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By BENEDICT CAREY Behind all those canned compliments for older adults — spry! wily! wise! — is an appreciation for something that scientists have had a hard time characterizing: mental faculties that improve with age. Knowledge is a large part of the equation, of course. People who are middle-aged and older tend to know more than young adults, by virtue of having been around longer, and score higher on vocabulary tests, crossword puzzles and other measures of so-called crystallized intelligence. Still, young adults who consult their elders (mostly when desperate) don’t do so just to gather facts, solve crosswords or borrow a credit card. Nor, generally, are they looking for help with short-term memory or puzzle solving. Those abilities, called fluid intelligence, peak in the 20s. No, the older brain offers something more, according to a new paper in the journal Psychological Science. Elements of social judgment and short-term memory, important pieces of the cognitive puzzle, may peak later in life than previously thought. The postdoctoral fellows Joshua Hartshorne of M.I.T. and Laura Germine of Harvard and Massachusetts General Hospital analyzed a huge trove of scores on cognitive tests taken by people of all ages. The researchers found that the broad split in age-related cognition — fluid in the young, crystallized in the old — masked several important nuances. “This dichotomy between early peaks and later peaks is way too coarse,” Dr. Hartshorne said. “There are a lot more patterns going on, and we need to take those into account to fully understand the effects of age on cognition.” The new paper is hardly the first challenge to the scientific literature on age-related decline, and it won’t be the last. A year ago, German scientists argued that cognitive “deficits” in aging were caused largely by the accumulation of knowledge — that is, the brain slows down because it has to search a larger mental library of facts. That idea has stirred some debate among scientists. Experts said the new analysis raised a different question: Are there distinct, independent elements of memory and cognition that peak at varying times of life? © 2015 The New York Times Company

Keyword: Intelligence; Development of the Brain
Link ID: 20693 - Posted: 03.17.2015

By Camilla Turner It is one of life’s most enduring mysteries. A question that music, poetry, myth and legend has, for thousands of years, tried but failed to answer. However, we may now be a step closer to discovering what love is, thanks to a scientific study that has obtained the first empirical evidence of love-related alterations in the brain. A team of researchers from universities in China and New York used MRI scans to track the physical effects of love on the brain and has pieced together a “love map” of the human mind. The study found that several areas of the brain showed increased activity in those who were in love, including in the parts of the brain linked to reward and motivation. The researchers said their results shed light on the “underlying mechanisms of romantic love” and would pave the way for a brain scan that could act as a “love test”. Scientists recruited 100 students from Southwest University in Chongqing, China, who were divided into three groups according to their relationship status: an “in-love” group, comprised of those who were in love at the time; an “ended-love” group, who had recently ended loving relationships; and a “single” group, who had never been in love. Participants were told not to think of anything while their brains were scanned, so that researchers could monitor the differences between the brains of students in all three groups. © Copyright of Telegraph Media Group Limited 2015

Keyword: Sexual Behavior
Link ID: 20692 - Posted: 03.17.2015

By RENEE ENGELN ON Tuesday, in the wake of an online petition signed by thousands of people, Facebook announced that it was removing “feeling fat” from its list of status update emoticons. The petition argued that the offending emoticon, with its chubby cheeks and double chin, reinforced negative body images, and Facebook seemed to agree. Is it really such a big deal if you tell everyone how fat you feel? After all, a simple “I’m so fat!” can result in a chorus of empathetic voices, saying, “Me, too!” or “You’re beautiful just the way you are!” And that will help you feel better, and help others feel better, too — right? Wrong. As someone who studies this type of public body self-disparagement, known as “fat talk,” I can say that it probably will make you feel worse. And it may drag down other people with you. Conversational shaming of the body has become practically a ritual of womanhood (though men also engage in it). In a survey that a colleague and I reported in 2011 in the Psychology of Women Quarterly, we found that more than 90 percent of college women reported engaging in fat talk — despite the fact that only 9 percent were actually overweight. In another survey, which we published in December in the Journal of Health Psychology, we canvassed thousands of women ranging in age from 16 to 70. Contrary to the stereotype of fat talk as a young woman’s practice, we found that fat talk was common across all ages and all body sizes. Most important, fat talk is not a harmless social-bonding ritual. According to an analysis of several studies that my colleagues and I published in 2012 in the Psychology of Women Quarterly, fat talk was linked with body shame, body dissatisfaction and eating-disordered behavior. Fat talk does not motivate women to make healthier choices or take care of their bodies; in fact, the feelings of shame it brings about tend to encourage the opposite. © 2015 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 20691 - Posted: 03.17.2015

By Emily Underwood Deep brain stimulation, which now involves surgically inserting electrodes several inches into a person's brain and connecting them to a power source outside the skull, can be an extremely effective treatment for disorders such as Parkinson's disease, obsessive compulsive disorder, and depression. The expensive, invasive procedure doesn't always work, however, and can be risky. Now, a study in mice points to a less invasive way to massage neuronal activity, by injecting metal nanoparticles into the brain and controlling them with magnetic fields. Major technical challenges must be overcome before the approach can be tested in humans, but the technique could eventually provide a wireless, nonsurgical alternative to traditional deep brain stimulation surgery, researchers say. "The approach is very innovative and clever," says Antonio Sastre, a program director in the Division of Applied Science & Technology at the National Institute of Biomedical Imaging and Bioengineering in Bethesda, Maryland. The new work provides "a proof of principle." The inspiration to use magnets to control brain activity in mice first struck materials scientist Polina Anikeeva while working in the lab of neuroscientist-engineer Karl Deisseroth at Stanford University in Palo Alto, California. At the time, Deisseroth and colleagues were refining optogenetics, a tool that can switch specific ensembles of neurons on and off in animals with beams of light. © 2015 American Association for the Advancement of Science.

Keyword: Brain imaging
Link ID: 20690 - Posted: 03.14.2015

By John Horgan In 1990 The New York Times published a front-page article by Lawrence Altman, a reporter with a medical degree, announcing that scientists had discovered “a link between alcoholism and a specific gene.” The evidence for the "feel-good gene," which supposedly reduces anxiety, is flimsy, just like the evidence linking specific genes to high intelligence, violent aggression, homosexuality, bipolar disorder and countless other complex human traits and ailments. That was merely one in a string of reports in which the Times and other major media hyped what turned out to be erroneous claims linking complex traits and disorders—from homosexuality and high intelligence to schizophrenia and bipolar disorder—to specific genes. I thought those days were over, and that scientists and the media have learned to doubt extremely reductionist genetic accounts of complex traits and behaviors. I was wrong. Last Sunday, the “Opinion” section of the Times published an essay, “The Feel-Good Gene,” which states: “For the first time, scientists have demonstrated that a genetic variation in the brain makes some people inherently less anxious, and more able to forget fearful and unpleasant experiences. This lucky genetic mutation produces higher levels of anandamide–the so-called bliss molecule and our natural marijuana–in our brains. In short, some people are prone to be less anxious simply because they won the genetic sweepstakes and randomly got a genetic mutation that has nothing at all to do with strength of character.” This article, like the one touting the alcoholism gene 25 years ago, was written by a physician, Richard Friedman, professor of psychiatry at Weill Cornell Medical College. I emphasize this fact because scientific hype is often blamed on supposedly ignorant journalists like me rather than on physicians and other so-called experts. © 2015 Scientific American

Keyword: Drug Abuse; Genes & Behavior
Link ID: 20689 - Posted: 03.14.2015

By Matthew J.X. Malady One hour and seven minutes into the decidedly hit-or-miss 1996 comedy Black Sheep, the wiseass sidekick character played by David Spade finds himself at an unusually pronounced loss for words. While riding in a car driven by Chris Farley’s character, he glances at a fold-up map and realizes he somehow has become unfamiliar with the name for paved driving surfaces. “Robes? Rouges? Rudes?” Nothing seems right. Even when informed by Farley that the word he’s looking for is roads, Spade’s character continues to struggle: “Rowds. Row-ads.” By this point, he’s become transfixed. “That’s a total weird word,” he says, “isn’t it?” Now, it’s perhaps necessary to mention that, in the context of the film, Spade’s character is high off nitrous oxide that has leaked from the car’s engine boosters. But never mind that. Row-ad-type word wig outs similar to the one portrayed in that movie are things that actually happen, in real life, to people with full and total control over their mental capacities. These wordnesias sneak up on us at odd times when we’re writing or reading text. I was in a full-on wordnesiac state. On one of my spelling attempts, I think I even threw a K into the mix. It was bad. Here’s how they work: Every now and again, for no good or apparent reason, you peer at a standard, uncomplicated word in a section of text and, well, go all row-ads on it. If you’re typing, that means inexplicably blanking on how to spell something easy like cake or design. The reading version of wordnesia occurs when a common, correctly spelled word either seems as though it can’t possibly be spelled correctly, or like it’s some bizarre combination of letters you’ve never before seen—a grouping that, in some cases, you can’t even imagine being the proper way to compose the relevant term. © 2014 The Slate Group LLC.

Keyword: Language
Link ID: 20688 - Posted: 03.14.2015

By Maggie Fox Teenagers who use marijuana heavily grow up to have poor memories and also have brain abnormalities, a new study shows. The study cannot say which came first — the brain structure differences or the pot use. But it suggests there could be long-term effects of heavy marijuana use. A team at Northwestern University looked at 97 volunteers with and without mental illness. The dope smokers said they'd used marijuana daily starting at age 16 or 17, and said they had not used other drugs. The daily marijuana users had an abnormally shaped hippocampus and performed about 18 percent more poorly on long-term memory tasks, the researchers reported in the journal Hippocampus. The hippocampus is a part of the brain used in storing long-term memory. "The memory processes that appear to be affected by cannabis are ones that we use every day to solve common problems and to sustain our relationships with friends and family," said Dr. John Csernansky, who worked on the study. Previous research by the same Northwestern team showed heavy pot smokers had poor short-term and working memory and abnormally shaped brain structures including the striatum, globus pallidus and thalamus. "It is possible that the abnormal brain structures reveal a pre-existing vulnerability to marijuana abuse," Matthew Smith, who led the study, said in a statement.

Keyword: Drug Abuse; Learning & Memory
Link ID: 20687 - Posted: 03.14.2015

When it comes to fight or flight for brawling crickets, a chemical in the brain is in charge. Being roughed up in a skirmish can trigger nerve cells in Mediterranean field crickets (Gryllus bimaculatus) to release nitric oxide, making the losing cricket run away, scientists report online March 13 in Science Advances. Watch in this video as two crickets face off. When the loser hits its limit, it flees the fight. In a second bout, the loser then tries to avoid the winner. Nitric oxide prompts this continued submissive behavior, which lasts several hours before a cricket’s will to fight returns. “If you block nitric oxide they recover quickly, and if you give them nitric oxide they don’t,” says Paul Stevenson, a coauthor of the new research and behavioral neurobiologist at Leipzig University in Germany. “It’s a very simple algorithm for controlling a very complicated social situation.” P. Stevenson and J. Rillich. Adding up the odds—Nitric oxide signaling underlies the decision to flee and post-conflict depression of aggression. Science Advances. Published online March 13, 2015.doi: 10.1126/sciadv.1500060. © Society for Science & the Public 2000 - 2015.

Keyword: Aggression
Link ID: 20686 - Posted: 03.14.2015

By Emily Underwood From imaging babies to blasting apart kidney stones, ultrasound has proved to be a versatile tool for physicians. Now, several research teams aim to unleash the technology on some of the most feared brain diseases. The blood-brain barrier, a tightly packed layer of cells that lines the brain's blood vessels, protects it from infections, toxins, and other threats but makes the organ frustratingly hard to treat. A strategy that combines ultrasound with microscopic blood-borne bubbles can briefly open the barrier, in theory giving drugs or the immune system access to the brain. In the clinic and the lab, that promise is being evaluated. This month, in one of the first clinical tests, Todd Mainprize, a neurosurgeon at the University of Toronto in Canada, hopes to use ultrasound to deliver a dose of chemotherapy to a malignant brain tumor. And in some of the most dramatic evidence of the technique's potential, a research team reports this week in Science Translational Medicine that they used it to rid mice of abnormal brain clumps similar to those in Alzheimer's disease, restoring lost memory and cognitive functions. If such findings can be translated from mice to humans, “it will revolutionize the way we treat brain disease,” says biophysicist Kullervo Hynynen of the Sunnybrook Research Institute in Toronto, who originated the ultrasound method. Some scientists stress that rodent findings can be hard to translate to humans and caution that there are safety concerns about zapping the brain with even the low-intensity ultrasound used in the new study, which is similar to that used in diagnostic scans. © 2015 American Association for the Advancement of Science.

Keyword: Alzheimers
Link ID: 20685 - Posted: 03.12.2015

|By Daisy Yuhas The brain is a hotbed of electrical activity. Scientists have long known that brain cells communicate via electrical missives, created by charged atoms and molecules called ions as they travel across the membranes of those cells. But a new study suggests that in the days and weeks that lead up to a brain forming in an embryo or fetus, altering the electrical properties of these cells can dramatically change how the ensuing brain develops. Researchers at Tufts University and the University of Minnesota have investigated how the difference in charge on either side of a resting cell’s membrane—its electrical potential—helps build the brain. In previous work Tufts University developmental biologist Michael Levin found that patterns of electrical potentials in the earliest stages of an embryo’s development can direct how an animal’s body grows, and that manipulating those potentials can cause a creature to sprout extra limbs, tails or functioning eyes. Now, Levin’s group has investigated how these potentials shape the brain. Working with frog embryos the researchers first used dyes to see the patterns of electrical potentials that precede brain development. They noticed that before the development of a normal brain the cells lining the neural tube, a structure that eventually becomes the brain and spinal cord, have extreme differences in ionic charge within and outside the membrane that houses the cells. In other words, these cells are extremely polarized. © 2015 Scientific American

Keyword: Development of the Brain
Link ID: 20684 - Posted: 03.12.2015

Older people could improve or maintain their mental function through heart healthy lifestyle changes, a large randomized trial for dementia prevention shows. Researchers in Finland and Sweden designed a trial to tackle risk factors for Alzheimer's disease. The 1,260 Finns aged 60 to 77 participating in the study were all considered at risk of dementia based on standard test scores. Half were randomly assigned to receive advice from health professionals on maintaining a healthy diet, aerobic and muscle training exercises, brain training exercises and regular checks of blood pressure, height and weight for body mass index and physical exams for two years or regular health advice. Participants in the Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability or FINGER study had their cognitive function measured in a battery of mental tests. "The main hypothesis was that simultaneous changes in several risk factors (even of smaller magnitude) would lead to a protective effect on cognition," Miia Kivipelto from the Karolinska Institute in Stockholm and her co-authors said in Wednesday's issue of The Lancet. Overall, test scores were 25 per cent in the diet and training group than the control group. There was no effect on memory. ©2015 CBC/Radio-Canada.

Keyword: Alzheimers
Link ID: 20683 - Posted: 03.12.2015

Mutations in the presenilin-1 gene are the most common cause of inherited, early-onset forms of Alzheimer’s disease. In a new study, published in Neuron, scientists replaced the normal mouse presenilin-1 gene with Alzheimer’s-causing forms of the human gene to discover how these genetic changes may lead to the disorder. Their surprising results may transform the way scientists design drugs that target these mutations to treat inherited or familial Alzheimer’s, a rare form of the disease that affects approximately 1 percent of people with the disorder. The study was partially funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. For decades, it has been unclear exactly how the presenilin mutations cause Alzheimer’s disease. Presenilin is a component of an important enzyme, gamma secretase, which cuts up amyloid precursor protein into two protein fragments, Abeta40 and Abeta42. Abeta42 is found in plaques, the abnormal accumulations of protein in the brain which are a hallmark of Alzheimer’s. Numerous studies suggested that presenilin-1 mutations increased activity of gamma-secretase. Investigators have developed drugs that block gamma-secretase, but they have so far failed in clinical trials to halt the disease. The study led by Raymond Kelleher, M.D., Ph.D. and Jie Shen, Ph.D., professors of neurology at Harvard Medical School, Boston, provides a plot twist in the association of presenilin-1 mutations and inherited Alzheimer’s disease. Using mice with altered forms of the presenilin gene, Drs. Kelleher and Shen discovered that the mutations may cause the disease by decreasing, rather than increasing, the activity of gamma-secretase.

Keyword: Alzheimers; Genes & Behavior
Link ID: 20682 - Posted: 03.12.2015

|By Esther Landhuis As we age, we seem to get worse at ignoring irrelevant stimuli. It's what makes restaurant conversations challenging—having to converse while also shutting out surrounding chatter. New research bears out the aging brain's distractibility but also suggests that training may help us tune out interference. Scientists at Brown University recruited seniors and twentysomethings for a visual experiment. Presented with a sequence of letters and numbers, participants were asked to report back only the numbers—all the while disregarding a series of meaningless dots. Sometimes the dots moved randomly, but other times they traveled in a clear direction, making them harder to ignore. Older participants ended up accidentally learning the dots' patterns, based on the accuracy of their answers when asked which way the dots were moving, whereas young adults seemed able to suppress that information and focus on the numbers, the researchers reported last November in Current Biology. In a separate study published in Neuron, scientists at the University of California, San Francisco, showed they could train aging brains to become less distractible. Their regimen helped aging rats as well as older people. The researchers played three different sounds and rewarded trainees for identifying a target tone while ignoring distracter frequencies. As the subjects improved, the task grew more challenging—the distracting tone became harder to discriminate from the target. © 2015 Scientific American,

Keyword: Attention; Alzheimers
Link ID: 20681 - Posted: 03.12.2015

By Gretchen Reynolds An easy, two-minute vision test administered on the sidelines after a young athlete has hit his or her head can help to reliably determine whether the athlete has sustained a concussion, according to a new study of student athletes, some as young as 5. The test is so simple and inexpensive that any coach or parent potentially could administer it, the study’s authors believe, and any league afford to provide it as a way to help evaluate and safeguard players. Those of us who coach or care for young athletes know by now that an athlete who falls or collides with something during play or seems dazed, dizzy, loses consciousness or complains of head pain should be tested for a concussion, which occurs when the brain is physically jostled within the skull. But most of us are clueless about how to test young athletes. The most commonly recommended sideline test is the Standardized Assessment of Concussion, a multipart examination during which athletes are asked to name the date, describe how they feel, memorize and recall lists of words, and do jumping jacks and other tests of coordination. Ideally, this assessment should be administered and evaluated by a medical professional. But while the sidelines of college and professional games are crowded with doctors and certified athletic trainers, few high schools and youth leagues have those resources. Most of the time, concussion testing in youth sports falls to volunteer coaches or parents with little if any medical experience. That situation prompted researchers at New York University’s Langone Concussion Center to begin wondering recently whether there might be other, easier diagnostic tools to check young players for concussions. Their thoughts soon turned to vision. “About 50 percent of the brain’s pathways are tied in some to way to vision and visual processing,” said Dr. Steven Galetta, chairman of neurology at N.Y.U. Langone Medical Center and senior author of the study, which was published in The Journal of Neuro-Ophthalmology. © 2015 The New York Times Company

Keyword: Brain Injury/Concussion
Link ID: 20680 - Posted: 03.12.2015

By Douglas Starr In 1906, Hugo Münsterberg, the chair of the psychology laboratory at Harvard University and the president of the American Psychological Association, wrote in the Times Magazine about a case of false confession. A woman had been found dead in Chicago, garroted with a copper wire and left in a barnyard, and the simpleminded farmer’s son who had discovered her body stood accused. The young man had an alibi, but after questioning by police he admitted to the murder. He did not simply confess, Münsterberg wrote; “he was quite willing to repeat his confession again and again. Each time it became richer in detail.” The young man’s account, he continued, was “absurd and contradictory,” a clear instance of “the involuntary elaboration of a suggestion” from his interrogators. Münsterberg cited the Salem witch trials, in which similarly vulnerable people were coerced into self-incrimination. He shared his opinion in a letter to a Chicago nerve specialist, which made the local press. A week later, the farmer’s son was hanged. Münsterberg was ahead of his time. It would be decades before the legal and psychological communities began to understand how powerfully suggestion can shape memory and, in turn, the course of justice. In the early nineteen-nineties, American society was recuperating from another panic over occult influence; Satanists had replaced witches. One case, the McMartin Preschool trial, hinged on nine young victims’ memories of molestation and ritual abuse—memories that they had supposedly forgotten and then, after being interviewed, recovered. The case fell apart, in 1990, because the prosecution could produce no persuasive evidence of the victims’ claims. A cognitive psychologist named Elizabeth Loftus, who had consulted on the case, wondered whether the children’s memories might have been fabricated—in Münsterberg’s formulation, involuntarily elaborated—rather than actually recovered.

Keyword: Learning & Memory
Link ID: 20679 - Posted: 03.12.2015

|By Anne Skomorowsky On a Saturday night last month, 12 students at Wesleyan University in Connecticut were poisoned by “Molly,” a hallucinogenic drug they had taken to enhance a campus party. Ambulances and helicopters transported the stricken to nearby hospitals, some in critical condition. Molly—the street name for the amphetamine MDMA—can cause extremely high fevers, liver failure, muscle breakdown, and cardiac arrest. Given the risks associated with Molly, why would anybody take it? The obvious answer—to get high—is only partly true. Like many drugs of abuse, Molly causes euphoria. But Molly is remarkable for its “prosocial” effects. Molly makes users feel friendly, loving, and strongly connected to one another. Molly is most commonly used in settings where communion with others is highly valued, such as raves, music festivals, and college parties. Recently, psychiatrists have taken an interest in its potential to enhance psychotherapy; this has led to new research into the mechanisms by which MDMA makes people feel closer. It appears that MDMA works by shifting the user’s attention towards positive experiences while minimizing the impact of negative feelings. To investigate this, a 2012 study by Cedric Hysek and colleagues used the Reading the Mind in the Eyes Test (RMET), which was developed to evaluate people with autism. In the RMET, participants are shown 36 pictures of the eye region of faces. Their task is to describe what the person in the picture is feeling. Volunteers taking MDMA, under carefully controlled conditions, improved in their recognition of positive emotions; but their performance in recognizing negative emotions declined. In other words, they incorrectly attributed positive or neutral feelings to images that were actually negative in emotional tone. They mistook negative and threat-related images for friendly ones. © 2015 Scientific American

Keyword: Drug Abuse
Link ID: 20678 - Posted: 03.12.2015

Mo Costandi Neuroscientists in France have implanted false memories into the brains of sleeping mice. Using electrodes to directly stimulate and record the activity of nerve cells, they created artificial associative memories that persisted while the animals snoozed and then influenced their behaviour when they awoke. Manipulating memories by tinkering with brain cells is becoming routine in neuroscience labs. Last year, one team of researchers used a technique called optogenetics to label the cells encoding fearful memories in the mouse brain and to switch the memories on and off, and another used it to identify the cells encoding positive and negative emotional memories, so that they could convert positive memories into negative ones, and vice versa. The new work, published today in the journal Nature Neuroscience, shows for the first time that artificial memories can be implanted into the brains of sleeping animals. It also provides more details about how populations of nerve cells encode spatial memories, and about the important role that sleep plays in making such memories stronger. Karim Benchenane of the French National Centre for Scientific Research (CNRS) in Paris and his colleagues implanted electrodes into the brains of 40 mice, targeting the medial forebrain bundle (MFB), a component of the reward circuitry, and the CA1 region of the hippocampus, which contains at least three different cell types that encode the memories needed for spatial navigation. © 2015 Guardian News and Media Limited

Keyword: Learning & Memory; Sleep
Link ID: 20677 - Posted: 03.10.2015

By Nicholas Bakalar People sometimes take Valium or Ativan to relieve anxiety before surgery, but a new study suggests that these benzodiazepine drugs have little beneficial effect and may even delay recovery. Researchers studied 1,062 patients admitted to French hospitals for surgery requiring general anesthesia. A third took 2.5 milligrams of lorazepam (brand name Ativan), a third received a placebo, and a third were given no premedication. Patients completed questionnaires assessing anxiety, pain levels and quality of sleep before and a day after their operations, while researchers recorded their time to having ventilation tubes removed and to recovering full wakefulness. The study was published in JAMA. Lorazepam was associated with more postsurgery amnesia and a longer time to recover cognitive abilities. Quality of sleep was impaired in the lorazepam group, but not in the others. And ventilation tubes were kept in significantly longer in the lorazepam group. Pain scores did not differ between the lorazepam and the no-medication groups, but there was more pain in the group given the placebo. The lead author, Dr. Axel Maurice-Szamburski, an anesthesiologist at Timone Hospital in Marseille, cited recent surveys showing that benzodiazepines are widely prescribed before surgery. “But until now,” he added, “sedatives have not been evaluated from the patient’s point of view. It’s the patient who should be happy, not the doctor.” © 2015 The New York Times Company

Keyword: Emotions
Link ID: 20676 - Posted: 03.10.2015

Jon Hamilton Alzheimer's, Parkinson's and amyotrophic lateral sclerosis ravage the brain in very different ways. But they have at least one thing in common, says Corinne Lasmezas, a neuroscientist and professor at Scripps Research Institute, in Jupiter, Fla. Each spreads from brain cell to brain cell like an infection. "So if we could block this [process], that might prevent the diseases," Lasmezas says. It's an idea that's being embraced by a growing number of researchers these days, including Nobel laureate Dr. Stanley Prusiner, who first recognized in the 1980s the infectious nature of brain proteins that came to be called prions. But the idea that mad cow prions could cause disease in people has its origins in an epidemic of mad cow disease that occurred in Europe and the U.K. some 15 years ago. Back then, Lasmezas was a young researcher in France studying how mad cow, formally known as bovine spongiform encephalopathy, was transmitted. "At that time, nobody knew if this new disease in cows was actually transmissible to humans," she says. In 1996, Lasmezas published a study strongly suggesting that it was. "So that was my first great research discovery," she says. Prions, it turns out, become toxic to brain cells when folded into an abnormal shape. "This misfolded protein basically kills the neurons," Lasmezas says. © 2015 NPR

Keyword: Prions; Parkinsons
Link ID: 20675 - Posted: 03.10.2015

By CELIA WATSON SEUPEL Every year, nearly 40,000 Americans kill themselves. The majority are men, and most of them use guns. In fact, more than half of all gun deaths in the United States are suicides. Experts and laymen have long assumed that people who died by suicide will ultimately do it even if temporarily deterred. “People think if you’re really intent on dying, you’ll find a way,” said Cathy Barber, the director of the Means Matters campaign at Harvard Injury Control Research Center. Prevention, it follows, depends largely on identifying those likely to harm themselves and getting them into treatment. But a growing body of evidence challenges this view. Suicide can be a very impulsive act, especially among the young, and therefore difficult to predict. Its deadliness depends more upon the means than the determination of the suicide victim. Now many experts are calling for a reconsideration of suicide-prevention strategies. While mental health and substance abuse treatment must always be important components in treating suicidality, researchers like Ms. Barber are stressing another avenue: “means restriction.” Instead of treating individual risk, means restriction entails modifying the environment by removing the means by which people usually die by suicide. The world cannot be made suicide-proof, of course. But, these researchers argue, if the walkway over a bridge is fenced off, a struggling college freshman cannot throw herself over the side. If parents leave guns in a locked safe, a teenage son cannot shoot himself if he suddenly decides life is hopeless. With the focus on who dies by suicide, these experts say, not enough attention has been paid to restricting the means to do it — particularly access to guns. © 2015 The New York Times Company

Keyword: Depression
Link ID: 20674 - Posted: 03.10.2015