By Simon Makin Brain science draws legions of eager students to the field and countless millions in dollars, euros and renminbi to fund research. These endeavors, however, have not yielded major improvements in treating patients who suffer from psychiatric disorders for decades. The languid pace of translating research into therapies stems from the inherent difficulties in understanding mental illness. “Psychiatry deals with brains interacting with the world and with other brains, so we're not just considering a brain's function but its function in complex situations,” says Quentin Huys of the Swiss Federal Institute of Technology (E.T.H. Zurich) and the University of Zurich, lead author of a review of the emerging field of computational psychiatry, published this month in Nature Neuroscience. Computational psychiatry sets forth the ambitious goal of using sophisticated numerical tools to understand and treat mental illness. Psychiatry currently defines disorders using lists of symptoms. Researchers have been devoting enormous energies to find biological markers that make diagnosis more objective with only halting success. Part of the problem is there is usually no one-to-one correspondence between biological causes and disorders defined by their symptoms, such as those in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). A specific disorder, like depression or schizophrenia, may result from a range of different underlying causes (biological or otherwise). On the other hand, the same cause might ultimately lead to different disorders in different people, depending on anything from their genetics to their life experiences. One of the goals of computational psychiatry is to draw connections between symptoms and causes, regardless of diagnoses. © 2016 Scientific American

Keyword: Schizophrenia; Depression
Link ID: 22013 - Posted: 03.22.2016

By Manuel Valdes For nearly every step of his almost 12-mile walks around Seattle, Darryl Dyer has company. Flocks of crows follow him, signaling each other, because they all know that he’s the guy with the peanuts. “They know your body type. The way you walk,” Dyer said. “They’ll take their young down and say: ‘You want to get to know this guy. He’s got the food.’ ” Scientists have known for years that crows have great memories, that they can recognize a human face and behavior, that they can pass that information on to their offspring. Researchers are trying to understand more about the crow’s brain and behavior, specifically what the birds do when they see one of their own dead. They react loudly, but the reasons aren’t entirely known. Among the guesses is that they are mourning; given that crows mate for life, losing a partner could be a significant moment for the social animals. There are anecdotes of crows placing sticks and other objects on dead birds — a funeral of sorts. Using masks with dark-haired wigs that looked creepily nonhuman, researchers showed up at Seattle parks carrying a stuffed crow and recorded the reactions. One crow signals an alarm, then dozens show up. They surround the dead crow, looking at it as they perch on trees or fly above it, a behavior called mobbing. “Crows have evolved to have these complex social relationships, and they have a big brain,” said Kaeli Swift, a University of Washington graduate student who led the study.

Keyword: Learning & Memory; Evolution
Link ID: 22012 - Posted: 03.22.2016

By Emily Underwood When pharmaceutical company Eli Lilly in Indianapolis last week announced a major change to its closely watched clinical trial for the Alzheimer’s drug solanezumab, some in the scientific community and drug development industry cried foul. To critics, the company’s decision to eliminate changes in a person’s daily ability to function as a primary measure of solanezumab’s efficacy and focus solely on a cognitive test seemed like a last-ditch attempt to keep a doomed drug from failing its third trial. Lilly’s stock plunged by nearly 5%, apparently reflecting that sentiment. Largely lost in the online “chatter,” however, was that Lilly’s move reflects a growing scientific consensus about how the early stages of Alzheimer’s disease progress, says Dennis Selkoe, a neurologist at Brigham and Women’s Hospital in Boston, who is not involved in the Lilly trial. “From the point of view of a neurologist who’s seen hundreds of patients, [Lilly’s decision] makes clinical sense,” he says. Solanezumab is an antibody designed to bind to and promote the clearance of the β-amyloid protein, which forms plaques around the neurons of people with Alzheimer’s. Not everyone agrees that these plaques are at the root of the disease—a concept called the amyloid hypothesis, of which Selkoe is a major proponent—but fighting them is the foundation of nearly all current efforts in Alzheimer’s drug development. By helping destroy the plaques in people with early stages of Alzheimer’s, Lilly hopes solanezumab can slow the disease’s progression. © 2016 American Association for the Advancement of Science.

Keyword: Alzheimers
Link ID: 22011 - Posted: 03.22.2016

By Emily Underwood People with autism spectrum disorder (ASD) die on average 18 years before the general population, according to a report released today by Autistica, a philanthropic group based in the United Kingdom. People with both ASD and an intellectual disability die even younger, on average 30 years earlier than those without the conditions. Fatal accidents—often by drowning, when a child or adult with ASD wanders away from caregivers—are one of the classic causes of premature death in people who have both ASD and an intellectual disability, says Sven Bölte, a clinical psychologist at the Karolinksa Institute in Stockholm, whose research is cited in the Autistica report. Epilepsy, along with several other neurological disorders, is another common cause of death among people with both ASD and learning difficulties, suggesting that early disruption of neurodevelopment is to blame. These “classic” causes of premature death in autism, however, do not fully account for a decades-long life span gap between autistic and nonautistic people, or the difference in mortality between autistic people with and without an intellectual disability, Bölte says. To explore these gaps, in 2015 Bölte’s group published a large epidemiological study of more than 27,000 Swedish people with ASD, 6500 of whom had an intellectual disability. They found that risk of premature death was about 2.5 times higher for the entire group, a gap largely due to increased prevalence of common health problems such as diabetes and respiratory disease. Patients may be being diagnosed too late because they do not know how to express health concerns to their doctors, Bölte says, making it “extremely important” for general practitioners to thoroughly explore autistic patients’ symptoms and histories. © 2016 American Association for the Advancement of Scienc

Keyword: Autism
Link ID: 22010 - Posted: 03.19.2016

By John Elder Robison What happens to your relationships when your emotional perception changes overnight? Because I’m autistic, I have always been oblivious to unspoken cues from other people. My wife, my son and my friends liked my unflappable demeanor and my predictable behavior. They told me I was great the way I was, but I never really agreed. For 50 years I made the best of how I was, because there was nothing else I could do. Then I was offered a chance to participate in a study at Beth Israel Deaconess Medical Center, a teaching hospital of Harvard Medical School. Investigators at the Berenson-Allen Center there were studying transcranial magnetic stimulation, or T.M.S., a noninvasive procedure that applies magnetic pulses to stimulate the brain. It offers promise for many brain disorders. Several T.M.S. devices have been approved by the Food and Drug Administration for the treatment of severe depression, and others are under study for different conditions. (It’s still in the experimental phase for autism.) The doctors wondered if changing activity in a particular part of the autistic brain could change the way we sense emotions. That sounded exciting. I hoped it would help me read people a little better. They say, be careful what you wish for. The intervention succeeded beyond my wildest dreams — and it turned my life upside down. After one of my first T.M.S. sessions, in 2008, I thought nothing had happened. But when I got home and closed my eyes, I felt as if I were on a ship at sea. And there were dreams — so real they felt like hallucinations. It sounds like a fairy tale, but the next morning when I went to work, everything was different. Emotions came at me from all directions, so fast that I didn’t have a moment to process them. © 2016 The New York Times Company

Keyword: Autism; Emotions
Link ID: 22009 - Posted: 03.19.2016

By Daisy Yuhas Something was wrong with Brayson Thibodeaux. At 15 months old, he still was not walking; his parents and grandparents were certain that his development was slower than normal. After pushing doctors for answers they finally got him to a neurologist who recommended a genetic test. Brayson had fragile X syndrome, the leading heritable cause of intellectual disability and of autism. The discovery sent ripples through the extended family, who live outside New Orleans. Brayson’s great-grandmother, Cheryl, recalled having heard of fragile X and discovered a cousin whose grandson had the same condition. She soon learned that many members of her family were confirmed carriers of a genetic condition—the fragile X pre-mutation—that put them at risk of having children with this syndrome. “Fragile X” refers to a mutation that alters the X chromosome in such a way that, viewed under a microscope, it would look like a piece was about to break off. That is because one gene contains multiple repetitions of noncoding DNA—specifically CGG (cytosine, guanine, guanine). The exact number of CGG repetitions is variable, but when it reaches more than 200, it is considered to be the full mutation, which causes the syndrome. People with between 55 and 200 repeats are said to have a partial or pre-mutation, an unstable gene that can expand into the full mutation in future generations. © 2016 Scientific American,

Keyword: Development of the Brain; Autism
Link ID: 22008 - Posted: 03.19.2016

Mo Costandi In order to remember, we must forget. Recent research shows that when your brain retrieves newly encoded information, it suppresses older related information so that it does not interfere with the process of recall. Now a team of European researchers has identified a neural pathway that induces forgetting by actively erasing memories. The findings could eventually lead to novel treatments for conditions such as post-traumatic stress disorder (PTSD). We’ve known since the early 1950s that a brain structure called the hippocampus is critical for memory formation and retrieval, and subsequent work using modern techniques has revealed a great deal of information about the underlying cellular mechanisms. The hippocampus contains neural circuits that loop through three of its sub-regions – the dentate gyrus and the CA3 and CA1 areas – and it’s widely believed that memories form by the strengthening and weakening of synaptic connections within these circuits. The dentate gyrus gives rise to so-called mossy fibres, which form the main ‘input’ to the hippocampus, by relaying sensory information from an upstream region called the entorhinal cortex first to CA3 and then onto CA1. It’s thought that the CA3 region integrates the information to encode, store, and retrieve new memories, before transferring them to the cerebral cortex for long-term storage. Exactly how each of these hippocampal sub-regions contribute to memory formation, storage, and retrieval is still not entirely clear, however. © 2016 Guardian News and Media Limited

Keyword: Learning & Memory
Link ID: 22007 - Posted: 03.19.2016

Results from a new study, funded in part by the National Center for Complementary and Integrative Health, demonstrate that mindfulness meditation works on a different pain pathway in the brain than opioid pain relievers. The researchers noted that because opioid and non-opioid mechanisms of pain relief interact synergistically, the results of this study suggest that combining mindfulness-based and pharmacologic/nonpharmacologic pain-relieving approaches that rely on opioid signaling may be particularly effective in treating pain. Previous research has shown that mindfulness meditation helps relieve pain, but researchers have been unclear about how the practice induces pain relief — specifically, if meditation is associated with the release of naturally occurring opiates. Researchers recorded pain reports in 78 healthy adults during meditation or a non-meditation control in response to painful heat stimuli and intravenous administration of the opioid antagonist naloxone (a drug that blocks the transmission of opioid activity) or placebo saline. Participants were randomized to one of four treatment groups: 1) meditation plus naloxone; 2) control plus naloxone; 3) meditation plus saline; or 4) control plus saline. People in the control groups were instructed to “close your eyes and relax until the end of the experiment.” The researchers found that participants who meditated during saline administration had significantly lower pain intensity and unpleasantness ratings compared to those who did not meditate while receiving saline. Importantly, data from the meditation plus naloxone group showed that naloxone did not block meditation’s pain-relieving effects. No significant differences in reductions of pain intensity or pain unpleasantness were seen between the meditation plus naloxone and the meditation plus saline groups. Participants who meditated during naloxone administration also had significantly greater reductions in pain intensity and unpleasantness than the control groups.

Keyword: Pain & Touch
Link ID: 22006 - Posted: 03.19.2016

Tracie McMillan When it comes to school breakfasts, two is better than none, says a new report released Thursday in the journal Pediatric Obesity. Researchers tracked nearly 600 middle-school students from fifth to seventh grade, looking to see if students ate no breakfast; ate breakfast at home or school; or ate both — and whether that affected obesity rates. The result: Weight gain among students who ate "double-breakfast" was no different than that seen among all other students. Meanwhile, the risk of obesity doubled among students who skipped breakfast or ate it inconsistently. "It seems it's a bigger problem to have kids skipping breakfast than to have these kids eating two breakfasts," says Marlene Schwartz of the Rudd Center for Food Policy and Obesity and one of the study's authors. "This study ... debunks an important misconception that school breakfast contributes to childhood obesity," says Duke Storen from Share Our Strength, a national group that runs anti-hunger and nutrition programs for children. While direct opposition to free school breakfast is unusual, says Storen, officials sometimes balk at implementing "alternative breakfast models" designed to encourage use of the program — such as offering breakfast in grab-and-go bags or in classrooms, rather than traditional sit-down meals in a cafeteria. That's a concern, say hunger advocates, because while eligibility rules for free and reduced-price breakfast are the same as for lunch, only about half as many children get subsidized breakfast as receive lunch, according to the Food Research and Action Center, an advocacy group. Indeed, the study was inspired in part by real-world concerns that school breakfast programs might promote obesity, says Schwartz. © 2016 npr

Keyword: Obesity
Link ID: 22005 - Posted: 03.19.2016

By C. CLAIBORNE RAY Current treatments for the so-called wet form of macular degeneration, involving injections inside the eye, are already “very effective” compared with laser treatments, which were used before intravitreal injections, said Dr. Ronald C. Gentile, the surgeon director at the New York Eye and Ear Infirmary of Mount Sinai. But several ways to improve their results are in the works, he said. The shots deliver drugs that fight a substance called vascular endothelial growth factor, and thus shrink the growth of what amounts to an abnormal blood vessel harming the retina. A major hurdle now involves the frequency and cost of the needed treatments. Once the drug is inside the eye, the effects wear off and a new injection is needed, Dr. Gentile said. The shots are also less effective in some patients. Even when they work well, some people need a shot as often as every four weeks, while some can wait two or three months. If both eyes are affected and the period of effectiveness is short, doctor visits can be very frequent, so drugs that last longer in the eyeball are being pursued. Researchers are working on slow-release medications as well as a delivery system that acts like a tiny pump in the eye, with a tank that can be refilled every six months. There is also a new drug target: a substance called platelet-derived growth factor that causes abnormal vessel growth as well. Combination drug treatments may be more effective against macular degeneration, Dr. Gentile said. The so-called dry form of macular degeneration, which often underlies the wet form, is harder to fight, he said, and although advances are being made, current antioxidant treatments with vitamins and minerals do not to improve vision; they just prevent it from worsening. © 2016 The New York Times Company

Keyword: ADHD
Link ID: 22004 - Posted: 03.19.2016

Alison Abbott In the 25 years that John Collinge has studied neurology, he has seen hundreds of human brains. But the ones he was looking at under the microscope in January 2015 were like nothing he had seen before. He and his team of pathologists were examining the autopsied brains of four people who had once received injections of growth hormone derived from human cadavers. It turned out that some of the preparations were contaminated with a misfolded protein — a prion — that causes a rare and deadly condition called Creutzfeldt–Jakob disease (CJD), and all four had died in their 40s or 50s as a result. But for Collinge, the reason that these brains looked extraordinary was not the damage wrought by prion disease; it was that they were scarred in another way. “It was very clear that something was there beyond what you'd expect,” he says. The brains were spotted with the whitish plaques typical of people with Alzheimer's disease. They looked, in other words, like young people with an old person's disease. For Collinge, this led to a worrying conclusion: that the plaques might have been transmitted, alongside the prions, in the injections of growth hormone — the first evidence that Alzheimer's could be transmitted from one person to another. If true, that could have far-reaching implications: the possibility that 'seeds' of the amyloid-β protein involved in Alzheimer's could be transferred during other procedures in which fluid or tissues from one person are introduced into another, such as blood transfusions, organ transplants and other common medical procedures. © 2016 Nature Publishing Group,

Keyword: Alzheimers; Prions
Link ID: 22003 - Posted: 03.17.2016

Laura Sanders Using flashes of blue light, scientists have pulled forgotten memories out of the foggy brains of mice engineered to have signs of early Alzheimer’s disease. This memory rehab feat, described online March 16 in Nature, offers new clues about how the brain handles memories, and how that process can go awry. The result “provides a theoretical mechanism for reviving old, forgotten memories,” says Yale School of Medicine neurologist Arash Salardini. Memory manipulations, such as the retrieval of lost memories and the creation of false memories, were “once the realm of science fiction,” he says. But this experiment and other recent work have now accomplished these feats, at least in rodents (SN: 12/27/14, p. 19), he says. To recover a lost memory, scientists first had to mark it. Neuroscientist Susumu Tonegawa of MIT and colleagues devised a system that tagged the specific nerve cells that stored a memory — in this case, an association between a particular cage and a shock. A virus delivered a gene for a protein that allowed researchers to control this collection of memory-holding nerve cells. The genetic tweak caused these cells to fire off signals in response to blue laser light, letting Tonegawa and colleagues call up the memory with light delivered by an optic fiber implanted in the brain. A day after receiving a shock in a particular cage, mice carrying two genes associated with Alzheimer’s seemed to have forgotten their ordeal; when put back in that cage, these mice didn’t seem as frightened as mice without the Alzheimer’s-related genes. But when the researchers used light to restore this frightening memory, it caused the mice to freeze in place in a different cage. (Freezing in a new venue showed that laser activation of the memory cells, and not environmental cues, caused the fear reaction.) © Society for Science & the Public 2000 - 2016. All rights reserved.

Keyword: Learning & Memory; Alzheimers
Link ID: 22002 - Posted: 03.17.2016

THERE they are! Newborn neurons vital for memory have been viewed in a live brain for the first time. The work could aid treatments for anxiety and stress disorders. Attila Losonczy at Columbia University Medical Center in New York and his team implanted a tiny microscope into the brains of live mice, the brain cells of which had been modified to make newly made neurons glow. The mice then ran on a treadmill as the team tweaked the surrounding sights, smells and sounds. The researchers paired a small electric shock with some cues, so the mice learned to associate these with an unpleasant experience. They then deactivated the newborn neurons – present in areas of the brain responsible for learning and memory – using optogenetics, which switches off specific cells with light. After this, the mice were unable to tell the difference between the scary and safe cues, becoming fearful of them all (Neuron, doi.org/bc7v). “It suggests that newborn cells do something special that allows animals to tell apart and separate memories,” says Losonczy. An inability to discriminate between similar sensory information triggered by different events – such as the sound of a gunshot and a car backfiring – is often seen in panic and anxiety disorders, such as PTSD. This suggests that new neurons, or a lack of them, plays a part in such conditions and could guide novel treatments. © Copyright Reed Business Information Ltd.

Keyword: Neurogenesis; Learning & Memory
Link ID: 22001 - Posted: 03.17.2016

Nicola Davis Electrical brain stimulation could benefit stroke patients by boosting the effects of rehabilitation therapy, new research suggests. Writing in the journal Science Translational Medicine, the authors reveal that patients who were given electrical brain stimulation during a rehabilitation programme performed better on a range of tasks than those taking part in the rehabilitation programme. “It is an exciting message because there is so much frustration about people not reaching their true recovery potential,” said Professor Heidi Johansen-Berg, an author of the study from the University of Oxford, highlighting the fact that the cost of programmes and limited availability of therapists often restricts the amount of rehabilitation offered to patients. To probe the effects of brain stimulation, the researchers chose 24 patients who had experienced a stroke at least six months before, and who had difficulties with moving one hand. The participants were then split into two groups. The first group underwent nine consecutive days of rehabilitation training, with each session lasting an hour. For the first 20 minutes, the patients had two electrodes placed on their heads and a direct current applied, a process known as anodal transcranial direct current stimulation (tDCS). This is stimulation is thought to prime the brain for learning. © 2016 Guardian News and Media Limited

Keyword: Stroke
Link ID: 22000 - Posted: 03.17.2016

BRAINS get data about the world through senses – sight, hearing, taste, smell and touch. In a lab in North Carolina, a group of rats is getting an extra one. Thanks to implants in their brains, they have learned to sense and react to infrared light. The rats show the brain’s ability to process unfamiliar data– an early step towards augmenting the human brain. Miguel Nicolelis of Duke University School of Medicine is leading the experiment. His team implanted four clusters of electrodes in the rats’ barrel cortex – the part of the brain that handles whisker sensation (doi.org/bdb6). Each cluster is connected to a sensor that converts infrared light into an electrical signal. Feeding stations placed at the four corners of the rats’ cage take turns emitting infrared signals that guide the rats to them, releasing a reward only when the rats press a button on the feeding station that is emiting the infrared signal. In an older, single sensor version of the experiment, it took the rats one month to adapt. With four sensors, it took them just three days. “This is a truly remarkable demonstration of the plasticity of the mammalian brain,” says Christopher James of the University of Warwick, UK. All the extra data that goes into making the rats’ new sense doesn’t appear to diminish their original senses. “The results show that nature has apparently designed the adult mammalian brain with the possibility of upgrades, and Nicolelis’ team is leading the way showing how to do it,” says Andrea Stocco of the University of Washington in Seattle. © Copyright Reed Business Information Ltd.

Keyword: Robotics; Vision
Link ID: 21999 - Posted: 03.17.2016

By Gretchen Reynolds Meditating before running could change the brain in ways that are more beneficial for mental health than practicing either of those activities alone, according to an interesting study of a new treatment program for people with depression. As many people know from experience, depression is characterized in part by an inability to stop dwelling on gloomy thoughts and unhappy memories from the past. Researchers suspect that this thinking pattern, known as rumination, may involve two areas of the brain in particular: the prefrontal cortex, a part of the brain that helps to control attention and focus, and the hippocampus, which is critical for learning and memory. In some studies, people with severe depression have been found to have a smaller hippocampus than people who are not depressed. Interestingly, meditation and exercise affect those same portions of the brain, although in varying ways. In brain-scan studies, people who are long-term meditators, for instance, generally display different patterns of brain-cell communication in their prefrontal cortex during cognitive tests than people who don’t meditate. Those differences are believed to indicate that the meditators possess a more honed ability to focus and concentrate. Meanwhile, according to animal studies, aerobic exercise substantially increases the production of new brain cells in the hippocampus. Both meditation and exercise also have proven beneficial in the treatment of anxiety, depression and other mood disorders. These various findings about exercise and meditation intrigued researchers at Rutgers University in New Brunswick, N.J., who began to wonder whether, since meditation and exercise on their own improve moods, combining the two might intensify the impacts of each. So, for the new study, which was published last month in Translational Psychiatry, the scientists recruited 52 men and women, 22 of whom had been given diagnoses of depression. The researchers confirmed that diagnosis with their own tests and then asked all of the volunteers to complete a computerized test of their ability to focus while sensors measured electrical signals in their brains. © 2016 The New York Times Company

Keyword: Depression
Link ID: 21998 - Posted: 03.17.2016

By KEN BELSON and ALAN SCHWARZ Perhaps no one will remember the setting, a hearing room for the House Energy and Commerce Committee, or the person who asked the question, a member of the House of Representatives from Illinois. But seven words spoken in the Rayburn House Office Building in Washington on Monday could profoundly affect the country’s most popular sport. After years of the N.F.L.‘s disputing evidence that connected football to chronic traumatic encephalopathy, the degenerative brain disease found in nearly 100 former players, a top official for the league for the first time acknowledged the link. To many, it was an echo of big tobacco’s confession in 1997 that smoking causes cancer and heart disease. Representative Jan Schakowsky, Democrat of Illinois, asked during a round-table discussion about concussions whether “there is a link between football and degenerative brain disorders like C.T.E.” Jeff Miller, the N.F.L.’s senior vice president for health and safety policy, said, “The answer to that is certainly, yes.” His response signaled a stunning about-face for the league, which has been accused by former players and independent experts of hiding the dangers of head injuries for decades. His reply came moments after a leading C.T.E. researcher — Dr. Ann McKee — had presented her findings, showing that dozens of former players who had died were afflicted with the disease. “The comments made by Jeff Miller yesterday accurately reflect the view of the N.F.L.,” Brian McCarthy, a league spokesman, said Tuesday, confirming that Mr. Miller had not misspoken. © 2016 The New York Times Company

Keyword: Brain Injury/Concussion
Link ID: 21997 - Posted: 03.16.2016

Barbara Bradley Hagerty Faced with her own forgetfulness, former NPR correspondent and author Barbara Bradley Hagerty tried to do something about it. She's written about her efforts in her book on midlife, called Life Reimagined. To her surprise, she discovered that an older dog can learn new tricks. A confession: I loathe standardized tests, and one of the perks of reaching midlife is that I thought I'd never have to take another. But lately I've noticed that in my 50s, my memory isn't the same as it once was. And so I decided to take a radical leap into the world of brain training. At the memory laboratory at the University of Maryland, manager Ally Stegman slides a sheet of paper in front of me. It has a series of boxes containing different patterns and one blank space. My job is to figure out the missing pattern. The test measures a sort of raw intelligence, the ability to figure out novel problems. Time races by. It takes me two minutes to crack the first question. I am stumped by the second and third. Finally, I begin to guess. After 25 minutes, the test is over, and to my relief, Stegman walks in. This test was really, really hard. The reason I am here, voluntarily reliving my nightmare, is simple: I want to tune up my 50-something brain. So over the next month, I will do brain-training exercises, then come back, take the test again and see if I made myself smarter. © 2016 npr

Keyword: Learning & Memory; Development of the Brain
Link ID: 21996 - Posted: 03.16.2016

Nicola Davis Suppressing bad memories from the past can block memory formation in the here and now, research suggests. The study could help to explain why those suffering from post-traumatic stress disorder (PTSD) and other psychological conditions often experience difficulty in remembering recent events, scientists say. Writing in Nature Communications, the authors describe how trying to forget past incidents by suppressing our recollections can create a “virtual lesion” in the brain that casts an “amnesiac shadow” over the formation of new memories. “If you are motivated to try to prevent yourself from reliving a flashback of that initial trauma, anything that you experience around the period of time of suppression tends to get sucked up into this black hole as well,” Dr Justin Hulbert, one of the study’s authors, told the Guardian. “I think it makes perfect sense because we know that people with a wide range of psychological problems have difficulties with their everyday memories for ordinary events,” said Professor Chris Brewin, an expert in PTSD from University College, London, who was not involved in the study. “Potentially this could account for the memory deficits we find in depression and other disorders too.” The phenomenon came to the attention of the scientists during a lecture when a student admitted to having suffered bouts of amnesia after witnessing the 1999 Columbine high school massacre. When the student returned to the school for classes after the incident she found she could not remember anything from the lessons she was in. “Here she was surrounded by all these reminders of these terrible things that she preferred not to think about,” said Hulbert. © 2016 Guardian News and Media Limited

Keyword: Learning & Memory; Stress
Link ID: 21995 - Posted: 03.16.2016

By Victoria Sayo Turner Seasonal affective disorder was categorized under major depression to signify depression with a yearly recurrence, a condition far more debilitating than your average “winter blues.” Credit: ©iStock Around March, some of us take a kick at the snow mounded on the curb and wonder if spring is finally going to drop by. The sun sets before we go home, and the cold coops us up except for runs to the grocery store. All of this amounts to something known informally as the winter blues, because those wintry days and dead trees can put us in a glum mood. But in the 1980s, research at the National Institutes of Mental Health led to recognition of a form of depression known as seasonal affective disorder (shortened, of course, to SAD). Seasonal affective disorder was categorized under major depression to signify depression with a yearly recurrence, a condition far more debilitating than your average “winter blues.” Mention of SAD in research and books peaked in the 1990s, and today SAD is considered a diagnosable (and insurable) disorder. Treatment ranges from psychotherapy to antidepressants to light therapy — large boxes filled with lightbulbs that look like tanning beds for your face. However, a recent study questions the existence of seasonal depression entirely. Each year, the Centers for Disease Control conducts a large cross-sectional study of the US population. A group of researchers realized they could use the CDC results independently to investigate how much depression changes by season. The 2006 version of the CDC study included a set of questions typically used to screen for depression. By analyzing the answers gathered from 34,000 adults over the course of the year, the researchers might detect flareups of seasonal affective disorder. They might see wintertime surges in depression. “To be honest, we initially did not question the [SAD] diagnosis,” writes investigator Dr. Steven LoBello, the goal being “to determine the actual extent to which depression changes with the seasons.” © 2016 Scientific American

Keyword: Biological Rhythms; Depression
Link ID: 21994 - Posted: 03.16.2016