By HENRY ALFORD Here in the valley of my mid-50s, I try not to get into a swivet over my occasionally faulty memory: Sometimes the mind has a mind of its own. But when I read this chilling passage — “I am dementing. I am dementing. I am dementing.” — from Gerda Saunders’s recent memoir “Memory’s Last Breath: Field Notes on My Dementia,” I found myself starting to panic. In a world increasingly dominated by the Google/Apple/Facebook/Amazon hegemony, we hear a lot about the threat to privacy. But isn’t memory just as vulnerable? Now that, as the former New Republic editor Franklin Foer writes in “World Without Mind: The Existential Threat of Big Tech,” “our phone is an extension of our memory; we’ve outsourced basic functions to algorithms,” doesn’t the world seem like an ever-larger parking lot that has mysteriously swallowed our Toyota? Don’t we all wish, now more than ever, that acquaintances came equipped with their own “Previously on this series …” trailer? Mr. Foer and Ms. Saunders aren’t the only writers on this beat. Recent books by Robert Sapolsky, Michael Lemonick, Felicia Yap, Emily Barr, Dale Bredesen, Val Emmich, Oliver Sacks and Elizabeth Rosner, among others, have addressed the theme of non-historical memory. Last July alone, more than a dozen books specifically about the topic, most of them self-published, were released. You’d expect the themes of amnesia or powers of recall to be prevalent in thrillers or in memoirs by trauma survivors or over-beveraged rock stars, but even literary fiction is getting in on the act. In Rachel Khong’s sly, diaristic “Goodbye, Vitamin,” a 30-year-old who moves back home learns she has to care for a dementing father who has started leaving his pants in trees. In Alissa Nutting’s outrageous sex comedy “Made for Love,” a woman on the lam from her tech pioneer husband discovers that he has implanted a chip in her brain that allows him to download all her experiences. © 2018 The New York Times Company

Keyword: Learning & Memory
Link ID: 24499 - Posted: 01.08.2018

By Nicole Edison Worried you might say something you regret when talking in your sleep? Your concerns may be justified: According to a recent study from France, your midnight mumblings may be more negative and insulting than what you say while awake. In the study, researchers found that sleep talkers said the word “no” four times as often in their sleep as when awake. And the f-word popped up during sleep talking more than 800 times more frequently than while awake. To study sleep talking, the researchers recorded nearly 900 nighttime utterances from about 230 adults during one or two consecutive nights in a sleep lab. Because sleep talking is a relatively rare event, the majority of people in the study had certain types of sleep disorders, or parasomnias, which are unusual behaviors that happen during sleep, the researchers noted. Once recorded, the nocturnal episodes were analyzed for such factors as wordiness, silences, tone, politeness and abusive language. These results were compared to see how sleep speech matched up to everyday spoken French in form and content. The researchers found that the majority (59 percent) of the nighttime utterances were unintelligible or nonverbal, including mumbling, whispering and laughing. But among the utterances that were intelligible, a surprising amount of what was said was offensive or aggressive: 24 percent contained negative content, 22 percent had “nasty” language and almost 10 percent contained the word “no” in some form. (By comparison, the word “no” accounted for 2.5 percent of awake language.) © 1996-2018 The Washington Post

Keyword: Sleep
Link ID: 24498 - Posted: 01.08.2018

Nicola Davis The prospect of a non-addictive alternatives to morphine and other opioids has moved a step closer as scientists say they have cracked a key challenge in developing safe and effective substitute painkillers. Overuse of highly addictive opioids has led to a health crisis across the world, especially in the US where more than 60,000 people died after overdoses in 2016 alone; president Donald Trump has declared the epidemic a public health emergency. Researchers looking for alternatives examined a receptor protein that interacts with opioids in the brain, and have now revealed its structure as it binds to a molecule related to morphine. While the structure of the receptor had previously been reported, this is the first time scientists have unveiled its structure as it interacts with a drug. The development, they say, could prove pivotal. The protein, known as the kappa opioid receptor, is one of four that interacts with opioids, but – crucially – while it can trigger pain-killing effects, it is not linked to problems including constipation, addiction risk and death as a result of overdose. “Tens of thousands of people are dying every year in the US because of opioid overdoses; in the last year more than 50,000 people died. That is as many as died in the Vietnam war in the US. It is a terrible, terrible crisis,” said Bryan Roth, co-author of the research from the University of North Carolina at Chapel Hill. © 2018 Guardian News and Media Limited

Keyword: Drug Abuse; Pain & Touch
Link ID: 24497 - Posted: 01.06.2018

By Meredith Wadman For the first time, scientists have produced evidence in living humans that the protein tau, which mars the brain in Alzheimer’s disease, spreads from neuron to neuron. Although such movement wasn’t directly observed, the finding may illuminate how neurodegeneration occurs in the devastating illness, and it could provide new ideas for stemming the brain damage that robs so many of memory and cognition. Tau is one of two proteins—along with β-amyloid—that form unusual clumps in the brains of people with Alzheimer’s disease. Scientists have long debated which is most important to the condition and, thus, the best target for intervention. Tau deposits are found inside neurons, where they are thought to inhibit or kill them, whereas β-amyloid forms plaques outside brain cells. Researchers at the University of Cambridge in the United Kingdom combined two brain imaging techniques, functional magnetic resonance imaging and positron emission tomography (PET) scanning, in 17 Alzheimer’s patients to map both the buildup of tau and their brains’ functional connectivity—that is, how spatially separated brain regions communicate with each other. Strikingly, they found the largest concentrations of the damaging tau protein in brain regions heavily wired to others, suggesting that tau may spread in a way analogous to influenza during an epidemic, when people with the most social contacts will be at greatest risk of catching the disease. © 2018 American Association for the Advancement of Science.

Keyword: Alzheimers; Brain imaging
Link ID: 24496 - Posted: 01.06.2018

Veronique Greenwood TSUKUBA, Japan—Outside the International Institute for Integrative Sleep Medicine, the heavy fragrance of sweet Osmanthus trees fills the air, and big golden spiders string their webs among the bushes. Two men in hard hats next to the main doors mutter quietly as they measure a space and apply adhesive to the slate-colored wall. The building is so new that they are still putting up the signs. The institute is five years old, its building still younger, but already it has attracted some 120 researchers from fields as diverse as pulmonology and chemistry and countries ranging from Switzerland to China. An hour north of Tokyo at the University of Tsukuba, with funding from the Japanese government and other sources, the institute’s director, Masashi Yanagisawa, has created a place to study the basic biology of sleep, rather than, as is more common, the causes and treatment of sleep problems in people. Full of rooms of gleaming equipment, quiet chambers where mice slumber, and a series of airy work spaces united by a spiraling staircase, it’s a place where tremendous resources are focused on the question of why, exactly, living things sleep. Ask researchers this question, and listen as, like clockwork, a sense of awe and frustration creeps into their voices. In a way, it’s startling how universal sleep is: In the midst of the hurried scramble for survival, across eons of bloodshed and death and flight, uncountable millions of living things have laid themselves down for a nice, long bout of unconsciousness. This hardly seems conducive to living to fight another day. “It’s crazy, but there you are,” says Tarja Porkka-Heiskanen of the University of Helsinki, a leading sleep biologist. That such a risky habit is so common, and so persistent, suggests that whatever is happening is of the utmost importance. Whatever sleep gives to the sleeper is worth tempting death over and over again, for a lifetime. (c) 2018 by The Atlantic Monthly Group.

Keyword: Sleep
Link ID: 24495 - Posted: 01.06.2018

Nancy Shute It's just a cold. But even though I know I'm not horribly ill, I feel this overwhelming need to skip work, ignore my family and retreat to the far corner of the sofa. I'm not being a wimp, it turns out. Those feelings are a real thing called sickness behavior, which is sparked by the body's response to infection. The same chemicals that tell the immune system to rush in and fend off invading viruses also tell us to slow down, skip the eating, drinking and sex, shun social interactions and rest. "Those messages are so powerful they can't be ignored," says Philip Chen, a rhinologist at the University of Texas, San Antonio. But that doesn't mean we don't try. Symptoms like a stuffy nose are obvious, Chen notes, but we're less aware that changes in mood and behavior are also part of our bodies' natural response to infection. It might behoove us to pay attention. There's plenty of evidence that having a cold impairs mood, alertness and working memory, and that brain performance falls off with even minor symptoms. But for most people, having a cold does not equal "take the week off." And that means many people work sick, even when it can put others in danger. A 2015 survey of food workers found that half "always" or "frequently' went to work while sick. © 2018 npr

Keyword: Neuroimmunology; Stress
Link ID: 24494 - Posted: 01.06.2018

By Joshua Rothman One day in the nineteen-eighties, a woman went to the hospital for cancer surgery. The procedure was a success, and all of the cancer was removed. In the weeks afterward, though, she felt that something was wrong. She went back to her surgeon, who reassured her that the cancer was gone; she consulted a psychiatrist, who gave her pills for depression. Nothing helped—she grew certain that she was going to die. She met her surgeon a second time. When he told her, once again, that everything was fine, she suddenly blurted out, “The black stuff—you didn’t get the black stuff!” The surgeon’s eyes widened. He remembered that, during the operation, he had idly complained to a colleague about the black mold in his bathroom, which he could not remove no matter what he did. The cancer had been in the woman’s abdomen, and during the operation she had been under general anesthesia; even so, it seemed that the surgeon’s words had lodged in her mind. As soon as she discovered what had happened, her anxiety dissipated. Henry Bennett, an American psychologist, tells this story to Kate Cole-Adams, an Australian journalist, in her book “Anesthesia: The Gift of Oblivion and the Mystery of Consciousness.” Cole-Adams hears many similar stories from other anesthesiologists and psychologists: apparently, people can hear things while under anesthesia, and can be affected by what they hear even if they can’t remember it. One woman suffers from terrible insomnia after her hysterectomy; later, while hypnotized, she recalls her anesthesiologist joking that she would “sleep the sleep of death.” Another patient becomes suicidal after a minor procedure; later, she remembers that, while she was on the table, her surgeon exclaimed, “She is fat, isn’t she?” In the nineteen-nineties, German scientists put headphones on thirty people undergoing heart surgery, then, during the operation, played them an abridged version of “Robinson Crusoe.” None of the patients recalled this happening, but afterward, when asked what came to mind when they heard the word “Friday,” many mentioned the story. In 1985, Bennett himself asked patients receiving gallbladder or spinal surgeries to wear headphones. A control group heard the sounds of the operating theatre; the others heard Bennett saying, “When I come to talk with you, you will pull on your ear.” When they met with him, those who’d heard the message touched their ears three times more often than those who hadn’t. © 2018 Condé Nast.

Keyword: Consciousness; Sleep
Link ID: 24493 - Posted: 01.05.2018

By Richard Stone Even 3 decades later, Seyed Naser Emadi's first encounter with nerve agents haunts him. In 1987, as a soldier fighting for Iran in its war with Iraq, he came across a hillside strewn with comrades killed by an Iraqi nerve agent, perhaps tabun or sarin. Unable to breathe, the victims had clawed at their necks to try to open a hole in their throats, recalls Emadi, now a dermatologist in Tehran. In fact, their windpipes were clear; the nerve agent had shut down control of breathing in the central nervous system. They "had no choice except death," he says. The long-term effects of nerve agents remain uncertain, but with the right antidotes, these poisons need not be an immediate death sentence. A few years after Emadi's experience, U.S. soldiers in 1991's Gulf War carried autoinjectors filled with drugs that—in principle—would keep them breathing and protect them from seizures if Iraqi forces again unleashed nerve agents. They never did, most historians agree, but the threat remains real today, as chemical attacks in Syria's ongoing civil war make clear. It is spurring urgent efforts to find better countermeasures, with several promising compounds in the pipeline. First synthesized by German chemists on the eve of World War II, nerve agents kill by binding to acetylcholinesterase (AChE), an enzyme that dismantles the neurotransmitter acetylcholine when it is released into synapses. One of the most efficient enzymes known, a single AChE molecule can hydrolyze 600,000 acetylcholine molecules per minute, says Palmer Taylor, a pharmacologist at the University of California, San Diego. © 2018 American Association for the Advancement of Science

Keyword: Neurotoxins
Link ID: 24492 - Posted: 01.05.2018

By Alfonso Serrano Elvis Alonzo began smoking cannabis as a last resort. Three years as a Marine Corps officer and 13 years with the Glendale Police Department in Arizona—where he was exposed to murders, suicides and people dying in his arms—had left him emotionally crippled. Toward the end of his police service, doctors diagnosed Alonzo with post-traumatic stress disorder and prescribed various medications to temper his nightmares and flashbacks. The drugs “turned me into a zombie,” he says. “I was so out of it that I couldn’t even drive, so they (the police department) had to medically retire me.” Alonzo stopped showering. His wife left him, and he nearly lost his house. Then a friend suggested he try marijuana to relieve his symptoms. “It’s been a godsend,” he says. “It curbs my anxiety, and it makes me sleep fantastic for at least four hours. It needs to be studied.” Thousands of military veterans have echoed Alonzo’s claim for years. They have pressured federal and state legislators to legalize medicinal cannabis and ease rules on research into the plant’s apparent therapeutic properties, arguing that it could help reduce suicide rates among former soldiers. Backed by overwhelming public support for broader legalization, their demands are starting to resonate in statehouses across the country. This past November, New York Gov. Andrew Cuomo chose Veterans Day to make PTSD a qualifying condition for the state’s tightly controlled medical marijuana program. New York joined seven other states this year—and 27 overall—that include PTSD in their lists of conditions that qualify for medical cannabis. © 2018 Scientific America

Keyword: Drug Abuse; Stress
Link ID: 24491 - Posted: 01.05.2018

/ By Robin Lloyd Most Americans drink safely and in moderation, as many of us could attest earlier this week. But a steady annual increase in trips made to emergency rooms as a result of drinking alcohol added up to 61 percent more visits in 2014 compared with 2006, according to a study published this week in the journal Alcoholism: Clinical and Experimental Research. The increase is alarming but also a bit mysterious to neuroscientist Aaron White, one of the study’s authors, in part because the same nine-year period showed a mere 2 percent increase in per capita alcohol consumption overall, and an 8 percent increase in the number of emergency room visits for any reason. White and his four co-authors, three of whom work with him at the National Institute on Alcohol Abuse and Alcoholism, have yet to understand what’s behind the dramatic increase in alcohol-related ER visits. “The lowest hanging fruit in terms of hypotheses is that there must be an increase in risky drinking in some people,” White says. “Even though that is not showing up in increases in overall per capita consumption, it’s enough to drive the increase in alcohol-related emergency department visits.” But there is no strong evidence for a national increase in binge drinking, he added. The new finding comes from an analysis of a nationally representative data set that includes information on about 30 million visits to U.S. hospital-based emergency departments annually, from 945 hospitals in 33 states and Washington, D.C. Copyright 2018 Undark

Keyword: Drug Abuse
Link ID: 24490 - Posted: 01.05.2018

By RONI CARYN RABIN A. Studies have found a link between low levels of magnesium, an essential mineral that plays a crucial role in a wide range of bodily processes, and sleep disorders. But if you are concerned you aren’t getting enough magnesium, changing your diet may be a better option than taking a supplement, as “there is really sparse evidence that taking super-therapeutic doses of magnesium will give you a benefit,” said Dr. Raj Dasgupta, a professor of pulmonary and sleep medicine at the University of Southern California. The mineral is widely available in both plant and animal-based foods, and the kidneys limit urinary excretion of magnesium, so deficiencies are rare in healthy people. Leafy green vegetables, nuts, legumes and whole grains are good sources of magnesium; fish, chicken and beef also contain magnesium. Older adults and people with certain disorders, such as Type 2 diabetes, gastrointestinal diseases and alcoholism, however, may have inadequate amounts. “Magnesium deficiency has been associated with higher levels of stress, anxiety and difficulty relaxing, which are key ingredients to getting good sleep at night,” Dr. Dasgupta said. He noted that magnesium interacts with an important neurotransmitter that favors sleep. One small double-blinded clinical trial of 43 elderly people in Tehran who were randomly assigned to receive either 500 milligrams of magnesium or a placebo for eight weeks found that those who received the supplement fell asleep faster and spent more of their time in bed asleep, but their total sleep time was not necessarily longer. An even smaller study of 10 people done nearly 20 years ago found that taking a magnesium supplement helped people with restless leg syndrome get more sleep. © 2018 The New York Times Company

Keyword: Sleep
Link ID: 24489 - Posted: 01.05.2018

By Meredith Wadman Chya* (pronounced SHY-a), who is not quite 10 years old, recently spent an unusual day at the University of Maryland School of Medicine in Baltimore. Part of the time she was in a "cool" brain scanner while playing video games designed to test her memory and other brain-related skills. At other points, she answered lots of questions about her life and health on an iPad. A slender Baltimore third grader who likes drawing, hip hop, and playing with her pet Chihuahua, Chya is one of more than 6800 children now enrolled in an unprecedented examination of teenage brain development. The Adolescent Brain Cognitive Development Study—or ABCD Study—will complete its 2-year enrollment period in September, and this month will release a trove of data from 4500 early participants into a freely accessible, anonymized database. Ultimately, the study aims to follow 10,000 children for a decade as they grow from 9- and 10-year-olds into young adults. Supported by the first chunk of $300 million pledged by several institutes at the National Institutes of Health (NIH) in Bethesda, Maryland, teams at 21 sites around the United States are regularly using MRI machines to record the structure and activity of these young brains. They're also collecting reams of psychological, cognitive, and environmental data about each child, along with biological specimens such as their DNA. In addition to providing the first standardized benchmarks of healthy adolescent brain development, this information should allow scientists to probe how substance use, sports injuries, screen time, sleep habits, and other influences may affect—or be affected by—a maturing brain. © 2017 American Association for the Advancement of Science.

Keyword: Development of the Brain; Schizophrenia
Link ID: 24488 - Posted: 01.04.2018

Amy Maxmen Name a remedy, and chances are that Elizabeth Allen has tried it: acupuncture, antibiotics, antivirals, Chinese herbs, cognitive behavioural therapy and at least two dozen more. She hates dabbling in so many treatments, but does so because she longs for the healthy days of her past. The 34-year-old lawyer was a competitive swimmer at an Ivy-league university when she first fell ill with chronic fatigue syndrome, 14 years ago. Her meticulous records demonstrate that this elusive malady is much worse than ordinary exhaustion. “Last year, I went to 117 doctor appointments and I paid $18,000 in out-of-pocket expenses,” she says. Dumbfounded that physicians knew so little about chronic fatigue syndrome — also known as myalgic encephalomyelitis or ME/CFS — Allen resolved several years ago to take part in any study that would have her. In 2017, she got her chance: she entered a study assessing how women with ME/CFS respond to synthetic hormones. After decades of pleading, people with the condition have finally caught the attention of mainstream science — and dozens of exploratory studies are now under way. Scientists entering the field are using the powerful tools of modern molecular biology to search for any genes, proteins, cells and possible infectious agents involved. They hope the work will yield a laboratory test to diagnose ME/CFS — which might have several different causes and manifestations — and they want to identify molecular pathways to target with drugs. © 2018 Macmillan Publishers Limited,

Keyword: Depression; Neuroimmunology
Link ID: 24487 - Posted: 01.04.2018

By Catherine Offord Graduate student Anne Murphy had run out of rats. Or rather, she’d run out of male rats, the animals she was using to study brain regions involved in pain modulation for her PhD at the University of Cincinnati in the early 1990s. At a time when neuroscientists almost exclusively used male animals for research, what Murphy did next was unusual: she used a female rat instead. “I had the hardest time to get the female to go under the anesthesia; she wasn’t acting right,” Murphy says. Her advisor’s explanation? “‘Well, you know those females, they have hormones, and those hormones are always fluctuating and they’re so variable,’” Murphy recalls. The comments struck a nerve. “It really got to me,” she says. “I’m a female. I have hormones that fluctuate. . . . It made me determined to investigate the differences between males and females in terms of pain processing and alleviation.” Her decision was timely. Since the ’90s, evidence has been accumulating to suggest that not only do women experience a higher incidence of chronic pain syndromes than men do—fibromyalgia and interstitial cystitis, for example—females also generally report higher pain intensities. Additionally, Murphy notes, a handful of clinical studies has suggested that women require higher doses of opioid pain medications such as morphine for comparable analgesia; plus, they experience worse side effects and a higher risk of addiction. © 1986-2018 The Scientist

Keyword: Pain & Touch; Sexual Behavior
Link ID: 24486 - Posted: 01.04.2018

Beyond the usual suspects of snakes, spiders, and scorpions, the animal kingdom is filled with noxious critters: snails, frogs, fish, anemones, and more make toxins for defense or predation. The noxious chemicals these animals produce are potent, and they often strike where it hurts: pain pathways. These compounds have long captivated researchers hoping to understand their effects and use that knowledge to develop drugs that suppress pain in a wide variety of ailments affecting humans. Paradoxically, some of these toxins are themselves analgesic, and researchers have worked to develop synthetic derivatives that can be tested as painkillers. Such is the case for the only toxin-derived analgesic to be approved by the US Food and Drug Administration (FDA): ziconotide (Prialt), a compound 1,000 times more potent than morphine that was inspired by a component of the venom of the cone snail Conus magus. Other toxins elicit pain, and researchers have used these compounds to identify inhibitors of ion channels on the pain-sensing neurons they target. Despite more than half a century of research in this field, however, scientists have had a frustrating time developing effective analgesics. Challenges include ensuring that the drugs are highly specific to their targets—each family of ion channels involved in pain sensing in humans contains several conserved proteins—and getting them to those targets, which often lie beyond the blood-brain barrier in the central nervous system. Nevertheless, several toxin-derived candidates are beginning to prove their worth in preclinical experiments and a handful of clinical trials, and bioprospectors continue to mine the animal kingdom’s vast library of venoms and poisons for more leads. The next big thing in painkillers could soon be slithering, creeping, hopping, or swimming into the pipeline. © 1986-2018 The Scientist

Keyword: Pain & Touch; Neurotoxins
Link ID: 24485 - Posted: 01.04.2018

Phil Plait I can't think of a better way to start off a new year than scrambling your brains. Just a little bit! But still: enough to make you scratch your head and wonder just what is wrong with that sack of wrinkly pink goo in your skull. One of my favorite optical illusionists is Akiyoshi Kitaoki. He has created hundreds, maybe thousands, of guaranteed brain-melting illusions that will make you swear that what you're seeing is real when it really, really isn't. He has ones that appear to move, that warp your sense of shape and size, destroy your notion of color, and will make you seriously question whether your eyes and brain are talking to each other in any sort of coherent way. He just posted a new one to Twitter, and I love it for its simplicity and efficiency: It creates two illusions at once. Are you ready? Here it is: I don't know about you, but when I look at this I see alternating squarish shapes (Kitaoka called them turtles, so I'll go with that) arranged like a chessboard, with half darked and half lighter. What's disturbing immediately though is that they don't appear to be separated along straight lines. The vertical border of the turtles on the left appear to curve to the right a bit, and the ones on the right curve left. It makes it look like there's a mound or bulge in the middle of the image.

Keyword: Vision
Link ID: 24484 - Posted: 01.04.2018

by Ben Guarino The next time a friend tells you that you look sick, hear the person out. We are better than chance at detecting illness in others simply by looking at their faces, according to new research led by a Swedish psychologist. “We can detect subtle cues related to the skin, eyes and mouth,” said John Axelsson of the Karolinska Institute, who co-wrote the study published Tuesday in the journal Proceedings of the Royal Society B. “And we judge people as sick by those cues.” Other species have more finely tuned disease radars, relying primarily on the sense of smell. And previous research, Axelsson noted, has shown that animals can sniff sickness in other animals. (A Canadian hospital enlisted the help of an English springer spaniel trained to smell bacterial spores that infect patients.) Yet while there is some evidence that an unhealthy person gives off odors that another individual can identify as sickness, the face is our primary source of “social information for communication,” Axelsson said. He and his colleagues, a team that included neuroscientists and psychologists in Germany and Sweden, injected eight men and eight women with a molecule found in bacterial membranes. Like animals — from insects to mammals — people react very strongly to this substance, lipopolysaccharide. “People did not really become sick from the bacteria,” Axelsson said, but their bodies did not know the bacteria weren't actually attacking. Their immune systems kicked into action, complete with feelings of sickness. The subjects, all white, received about $430 for their trouble. © 1996-2018 The Washington Post

Keyword: Attention; Neuroimmunology
Link ID: 24483 - Posted: 01.03.2018

By Mark R. Hutchinson When someone is asked to think about pain, he or she will typically envision a graphic wound or a limb bent at an unnatural angle. However, chronic pain, more technically known as persistent pain, is a different beast altogether. In fact, some would say that the only thing that acute and persistent pain have in common is the word “pain.” The biological mechanisms that create and sustain the two conditions are very different. Pain is typically thought of as the behavioral and emotional results of the transmission of a neuronal signal, and indeed, acute pain, or nociception, results from the activation of peripheral neurons and the transmission of this signal along a connected series of so-called somatosensory neurons up the spinal cord and into the brain. But persistent pain, which is characterized by the overactivation of such pain pathways to cause chronic burning, deep aching, and skin-crawling and electric shock–like sensations, commonly involves another cell type altogether: glia.1 Long considered to be little more than cellular glue holding the brain together, glia, which outnumber neurons 10 to 1, are now appreciated as critical contributors to the health of the central nervous system, with recognized roles in the formation of synapses, neuronal plasticity, and protection against neurodegeneration. And over the past 15 to 20 years, pain researchers have also begun to appreciate the importance of these cells. Research has demonstrated that glia seem to respond and adapt to the cumulative danger signals that can result from disparate kinds of injury and illness, and that they appear to prime neural pathways for the overactivation that causes persistent pain. In fact, glial biology may hold important clues to some of the mysteries that have perplexed the pain research field, such as why the prevalence of persistent pain differs between the sexes and why some analgesic medications fail to work. © 1986-2018 The Scientist

Keyword: Pain & Touch; Glia
Link ID: 24482 - Posted: 01.03.2018

Samantha Raphelson Jennifer Brea was a PhD candidate at Harvard University when flu-like symptoms and a high fever brought her down for more than five years. After her condition stumped several doctors, the 28-year-old filmed herself on her iPhone, including an episode when she was unable to move or speak. She showed the footage to her doctor, and in 2012 – a year and a half after her initial fever – she was diagnosed with a condition called myalgic encephalomyelitis, or chronic fatigue syndrome. Even though an estimated 836,000 to 2.5 million Americans suffer from ME/CFS, the disease is largely misunderstood and many sufferers have not been diagnosed. The annual federal research budget for the disease is $4 million to $6 million, which is slim compared to, for example, the nearly $109 million allocated annually to multiple sclerosis research. That's part of the problem, Brea says. "It's a disease that is twice as common as multiple sclerosis and on average can be even more debilitating, and yet we get almost no research funding and no access to medical care," she says. Brea tells Here & Now's Robin Young that her new documentary, Unrest, seeks to lift the veil on this invisible illness. The Sundance-award-winning film, which began with that initial iPhone footage, premieres on PBS next Monday. ME/CFS follows an infection that leaves 75 percent of those affected unable to work and 25 percent homebound or bedridden. The disease is characterized by severe physical and mental fatigue, sleep problems and cognitive dysfunction, according to the Centers for Disease Control and Prevention. © 2018 npr

Keyword: Depression; Neuroimmunology
Link ID: 24481 - Posted: 01.03.2018

/ By Drew Smith For decades, no industry has been a more reliable moneymaker than pharmaceuticals. Immune to recession, drug companies regularly score 15 percent profit margins year after year. There is no danger of market saturation and, in the U.S., little prospect of government restraint of prices. Nearly all regulatory submissions win approval, and turnaround times are steadily decreasing. If you are an investor, what’s not to like? But all dominant and expanding industries are fueled by resources of one type or another. Some of these are tangible and obvious, like gold deposits. Their exploitation follows a familiar arc. There is an initial rush to simply pick nuggets up off the ground. When the nuggets have been picked, miners must search for pebbles, then sand, then dust. There are still fortunes to be made, but more and more capital investment is needed to separate the gold from the dross. If you are a drug company, drug targets are your resource. Our conception of disease has progressed through many understandings — as demonic possession, humoral imbalance, blockage of chi, disordering of machinery — and has now landed on the notion that it is either an invasion by microscopic creatures or bad behavior by large protein molecules. Health is restored by poisoning the invaders or correcting the proteins. Drugs are the agents that accomplish these goals. To a first approximation, drugs are small molecules that bind to specific large molecules. This is the one-disease, one-protein, one-drug paradigm, and it is the essential value proposition of the pharmaceutical industry. Companies identify protein targets and make drugs that alter target behavior. They are very, very good at this. So good that the supply of new drugs largely depends on the supply of new drug targets. Copyright 2018 Undark

Keyword: Depression; Schizophrenia
Link ID: 24480 - Posted: 01.03.2018