to the brain that reflect the severity of the injury. But that model failed to explain not only battlefield experience but also a host of clinical findings and everyday salves. Most notably, rubbing a wound lessens its sting — and accounting for just that common sensation proved central to the new theory. Doctors knew that massaging the skin activated so-called large nerve fibers, which are specialized to detect subtle variations of touch; and that deeper, small fibers sounded the alarm of tissue damage. The two researchers reasoned that all these sensations must pass through a “gate” in the spinal cord, which adds up their combined signals before sending a message to the brain. In effect, activating the large fibers blocks signals from the smaller ones, by closing the gate. © 2020 The New York Times Company

Keyword: Pain & Touch
Link ID: 26950 - Posted: 01.13.2020