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Laura Sanders A busy protein known for its role in aging may also have a hand in depression, a study on mice hints. Under certain circumstances, the aging-related SIRT1 protein seems to make mice despondent, scientists report August 10 in the Journal of Neuroscience. The results are preliminary, but they might ultimately help find new depression treatments. Today’s treatments aren’t always effective, and new approaches are sorely needed. “This is one potential new avenue,” says study coauthor Deveroux Ferguson of the University of Arizona College of Medicine in Phoenix. Ferguson and colleagues subjected mice to 10 days of stressful encounters with other mice. After their demoralizing ordeal, the mice showed signs of depression, such as eschewing sugar water and giving up attempts to swim. Along with these signs of rodent despair, the mice had more SIRT1 gene activity in the nucleus accumbens, a brain area that has been linked to motivation and depression. Resveratrol, a compound found in red grapes, supercharges the SIRT1 protein, making it more efficient at its job. When Ferguson and colleagues delivered resveratrol directly to the nucleus accumbens, mice displayed more signs of depression and anxiety. When the researchers used a different compound to hinder SIRT1 activity, the mice showed the opposite effect, appearing bolder in some tests than mice that didn’t receive the compound. |© Society for Science & the Public 2000 - 2016.
By Ann Griswold, Autism shares genetic roots with obsessive-compulsive disorder (OCD) andattention deficit hyperactivity disorder (ADHD). The three conditions have features in common, such as impulsivity. New findings suggest that they also share a brain signature. The first comparison of brain architecture across these conditions has found that all are associated with disruptions in the structure of the corpus callosum. The corpus callosum is a bundle of nerve fibers that links the brain’s left and right hemispheres. The results appeared July 1 in the American Journal of Psychiatry. Clinicians may find it difficult to distinguish autism from ADHD based on symptoms alone. But if the conditions are marked by similar structural problems in the brain, the same interventions might be useful no matter what the diagnosis is, says lead researcher Stephanie Ameis, assistant professor of psychiatry at the University of Toronto. The unique aspects of each condition might arise from other brain attributes, such as differences in the connections between neurons, says Thomas Frazier, director of research at the Cleveland Clinic Foundation. “A reasonable conclusion is that autism and ADHD don’t differ dramatically in a structural way, but could differ in connectivity,” says Frazier, who was not involved in the study. Ameis’ team examined the brains of 71 children with autism, 31 with ADHD, 36 with OCD and 62 typical children using diffusion tensor imaging. This method provides a picture of the brain’s white matter, the long fibers that connect nerve cells, by measuring the diffusion of water across these fibers. © 2016 Scientific American
Amy McDermott You’ve got to see it to be it. A heightened sense of red color vision arose in ancient reptiles before bright red skin, scales and feathers, a new study suggests. The finding bolsters evidence that dinosaurs probably saw red and perhaps displayed red color. The new finding, published in the Aug. 17 Proceedings of the Royal Society B, rests on the discovery that birds and turtles share a gene used both for red vision and red coloration. More bird and turtle species use the gene, called CYP2J19, for vision than for coloration, however, suggesting that its first job was in sight. “We have this single gene that has two very different functions,” says evolutionary biologist Nicholas Mundy of the University of Cambridge. Mundy’s team wondered which function came first: the red vision or the ornamentation. In evolution, what an animal can see is often linked with what others can display, says paleontologist Martin Sander of the University of Bonn in Germany, who did not work on the new study. “We’re always getting at color from these two sides,” he says, because the point of seeing a strong color is often reading visual signals. Scientists already knew that birds use CYP2J19 for vision and color. In bird eyes, the gene contains instructions for making bright red oil droplets that filter red light. Other forms of red color vision evolved earlier in other animals, but this form allows birds to see more shades of red than humans can. Elsewhere in the body, the same gene can code for pigments that stain feathers red. Turtles are the only other land vertebrates with bright red oil droplets in their eyes. But scientists weren’t sure if the same gene was responsible, Mundy says. |© Society for Science & the Public 2000 - 2016
By BENEDICT CAREY HOLYOKE, Mass. — Some of the voices inside Caroline White’s head have been a lifelong comfort, as protective as a favorite aunt. It was the others — “you’re nothing, they’re out to get you, to kill you” — that led her down a rabbit hole of failed treatments and over a decade of hospitalizations, therapy and medications, all aimed at silencing those internal threats. At a support group here for so-called voice-hearers, however, she tried something radically different. She allowed other members of the group to address the voice, directly: What is it you want? “After I thought about it, I realized that the voice valued my safety, wanted me to be respected and better supported by others,” said Ms. White, 34, who, since that session in late 2014, has become a leader in a growing alliance of such groups, called the Hearing Voices Network, or HVN. At a time when Congress is debating measures to extend the reach of mainstream psychiatry — particularly to the severely psychotic, who often end up in prison or homeless — an alternative kind of mental health care is taking root that is very much anti-mainstream. It is largely nonmedical, focused on holistic recovery rather than symptom treatment, and increasingly accessible through an assortment of in-home services, residential centers and groups like the voices network Ms. White turned to, in which members help one another understand each voice, as a metaphor, rather than try to extinguish it. For the first time in this country, experts say, psychiatry’s critics are mounting a sustained, broadly based effort to provide people with practical options, rather than solely alleging abuses like overmedication and involuntary restraint. “The reason these programs are proliferating now is society’s shameful neglect of the severely ill, which creates a vacuum of great need,” said Dr. Allen Frances, a professor emeritus of psychiatry at Duke University. © 2016 The New York Times Company
Link ID: 22534 - Posted: 08.09.2016
By Simon Makin A technology with the potential to blur the boundaries between biology and electronics has just leaped a major hurdle in the race to demonstrate its feasibility. A team at the University of California, Berkeley, led by neuroscientist Jose Carmena and electrical and computer engineer Michel Maharbiz, has provided the first demonstration of what the researchers call “ultrasonic neural dust” to monitor neural activity in a live animal. They recorded activity in the sciatic nerve and a leg muscle of an anesthetized rat in response to electrical stimulation applied to its foot. “My lab has always worked on the boundary between biology and man-made things,” Maharbiz says. “We build tiny gadgets to interface synthetic stuff with biological stuff.” The work was published last week in the journal Neuron. The system uses ultrasound for both wireless communication and the device’s power source, eliminating both wires and batteries. It consists of an external transceiver and what the team calls a “dust mote” about 0.8x1x3 mm size, which is implanted inside the body. The transceiver sends ultrasonic pulses to a piezoelectric crystal in the implant, which converts them into electricity to provide power. The implant records electrical signals in the rat via electrodes, and uses this signal to alter the vibration of the crystal. These vibrations are reflected back to the transceiver, allowing the signal to be recorded—a technique known as backscatter. “This is the first time someone has used ultrasound as a method of powering and communicating with extremely small implantable systems,” says one of the paper’s authors, Dongjin Seo. “This opens up a host of applications in terms of embodied telemetry: being able to put something super-tiny, super-deep in the body, which you can park next to a nerve, organ, muscle or gastrointestinal tract, and read data out wirelessly.” © 2016 Scientific American
Keyword: Brain imaging
Link ID: 22533 - Posted: 08.09.2016
By ABBY GOODNOUGH TUSCALOOSA, Ala. — Roslyn Lewis was at work at a dollar store here in Tuscaloosa, pushing a heavy cart of dog food, when something popped in her back: an explosion of pain. At the emergency room the next day, doctors gave her Motrin and sent her home. Her employer paid for a nerve block that helped temporarily, numbing her lower back, but she could not afford more injections or physical therapy. A decade later, the pain radiates to her right knee and remains largely unaddressed, so deep and searing that on a recent day she sat stiffly on her couch, her curtains drawn, for hours. The experience of African-Americans, like Ms. Lewis, and other minorities illustrates a problem as persistent as it is complex: Minorities tend to receive less treatment for pain than whites, and suffer more disability as a result. While an epidemic of prescription opioid abuse has swept across the United States, African-Americans and Hispanics have been affected at much lower rates than whites. Researchers say minority patients use fewer opioids, and they offer a thicket of possible explanations, including a lack of insurance coverage and a greater reluctance among members of minority groups to take opioid painkillers even if they are prescribed. But the researchers have also found evidence of racial bias and stereotyping in recognizing and treating pain among minorities, particularly black patients. “We’ve done a good job documenting that these disparities exist,” said Salimah Meghani, a pain researcher at the University of Pennsylvania. “We have not done a good job doing something about them.” Dr. Meghani’s 2012 analysis of 20 years of published research found that blacks were 34 percent less likely than whites to be prescribed opioids for conditions such as backaches, abdominal pain and migraines, and 14 percent less likely to receive opioids for pain from traumatic injuries or surgery. © 2016 The New York Times Company
BENEDICT CAREY As a boy growing up in Massachusetts, Luke Dittrich revered his grandfather, a brain surgeon whose home was full of exotic instruments. Later, he learned that he was not only a prominent doctor but had played a significant role in modern medical history. In 1953, at Hartford Hospital, Dr. William Scoville had removed two slivers of tissue from the brain of a 27-year-old man with severe epilepsy. The operation relieved his seizures but left the patient — Henry Molaison, a motor repairman — unable to form new memories. Known as H. M. to protect his privacy, Mr. Molaison went on to become the most famous patient in the history of neuroscience, participating in hundreds of experiments that have helped researchers understand how the brain registers and stores new experiences. By the time Mr. Dittrich was out of college — and after a year and a half in Egypt, teaching English — he had become fascinated with H. M., brain science and his grandfather’s work. He set out to write a book about the famous case but discovered something unexpected along the way. His grandfather was one of a cadre of top surgeons who had performed lobotomies and other “psycho-surgeries” on thousands of people with mental problems. This was not a story about a single operation that went wrong; it was far larger. The resulting book — “Patient H. M.: A Story of Memory, Madness, and Family Secrets,” to be published Tuesday — describes a dark era of American medicine through a historical, and deeply personal, lens. Why should scientists and the public know this particular story in more detail? The textbook story of Patient H. M. — the story I grew up with — presents the operation my grandfather performed on Henry as a sort of one-off mistake. It was not. Instead, it was the culmination of a long period of human experimentation that my grandfather and other leading doctors and researchers had been conducting in hospitals and asylums around the country. © 2016 The New York Times Company
Keyword: Learning & Memory
Link ID: 22531 - Posted: 08.09.2016
By Julia Shaw Every memory you have ever had is chock-full of errors. I would even go as far as saying that memory is largely an illusion. This is because our perception of the world is deeply imperfect, our brains only bother to remember a tiny piece of what we actually experience, and every time we remember something we have the potential to change the memory we are accessing. I often write about the ways in which our memory leads us astray, with a particular focus on ‘false memories.’ False memories are recollections that feel real but are not based on actual experience. For this particular article I invited a few top memory researchers to comment on what they wish everyone knew about their field. First up, we have Elizabeth Loftus from the University of California, Irvine, who is one of the founders of the area of false memory research, and is considered one of the most ‘eminent psychologists of the 20th century.’ Elizabeth Loftus says you need independent evidence to corroborate your memories. According to Loftus: “The one take home message that I have tried to convey in my writings, and classes, and in my TED talk is this: Just because someone tells you something with a lot of confidence and detail and emotion, it doesn't mean it actually happened. You need independent corroboration to know whether you're dealing with an authentic memory, or something that is a product of some other process.” Next up, we have memory scientist Annelies Vredeveldt from the Vrije Universiteit Amsterdam, who has done fascinating work on how well we remember when we recall things with other people. © 2016 Scientific American,
Keyword: Learning & Memory
Link ID: 22530 - Posted: 08.09.2016
By TATIANA SCHLOSSBERG Need a laugh? Get online and take a look at videos of baby Japanese macaques smiling as they sleep. Their faces twitch, usually just on one side and for less than a second. A lip curls, a nose wrinkles — as if they were hairy, wry elves. Newborn Japanese macaques -- like humans and chimpanzees -- were found to make facial expressions called "spontaneous smiles." Watch the full video. Credit Kyoto University Primate Research Institute Maybe you don’t laugh, maybe you just smile back — O.K., fine. But you may owe that smile to the human version of this infant’s facial spasm. Some scientists suspect spontaneous smiles in these monkeys echo the development of our own expressions. Scientists from the Primate Research Institute at Kyoto University in Japan have observed these spontaneous smiles in Japanese macaques for the first time, according to a new study published in the journal Primates. Spontaneous smiles have previously been observed in infant humans and chimpanzees, but this is the first time they have been seen in another primate species. The scientists watched seven macaque monkeys for an average of 44 minutes, during which the monkeys happened to fall asleep. During REM sleep, each of the monkeys spontaneously smiled at least once, for a little less than a second on average. All told, the seven monkeys smiled 58 times, mostly on the left side of their faces. Human and macaque infants alike primarily smile on one side of their faces. But after two months, human babies begin to smile bilaterally. Around the same time, they also begin to offer up “social smiles,” indicating to others a feeling of happiness. According to the study, scientists think that the earliest spontaneous smiles are key to the development of the zygomaticus major muscle, which is responsible for moving your lips up or to the side, allowing you to smile, among other things. Spontaneous smiles in these monkeys echo the development of our own expressions. Watch the full video.
Seth Stephens-Davidowitz Feeling worried? These days, much of America is. Over the past eight years, Google search rates for anxiety have more than doubled. They are higher this year than they have been in any year since Google searches were first tracked in 2004. So far, 2016 has been tops for searches for driving anxiety, travel anxiety, separation anxiety, anxiety at work, anxiety at school and anxiety at home. Americans have also become increasingly terrified of the morning. Searches for “anxiety in the morning” have risen threefold over the past decade. But this is nothing compared with the fear of night. Searches for “anxiety at night” have risen ninefold. For years, I have confidently pontificated on topics that I think are important but that I have little experience of — child abuse, racism, sexism, sex. Now I am ready to tackle a topic I actually know something about. Over the past few weeks, I’ve taken a break from worrying about my own anxiety to studying our country’s. While I am not sure I totally nailed down why anxiety seems to have risen so much during the Obama era, I did learn a lot. The places where anxiety is highest are not where I would have expected. When I was growing up, if you had asked me which people were the most anxious, I would have said New York Jews. And a decade of interacting with our country’s urban intelligentsia, Jewish and otherwise, has confirmed that pretty much all of us are a neurotic mess. © 2016 The New York Times Company
Link ID: 22528 - Posted: 08.08.2016
By PHYLLIS KORKKI Ever experienced a bout of anxiety at work? I just did. One day last week I had several assignments to finish in quick succession. I could feel thoughts pinging around in my brain as I tried and failed to decide what to focus on first. Once I was able to get the pandemonium under control, my brain felt like mush. So what did I do? I breathed deeply from the middle of my body. I imagined the top of my head, and pictured arrows coming out the sides of my shoulders. I stood up for a while and then walked around the newsroom. And went back to work. These simple solutions to anxiety are not so easy to practice in an era of multitasking, multiple screens and mindless distractions. I learned them only after signing a contract to write a book — and becoming so anxious about it that I developed back and stomach pains. Unable to score a prescription for Klonopin (it’s addictive, my doctor said), I was reduced to seeking out natural methods to relieve my anxiety. The methods I learned helped me write the book. But they also made me realize that workers of all stripes could use them to reduce stress, and to think more clearly and creatively. My first stop was Belisa Vranich, a clinical psychologist who teaches — or rather reteaches — people how to breathe. Dimly I sensed that the way I was inhaling and exhaling was out of whack, and she confirmed it by giving me some tests. First off, like most people, I was a “vertical” breather, meaning my shoulders moved upward when I inhaled. Second, I was breathing from my upper chest, where the lungs don’t have much presence. © 2016 The New York Times Company
Link ID: 22527 - Posted: 08.08.2016
Pete Etchells Mind gamers: How good do you reckon your memory is? We might forget things from time to time, but the stuff we do remember is pretty accurate, right? The trouble is, our memory isn’t as infallible as we might want to believe, and you can test this for yourself using the simple experiment below. All done? Great. Now we’re going to do a simple recognition test – below is another list of words for you to look at. Without looking back, note down which of them appeared in the three lists you just scanned. No cheating! If you said that top, seat and yawn were in the lists, you’re spot on. Likewise, if you think that slow, sweet and strong didn’t appear anywhere, you’re also right. What about chair, mountain and sleep though? They sound like they should have been in the lists, but they never made an appearance. Some of you may have spotted this, but a lot of people tend to say, with a fair amount of certainty, that the words were present. This experiment comes from a classic 1995 study by Henry L. Roediger and Kathleen McDermott at Rice University in Texas. Based on earlier work by James Deese (hence the name Deese-Roediger-McDermott, or DRM, paradigm), participants heard a series of word lists, which they then had to recall from memory. After a brief conversation with the researcher, the participants were then given a new list of words. Critically, this new list contained some words that were associated with every single item on each of the initial lists – for example, while sleep doesn’t appear on list 3 above, it’s related to each word that does appear (bed, rest, tired, and so on). © 2016 Guardian News and Media Limited
Keyword: Learning & Memory
Link ID: 22526 - Posted: 08.08.2016
By EUGENE M. CARUSO, ZACHARY C. BURNS and BENJAMIN A. CONVERSE Watching slow-motion footage of an event can certainly improve our judgment of what happened. But can it also impair judgment? This question arose in the 2009 murder trial of a man named John Lewis, who killed a police officer during an armed robbery of a Dunkin’ Donuts in Philadelphia. Mr. Lewis pleaded guilty; the only question for the jury was whether the murder resulted from a “willful, deliberate and premeditated” intent to kill or — as Mr. Lewis argued — from a spontaneous, panicked reaction to seeing the officer enter the store unexpectedly. The key piece of evidence was a surveillance video of the shooting, which the jury saw both in real time and in slow motion. The jury found that Mr. Lewis had acted with premeditation, and he was sentenced to death. Mr. Lewis appealed the decision, arguing that the slow-motion video was prejudicial. Specifically, he claimed that watching the video in slow motion artificially stretched the relevant time period and created a “false impression of premeditation.” Did it? We recently conducted a series of experiments whose results are strikingly consistent with that claim. Our studies, published this week in the Proceedings of the National Academy of Sciences, show that seeing replays of an action in slow motion leads viewers to believe that the actor had more time to think before acting than he actually did. The result is that slow motion makes actions seem more intentional, more premeditated. In one of our studies, participants watched surveillance video of a fatal shooting that occurred outside a convenience store during an armed robbery. We gave them a set of instructions similar to those given to the jurors in Mr. Lewis’s case, asking them to decide whether the crime was premeditated or not. We assigned half our participants to watch the video in slow motion and the other half to watch it at regular speed. © 2016 The New York Times Company
Link ID: 22525 - Posted: 08.08.2016
By MARTHA C. WHITE A graphic 30-year-old drug education campaign from Partnership for a Drug-Free America is being updated. For a generation of commercial-watching adolescents, it was an indelible image: an egg, sizzling in a frying pan, representing “your brain on drugs.” It was a straightforward message, and the ad’s final line — “Any questions?” — asked as the egg white clouded and cooked, was strictly rhetorical. Three decades later, the Partnership for Drug-Free Kids (the group formerly known as the Partnership for a Drug-Free America) is bringing the frying pan out of retirement and firing up the stove again. But this time questions are the point. The group hopes it can tap into the nostalgia parents may have for the old frying egg ad while also letting them know their children do indeed want answers about drugs. “‘Any questions’ was the end. Now it’s the beginning,” said Scott Seymour, chief creative officer at BFG Communications, which created print and digital banner ads for the new campaign. “The landscape of drugs has really gotten a lot more complex, so we took this idea of having a succession of questions delivered by kids,” he said. The group drew on real inquiries from parents to develop the questions featured in the ads, which cover topics like prescription drugs and marijuana legalization. Children today feel empowered and entitled to ask questions about drugs, and parents are more willing to entertain those questions, observers say. “Because of parenting styles today, parents are engaged with their kids in a different way,” said Kristi Rowe, chief marketing officer at the Partnership for Drug-Free Kids. “They’re really stumped by the questions. They don’t know how to answer them.” © 2016 The New York Times Company
Keyword: Drug Abuse
Link ID: 22524 - Posted: 08.08.2016
Helen Thompson A roughly 27-million-year-old fossilized skull echoes growing evidence that ancient whales could navigate using high-frequency sound. Discovered over a decade ago in a drainage ditch by an amateur fossil hunter on the South Carolina coast, the skull belongs to an early toothed whale. The fossil is so well-preserved that it includes rare inner ear bones similar to those found in modern whales and dolphins. Inspired by the Latin for “echo hunter,” scientists have now named the ancient whale Echovenator sandersi. “It suggests that the earliest toothed whales could hear high-frequency sounds,” which is essential for echolocation, says Morgan Churchill, an anatomist at the New York Institute of Technology in Old Westbury. Churchill and his colleagues describe the specimen online August 4 in Current Biology. Modern whales are divided on the sound spectrum. Toothed whales, such as orcas and porpoises, use high-frequency clicking sounds to sense predators and prey. Filter-feeding baleen whales, on the other hand, use low-frequency sound for long-distance communication. Around 35 million years ago, the two groups split, and E. sandersi emerged soon after. CT scans show that E. sandersi had a few features indicative of ultrasonic hearing in modern whales and dolphins. Most importantly, it had a spiraling inner ear bone with wide curves and a long bony support structure, both of which allow a greater sensitivity to higher-frequency sound. A small nerve canal probably transmitted sound signals to the brain. © Society for Science & the Public 2000 - 2016. All rights reserved.
By Roxanne Khamsi, What if controlling the appetite were as easy as flipping a switch? It sounds like the stuff of science fiction, but Jeffrey Friedman of Rockefeller University and his colleagues did exactly this in genetically engineered mice to try to shed light on how the brain influences appetite. Friedman and his colleagues used magnetic stimulation to switch on neurons in a region of the brain called the ventromedial hypothalamus and found that doing so increased the rodents' blood sugar levels and decreased levels of the hormone insulin. Turning on the neurons also caused the mice to eat more than their control counterparts. The ultimate confirmation came when they inhibited these neurons and saw the opposite effects: it drove blood sugar down, elevated insulin levels and suppressed the animals' urge to consume their chow. That the brain influences hunger is not an unexpected finding, but scientists have recently narrowed in on how it has sway on what ends up in the gut—and how the gut talks to the mind. This two-way communication, defined as the 'gut–brain axis', happens not only through nerve connections between the organs, but also through biochemical signals, such as hormones, that circulate in the body. “The idea that there is bidirectional communication between the gastrointestinal tract and brain that affects metabolism traces back more than a century,” Friedman says, referring to the work of the nineteenth-century French scientist Claude Bernard, who made seminal discoveries into how the body maintains physiological equilibrium. “Our new findings that insulin-producing cells in the pancreas can be controlled by certain neurons in the brain that sense blood sugar provides further experimental evidence supporting this notion.” © 2016 Scientific American,
Link ID: 22522 - Posted: 08.06.2016
Tina Hesman Saey Alcoholism may stem from using genes incorrectly, a study of hard-drinking rats suggests. Rats bred either to drink heavily or to shun alcohol have revealed 930 genes linked to a preference for drinking alcohol, researchers in Indiana report August 4 in PLOS Genetics. Human genetic studies have not found most of the genetic variants that put people at risk for alcoholism, says Michael Miles, a neurogenomicist at Virginia Commonwealth University in Richmond. The new study takes a “significant and somewhat novel approach” to find the genetic differences that separate those who will become addicted to alcohol from those who drink in moderation. It took decades to craft the experiment, says study coauthor William Muir, a population geneticist at Purdue University in West Lafayette, Ind. Starting in the 1980s, rats bred at Indiana University School of Medicine in Indianapolis were given a choice to drink pure water or water mixed with 10 percent ethanol, about the same amount of alcohol as in a weak wine. For more than 40 generations, researchers selected rats from each generation that voluntarily drank the most alcohol and bred them to create a line of rats that consume the rat equivalent of 25 cans of beer a day. Simultaneously, the researchers also selected rats that drank the least alcohol and bred them to make a line of low-drinking rats. A concurrent breeding program produced another line of high-drinking and teetotaling rats. For the new study, Muir and colleagues collected DNA from 10 rats from each of the high- and low-drinking lines. Comparing complete sets of genetic instructions from all the rats identified 930 genes that differ between the two lines. |© Society for Science & the Public 2000 - 2016.
By Nicholas Bakalar A drug used to treat rheumatoid arthritis may have benefits against Alzheimer’s disease, researchers report. Rheumatoid arthritis is an autoimmune disease believed to be driven in part by tumor necrosis factor, or T.N.F., a protein that promotes inflammation. Drugs that block T.N.F., including an injectable drug called etanercept, have been used to treat rheumatoid arthritis for many years. T.N.F. is also elevated in the cerebrospinal fluid of Alzheimer’s patients. Researchers identified 41,109 men and women with a diagnosis of rheumatoid arthritis and 325 with both rheumatoid arthritis and Alzheimer’s disease. In people over 65, the prevalence of Alzheimer’s disease was more than twice as high in people with rheumatoid arthritis as in those without it. The study is in CNS Drugs. But unlike patients treated with five other rheumatoid arthritis drugs, those who had been treated with etanercept showed a significantly reduced risk for Alzheimer’s disease. Still, the lead author, Dr. Richard C. Chou, an assistant professor of medicine at Dartmouth, said that it is too early to think of using etanercept as a treatment for Alzheimer’s. “We’ve identified a process in the brain, and if you can control this process with etanercept, you may be able to control Alzheimer’s,” he said. “But we need clinical trials to prove and confirm it.” © 2016 The New York Times Company
Link ID: 22520 - Posted: 08.06.2016
By LUKE DITTRICH ‘Can you tell me who the president of the United States is at the moment?” A man and a woman sat in an office in the Clinical Research Center at the Massachusetts Institute of Technology. It was 1986, and the man, Henry Molaison, was about to turn 60. He was wearing sweatpants and a checkered shirt and had thick glasses and thick hair. He pondered the question for a moment. “No,” he said. “I can’t.” The woman, Jenni Ogden, was a visiting postdoctoral research fellow from the University of Auckland, in New Zealand. One of the greatest thrills of her time at M.I.T. was the chance to have sit-down sessions with Henry. In her field — neuropsychology — he was a legendary figure, something between a rock star and a saint. “Who’s the last president you remember?” “I don’t. ... ” He paused for a second, mulling over the question. He had a soft, tentative voice, a warm New England accent. “Ike,” he said finally. Dwight D. Eisenhower’s inauguration took place in 1953. Our world had spun around the sun more than 30 times since, though Henry’s world had stayed still, frozen in orbit. This is because 1953 was the year he received an experimental operation, one that destroyed most of several deep-seated structures in his brain, including his hippocampus, his amygdala and his entorhinal cortex. The operation, performed on both sides of his brain and intended to treat Henry’s epilepsy, rendered him profoundly amnesiac, unable to hold on to the present moment for more than 30 seconds or so. That outcome, devastating to Henry, was a boon to science: By 1986, Patient H.M. — as he was called in countless journal articles and textbooks — had become arguably the most important human research subject of all time, revolutionizing our understanding of how memory works. © 2016 The New York Times Company
Keyword: Learning & Memory
Link ID: 22519 - Posted: 08.04.2016
By Jonathan Webb Science reporter, BBC News Scientists have glimpsed activity deep in the mouse brain which can explain why we get thirsty when we eat, and why cold water is more thirst-quenching. A specific "thirst circuit" was rapidly activated by food and quietened by cooling down the animals' mouths. The same brain cells were already known to stimulate drinking, for example when dehydration concentrates the blood. But the new findings describe a much faster response, which predicts the body's future demand for water. The researchers went looking for this type of system because they were puzzled by the fact that drinking behaviour, in humans as well as animals, seems to be regulated very quickly. "There's this textbook model for homeostatic regulation of thirst, that's been around for almost 100 years, that's based on the blood," said the study's senior author Zachary Knight, from the University of California, San Francisco. "There are these neurons in the brain that… generate thirst when the blood becomes too salty or the blood volume falls too low. But lots of aspects of everyday drinking can't possibly be explained by that homeostatic model because they occur much too quickly." Take the "prandial thirst" that comes while we consume a big, salty meal - or the fact that we feel quenched almost as soon as we take a drink. © 2016 BBC.
Link ID: 22518 - Posted: 08.04.2016