By Suzy Gage When I started my PhD a few years ago, I thought that certain psychological findings were established fact. The next four years were an exercise in disillusionment. If the effects I was seeking to explore were so reliable, so established, why could I not detect them? There is growing interest in the need to improve reliability in science. Many drugs show promise at the design and pre-clinical phases, only to fail (at great expense) in clinical trials. Many of the most hyped scientific discoveries eventually cannot be replicated. Worryingly for science (but somewhat comforting for my self-esteem as a researcher) this may be because many of the conclusions drawn from published research findings are false. A major factor that influences the reliability of science is statistical power. We cannot measure everyone or everything, so we take samples and use statistical inference to determine the probability that the results we observe in our sample reflect some underlying scientific truth. Statistical power determines whether we accurately conclude if there is an effect or not. Statistical power is the ability of a study to detect an effect (eg higher rates of cancer in smokers) given that an effect actually exists (smoking actually is associated with increased risk of cancer). Power is related to the size of the study sample (the number of smokers and non-smokers we test) and the size of the real effect (the magnitude of the increased risk associated with smoking). Larger studies have more power and can detect smaller, more subtle effects. Small studies have lower power and can only detect larger effects reliably. © 2013 Guardian News and Media Limited

Keyword: Miscellaneous
Link ID: 18019 - Posted: 04.11.2013

by Sara Reardon The Brain Activity Map project launched recently by President Obama – and funded to the tune of $100 million in the US budget announcement earlier this month – highlights the need for research that focuses both on how individual neurons work and the ways that different regions of the brain work together as a unit. Looking at individual neurons requires slicing up brains into thin sections. However, this damages the axons – the arms that protrude from neurons to make connections with other cells – making it difficult to see exactly how brain cells link up. A few microscopic techniques can focus light deep into the intact brains of dead animals to study its structure without damaging the axons, but much of this light is scattered away by the fatty lipid membranes that surround individual cells, making the technique less than perfect. Now Kwanghun Chung, Karl Deisseroth and their team at Stanford University in California have developed a technique that provides a clearer picture. First, they remove the brain from a mouse and infuse it with a see-through gel that collects in the neurons' lipid membranes. As the gel solidifies, it takes the shape of the membranes and creates a matrix that holds the cells' proteins, DNA and RNA in place. Then the team adds a second chemical that dissolves the lipids, leaving a transparent brain made out of gel that retains the brain's proteins, DNA and RNA in their original positions. © Copyright Reed Business Information Ltd.

Keyword: Brain imaging
Link ID: 18018 - Posted: 04.11.2013

By JAMES GORMAN Scientists at Stanford University reported on Wednesday that they have made a whole mouse brain, and part of a human brain, transparent so that networks of neurons that receive and send information can be highlighted in stunning color and viewed in all their three-dimensional complexity without slicing up the organ. Even more important, experts say, is that unlike earlier methods for making the tissue of brains and other organs transparent, the new process, called Clarity by its inventors, preserves the biochemistry of the brain so well that researchers can test it over and over again with chemicals that highlight specific structures and provide clues to past activity. The researchers say this process may help uncover the physical underpinnings of devastating mental disorders like schizophrenia, autism, post-traumatic stress disorder and others. The work, reported on Wednesday in the journal Nature, is not part of the Obama administration’s recently announced initiative to probe the secrets of the brain, although the senior author on the paper, Dr. Karl Deisseroth at Stanford, was one of those involved in creating the initiative and is involved in planning its future. Dr. Thomas Insel, director of the National Institute of Mental Health, which provided some of the financing for the research, described the new work as helping to build an anatomical “foundation” for the Obama initiative, which is meant to look at activity in the brain. Dr. Insel added that the technique works in a human brain that has been in formalin, a preservative, for years, which means that long-saved human brains may be studied. “Frankly,” he said, “that is spectacular.” © 2013 The New York Times Company

Keyword: Brain imaging
Link ID: 18017 - Posted: 04.11.2013

A rat with some human genes could provide a better way to test Alzheimer's drugs. The genetically modified rat is the first rodent model to exhibit the full range of brain changes found in Alzheimer's, researchers in The Journal of Neuroscience. "It's a big step forward" for drug development, says , a program director at the National Institute of Neurological Disorders and Stroke, or NINDS, which helped fund the work. "The closer the model is to the human condition in representing the disease, the more likely the drug will behave and cure the way it would in humans." In recent years, drug companies have developed several Alzheimer's drugs that seemed to work in animals, but with the disease. A lack of good animal models for Alzheimer's may be one reason for those failures, researchers say. For the past couple of decades, Alzheimer's researchers have relied primarily on mice that carry human gene mutations that cause people to get the disease in their 40s or 50s. Like people, these mice develop so-called amyloid plaques in their brains. But that's where the similarity ends. In people with Alzheimer's, after plaques appear, huge numbers of brain cells die. That's never happened in mice, despite lots of genetic tinkering, Corriveau says. So researchers began to consider a different rodent model: the rat. "Rats are 4 [million] to 5 million years closer evolutionarily to humans," Corriveau says, which means their brains are more like ours. ©2013 NPR

Keyword: Alzheimers; Genes & Behavior
Link ID: 18016 - Posted: 04.11.2013

By GRETCHEN REYNOLDS Two new experiments, one involving people and the other animals, suggest that regular exercise can substantially improve memory, although different types of exercise seem to affect the brain quite differently. The news may offer consolation for the growing numbers of us who are entering age groups most at risk for cognitive decline. It was back in the 1990s that scientists at the Salk Institute for Biological Studies in La Jolla, Calif., first discovered that exercise bulks up the brain. In groundbreaking experiments, they showed that mice given access to running wheels produced far more cells in an area of the brain controlling memory creation than animals that didn’t run. The exercised animals then performed better on memory tests than their sedentary labmates. Since then, scientists have been working to understand precisely how, at a molecular level, exercise improves memory, as well as whether all types of exercise, including weight training, are beneficial. The new studies provide some additional and inspiring clarity on those issues, as well as, incidentally, on how you can get lab rats to weight train. For the human study, published in The Journal of Aging Research, scientists at the University of British Columbia recruited dozens of women ages 70 to 80 who had been found to have mild cognitive impairment, a condition that makes a person’s memory and thinking more muddled than would be expected at a given age. Mild cognitive impairment is also a recognized risk factor for increasing dementia. Seniors with the condition develop Alzheimer’s disease at much higher rates than those of the same age with sharper memories. Copyright 2013 The New York Times Company

Keyword: Learning & Memory
Link ID: 18015 - Posted: 04.10.2013

by Tanya Lewis, The lip-smacking vocalizations gelada monkeys make are surprisingly similar to human speech, a new study finds. Many nonhuman primates demonstrate lip-smacking behavior, but geladas are the only ones known to make undulating sounds, known as "wobbles," at the same time. (The wobbling sounds a little like a human hum would sound if the volume were being turned on and off rapidly.) The findings show that lip-smacking could have been an important step in the evolution of human speech, researchers say. "Our finding provides support for the lip-smacking origins of speech because it shows that this evolutionary pathway is at least plausible," Thore Bergman of the University of Michigan in Ann Arbor and author of the study published today (April 8) in the journal Current Biology,said in a statement. "It demonstrates that nonhuman primates can vocalize while lip-smacking to produce speechlike sounds." NEWS: Lip Smacks of Monkeys Prelude to Speech? Lip-smacking -- rapidly opening and closing the mouth and lips -- shares some of the features of human speech, such as rapid fluctuations in pitch and volume. (See Video of Gelada Lip-Smacking) Bergman first noticed the similarity while studying geladas in the remote mountains of Ethiopia. He would often hear vocalizations that sounded like human voices, but the vocalizations were actually coming from the geladas, he said. He had never come across other primates who made these sounds. But then he read a study on macaques from 2012 revealing how facial movements during lip-smacking were very speech-like, hinting that lip-smacking might be an initial step toward human speech. © 2013 Discovery Communications, LLC.

Keyword: Language; Evolution
Link ID: 18014 - Posted: 04.10.2013

Ed Yong Every autumn, millions of monarch butterflies (Danaus plexippus) converge on a small cluster of Mexican mountains to spend the winter. They have journeyed for up to 4,000 kilometres from breeding grounds across eastern North America. And according to a study, they accomplish this prodigious migration without ever knowing where they are relative to their destination. The monarchs can use the position of the Sun as a compass, but when Henrik Mouritsen, a biologist at the University of Oldenburg in Germany, displaced them by 2,500 kilometres, he found that they did not correct their heading. “People seemed to assume that they had some kind of a map that allowed them to narrow in on a site a few kilometres across after travelling several thousands of kilometres,” he says. Now, “it is clear that they don’t”. His results are published in the Proceedings of the National Academy of Sciences1. For more than five decades, scientists have teamed up with amateurs to tag and monitor free-flying monarchs, creating a database of their migrations. When Mouritsen analysed these records, he realized that the monarchs tend to spread out over the course of their migration. Their distribution was a good fit with the predictions of a mathematical model that assumed that the monarchs were flying with just a compass, rather than a compass and a map. Mouritsen also captured 76 southwesterly flying monarchs from fields near Guelph in Ontario, Canada, and transported them 2,500 kilometres to the west, to Calgary in the Canadian province of Alberta. He placed the butterflies in a “flight simulator” — a plastic cylinder that kept them from seeing any landmarks except the sky — and tethered them to a rod that let them point in any direction without actually flying away. © 2013 Nature Publishing Group

Keyword: Animal Migration
Link ID: 18013 - Posted: 04.10.2013

By PAULA SPAN The long list of roles Margaret Thatcher played during her 87 years — potent politician, free-market evangelist, labor antagonist, dominant global leader — includes the one she never publicly discussed: person with dementia. The stroke that killed her on Monday was not her first. Mrs. Thatcher suffered several small strokes more than a decade earlier, canceled all her speaking engagements in 2003 and largely withdrew from public life. Even before the strokes, her daughter, Carol, wrote in a 2008 memoir, she was losing cognitive ground, repeating questions and showing other signs of confusion. Heartbreakingly, she often forgot that her beloved husband, Denis, had died of cancer in 2003. “I had to keep giving her the bad news over and over again,” her daughter wrote. “Every time it finally sank in that she had lost her husband of more than 50 years, she’d look at me sadly and say, ‘Oh’, as I struggled to compose myself. ‘Were we all there?’ she’d ask softly.” At the time, members of her mother’s political circle and other British commentators denounced Carol Thatcher for invading her mother’s privacy and, supposedly, diminishing her dignity. The criticism arose again in some quarters last year, when Meryl Streep won an Oscar for her portrayal of Mrs. Thatcher’s dementia in “The Iron Lady.” © 2013 The New York Times Company

Keyword: Alzheimers
Link ID: 18012 - Posted: 04.10.2013

By Janice Lynch Schuster, My grandmother, who is 92, recently reported that she’d seen three giraffes in her Midwest back yard. She is otherwise sharp (and also kind and funny), but the giraffe episode was further evidence of the mild cognitive impairment that has been slowly creeping into her life. The question for my family has become: How should we respond? One of my sisters tried humor. (“Grandmom, I didn’t know you drank in the middle of the day!”) My father suggested that they were deer (to which she replied, “I’m 92 years old, and I know a giraffe when I see one.”) I tried to learn more about what, exactly, the giraffes were doing out there. (She didn’t seem to know, saying only that “the light shimmered.”) Communicating with a family member who has cognitive impairment can be frustrating and disheartening, even downright depressing for patient and caregiver alike. And it’s a problem faced by a growing number of Americans. According to a report published last week, about 4.1 million Americans have dementia. Alzheimer’s, one of the many forms of dementia, is the most expensive disease in the United States, costing $157 billion to $215 billion a year — more than heart disease and cancer, according to the study, which was sponsored by the National Institute on Aging. As baby boomers reach old age, these numbers are expected to increase dramatically. A number of techniques can not only reduce the frustration but also create new ways of connecting. Among the most effective and popular among experts is the “validation method,” a practice pioneered by geriatric social worker and researcher Naomi Feil in the 1980s. © 1996-2013 The Washington Post

Keyword: Alzheimers; Language
Link ID: 18011 - Posted: 04.10.2013

by Dr. Tyeese Gaines African-Americans with a particular gene are twice as likely to develop Alzheimer’s disease in old age as those without it, says a new study published in the Journal of the American Medical Association. This finding is a result of the largest database search for Alzheimer’s genes among African-Americans. “Until now, data on the genetics of Alzheimer’s in this patient population have been extremely limited,” said Dr. Richard Mayeux, chair of neurology at Columbia University Medical Center and senior author of the study. Alzheimer’s disease is the most common cause of dementia — a brain disease that affects memory, personality and the ability to reason. At age 65, only one percent of people have Alzheimer’s, yet over 80 years of age, it increases to 30 percent. A gene called APOE is associated with one in every five cases of Alzheimer’s – known to be a major genetic risk factor for whites and blacks. Yet, in this new research, Mayeux and his team identified an additional gene variant linked to a doubled risk in African-Americans alone, called ABCA7. “ABCA7 is the first major gene implicated in late-onset Alzheimer’s among African-Americans,” said Dr. Christine Reitz, assistant professor of neurology and lead author of the study. To reach this conclusion, researchers examined samples from nearly 6,000 African-American men and women collected between 1989 and 2011 – 2,000 had a diagnosis of probable Alzheimer’s disease and the other 4,000 had no cognitive difficulty. “Although this is a very significant finding, it does not change much for the everyday African-American male or female,” says Rick Kittles, PhD, a human genetics expert who has traced the ancestry of more than 100,000 African-Americans. “There is still much work to do [to] determine how exactly this gene plays a role in Alzheimer’s disease.” ©2013 NBCUniversal

Keyword: Alzheimers; Genes & Behavior
Link ID: 18010 - Posted: 04.10.2013

By Tara Haelle New evidence is confirming that the environment kids live in has a greater impact than factors such as genetics, insufficient physical activity or other elements in efforts to control child obesity. Three new studies, published in the April 8 Pediatrics, land on the import of the 'nurture' side of the equation and focus on specific circumstances in children's or teen's lives that potentially contribute to unhealthy bulk. In three decades child and adolescent obesity has tripled in the U.S., and estimates from 2010 classify more than a third of children and teens as overweight or obese. Obesity puts these kids at higher risk for type 2 diabetes, cardiovascular disease, sleep apnea, and bone or joint problems. The variables responsible are thought to range from too little exercise to too many soft drinks. Now it seems that blaming Pepsi or too little PE might neglect the bigger picture. "We are raising our children in a world that is vastly different than it was 40 or 50 years ago," says Yoni Freedhoff, an obesity doctor and assistant professor of medicine at the University of Ottawa. "Childhood obesity is a disease of the environment. It's a natural consequence of normal kids with normal genes being raised in unhealthy, abnormal environments." The environmental factors in these studies range from the seemingly minor, such as kids' plate sizes, to bigger challenges, such as school schedules that may keep teens from getting sufficient sleep. But they are part of an even longer list: the ubiquity of fast food, changes in technology, fewer home-cooked meals, more food advertising, an explosion of low-cost processed foods and increasing sugary drink serving sizes (pdf) as well as easy access to unhealthy snacks in vending machines, at sports games and in nearly every setting children inhabit—these are just a handful of environmental factors research has linked to increasing obesity, and researchers are starting to pick apart which among them play bigger or lesser roles in making kids supersized. © 2013 Scientific American

Keyword: Obesity; Genes & Behavior
Link ID: 18009 - Posted: 04.10.2013

Matt Kaplan By making noise that could potentially expose them to predators, young pied babblers get their parents to give them more attentions. Begging loudly has long been viewed as an offspring’s way of saying “I’m hungry”. But in predator-filled environments, these squawks can put young birds in harm's way, and may be a form of blackmail that forces parents to pay attention and feed the youngsters more than they might otherwise. The discovery comes from a three-year analysis of a well-studied community of pied babbler (Turdoides bicolor) in the Kalahari Desert of South Africa1. Alex Thompson of the University of Cape Town and colleagues from Britain and Australia, spent more than 200 hours observing the animals in the wild and recorded more than 3,000 incidents of parents feeding fledglings. Thompson and his team noted that fledglings were fed an average of 0.12 grams of food per minute when on the ground and away from cover, but just 0.03 grams per minute when begging from the safety of the trees. Furthermore, when the birds were played an audio recording of alarm calls indicating that a ground predator was in the vicinity, parents more than doubled the amount they gave to ground-based youngsters, but made no compensation for those in the trees. Fascinated, the team speculated that the young, which were slower than adults to respond to the alarm calls and cannot escape as quickly from danger, were intentionally putting themselves into a dangerous situation when hungry to force their parents to pay attention and feed them. © 2013 Nature Publishing Group,

Keyword: Sexual Behavior; Evolution
Link ID: 18008 - Posted: 04.10.2013

By KATIE HAFNER While undressing for bed one night in 2009, Susan Spencer-Wendel noticed that the muscles in her left palm had disappeared, leaving a scrawny pile of tendons and bones. Her right hand was fine. She let out a yelp and showed the hand to her husband, who told her to go to the doctor. She was 42. Ms. Spencer-Wendel then entered a protracted period of denial. Adopted as an infant in Florida, she traveled from her home in West Palm Beach to find blood relatives living in Cyprus, who confirmed that there was no family history of her worst fear: amyotrophic lateral sclerosis, or A.L.S., the relentless disease that lays waste to muscles while leaving the mind intact. In June 2011, a doctor in Miami gave her a definitive diagnosis of A.L.S., smiling “like he was inviting me to a birthday party,” she writes in “Until I Say Goodbye: My Year of Living With Joy.” Patients with A.L.S., which is also known as Lou Gehrig’s disease, typically live no more than four years after the onset of symptoms. There is no cure. Ms. Spencer-Wendel thought she had prepared herself fully — that she would burst off the starting block like a sprinter to greet her fate. Instead, when she heard the news, “I dropped my head for the start ... and began to cry.” Her heart-ripping book chronicles what she did immediately after her diagnosis: she decided to embrace life while death chased her down. Instead of letting the world close in on her, she resolved to travel as far and as wide for as long as she could. She went to the Yukon with her best friend, Budapest with her husband, and the Bahamas with her sister. © 2013 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 18007 - Posted: 04.09.2013

By Stephani Sutherland Scientists have long known that once we nod off, certain memories grow stronger. One recent theory suggests that forgetting, too, is an essential function of sleep [see “Sleep's Secret Repairs,” by Jason Castro; Scientific American Mind, May/June 2012]. Researchers now suspect that post-traumatic stress disorder (PTSD) may emerge from flaws in sleep's forgetting process. Two studies presented at the 2012 meeting of the Society for Neuroscience in New Orleans indicate that sleep might offer a window of opportunity for weakening memories and providing relief from lingering reminders of trauma. Neuroscientists believe that during sleep, a memory-elimination routine cleans out obsolete information by physically weakening synapses, the junctions between communicating neurons. Gina Poe, a neuroscientist at the University of Michigan, found in mice that for synapses to lose strength, levels of the neurotransmitter noradrenaline must drop. Noradrenaline levels typically fall during REM sleep in rodents and humans, but in people with PTSD the amount stays high throughout sleep. Normalizing noradrenaline with pharmaceuticals, Poe says, “could absolutely be a key target to actually cure PTSD through normal sleep.” In a separate experiment, researcher Asya Rolls of Stanford University hijacked memory remodeling in sleeping mice to make a traumatic association less scary. Rolls and her colleagues conditioned mice to fear the scent of jasmine flowers by pairing the smell with a foot shock. When the mice slept, they released a puff of jasmine. Under normal circumstances, the smell would reactivate and bolster the memory, a process that requires newly made structural proteins. The researchers gave some mice a drug that prevented the manufacture of these building blocks in a key fear-memory area. When these mice woke up, they no longer responded to the odor with fearful behavior, indicating that the memory had been successfully disrupted. The findings might someday translate to a new kind of sleep-based therapy in people whose traumatic experiences are tied to specific sounds and smells—such as the noise of a bomb going off—that can be presented to their sleeping brain. © 2013 Scientific American

Keyword: Sleep; Learning & Memory
Link ID: 18006 - Posted: 04.09.2013

By DENISE GRADY SAN FRANCISCO — Scientists are trained to be skeptics, and Elizabeth H. Blackburn considers herself one of the biggest. Show her the data, and be ready to defend it. But even though she relishes the give and take, Dr. Blackburn admits to impatience at times with the questions some scientists have raised about one of her ventures. “It’s just such a no-brainer, and yet people have such difficulty understanding it,” she said. At issue is a lab test that measures telomeres, stretches of DNA that cap the ends of chromosomes and help keep cells from aging too soon. Unusually short telomeres may be a sign of illness, and Dr. Blackburn, who shared the 2009 Nobel Prize in medicine for her work on telomeres (TEEL-o-meers), thinks measuring them could give doctors and patients a chance to intervene early and maybe even prevent disease. A company she helped found expects to begin offering tests to the public later this year. Other researchers have raised doubts about the usefulness of the measurement, which does not diagnose a specific disease. But Dr. Blackburn, 64, a professor of biology and physiology at the University of California, San Francisco, says she has been convinced by a decade of data from her own team and others, linking short telomeres to heart disease, diabetes, cancer and other diseases, and to chronic stress and post-traumatic stress disorder. With studies that explore the connections among emotional stress, health and telomeres, she has delved into questions that she would have shied away from earlier in her career, as a woman trying to establish herself in science. But now, she has enough confidence and autonomy to follow the leads that intrigue her. The scope of her research has expanded tremendously, from a tight focus on molecular biology to broader questions about the implications of her work for health and public policy. © 2013 The New York Times Company

Keyword: Stress; Genes & Behavior
Link ID: 18005 - Posted: 04.09.2013

By Scicurious In his State of the Union this year, President Obama referred to increasing support for science and technology, and mentioned the “Brain Activity Map”. Of course neuroscientists were instantly atwitter. It was the first we’d all heard of any Brain Activity Map. What is it? What did it mean? After a lot of speculation and some quickly formed opinions about whether or not it was a good idea…the White House has now unveiled what the project actually is: BRAIN, Brain Research through Advancing Innovative Neurotechnologies. And what is the project exactly? Will the BRAIN project end up as a BAM (Brain Activity Map)? Or a BUST (Badly Underfunded S**T)? I’d like to explore what I know, and I’d like to hear what everyone else knows as well. Am I wrong? Am I too optimistic? Too pessimistic? Have at. What is the BRAIN Project about? What are its goals? Well, nobody knows, actually. I certainly don’t know. But it appears that no one else knows either. “This working group, co-chaired by Dr. Cornelia “Cori” Bargmann (The Rockefeller University) and Dr. William Newsome (Stanford University), is being asked to articulate the scientific goals of the BRAIN initiative and develop a multi-year scientific plan for achieving these goals, including timetables, milestones, and cost estimates.” So basically, BRAIN is a very fancy initiative, with a fancy name…and so far, no goals. And of course, we’re all excited and trying to figure out what it’s going to be and whether or not it will work. Maybe it would have been in the better interest of the White House to wait until there were…you know, goals. But there is one goal that seems established here: new technologies. © 2013 Scientific American

Keyword: Brain imaging
Link ID: 18004 - Posted: 04.09.2013

By Sara Reardon and Bob Holmes, When President Obama called for $100 million in federal funding last week to map the human brain, he said he was hoping to “unlock the mystery of the three pounds of matter that sits between our ears.” Scientists hope that tracking brain activity neuron by neuron — an effort now called the Brain Research Through Advancing Innovative Neurotechnologies (BRAIN) Initiative — will revolutionize our understanding of brain function in the same way that the Human Genome Project is transforming our understanding of our genes. But just how do you go about mapping a brain? This is a question that two projects with similar lofty goals are already grappling with. The Human Brain Project aims to do it by creating a computer simulation of the entire brain. The Human Connectome Project is using magnetic resonance imaging to track the fibers that connect different regions of the brain on the millimeter scale, giving a rough-grained road map of the brain. To succeed, researchers will need to find noninvasive ways to record the firing of individual neurons, because all current methods involve opening the skull and, often, sticking electrodes into brain tissue. “Right now, you’re literally driving posts into the brain. It’s not very sophisticated,” says neurobiologist John Ngai of the University of California at Berkeley. A few groups are working on new approaches. The MindScope project at the Allen Institute for Brain Science in Seattle aims to map the visual cortex of mice. The team identifies where neurons are firing by injecting the brain with dyes or using genetically engineered proteins that bind to calcium molecules. When a neuron fires, calcium flows into the cell and activates the dye or protein. © 1996-2013 The Washington Post

Keyword: Brain imaging
Link ID: 18003 - Posted: 04.09.2013

By DOUGLAS QUENQUA The French geneticist Jérôme Lejeune discovered more than 50 years ago that Down syndrome is caused by the presence of an extra copy of chromosome 21. But to this day it has remained a mystery why that results in impaired physical and cognitive development. Now researchers at the Sanford-Burnham Medical Research Institute think they have found a clue. The scientists, who were investigating Alzheimer’s disease, found that mice that lacked a protein known as SNX27 had many of the same learning and memory defects as mice with Down syndrome. Looking at the brains of people with the syndrome, the researchers discovered that they, too, lacked SNX27. While chromosome 21 is not directly involved in SNX27 production, it does encode a regulator — miR-155 — that inhibits production. According to the study, published in the journal Nature Medicine, levels of miR-155 in the brains of people with Down syndrome correlate almost exactly with the decrease in SNX27. “In the brain, SNX27 keeps certain receptors on the cell surface — receptors that are necessary for neurons to fire properly,” said the study’s senior author, Huaxi Xu, in a statement released by the institute. “So in Down syndrome, we believe lack of SNX27 is at least partly to blame for developmental and cognitive defects.” To test their findings, Dr. Xu’s team introduced more SNX27 to mice with Down syndrome. As they expected, the mice showed immediate improvements in cognitive function and behavior. Now the researchers are investigating molecules that might increase production of SNX27 in the human brain. © 2013 The New York Times Company

Keyword: Development of the Brain; Genes & Behavior
Link ID: 18002 - Posted: 04.09.2013

By Linda Carroll, Kate Snow and Meghan Frank, NBC News As a little girl, Bonnie Ihme had big plans. Bright and artistically talented, she dreamed of becoming an architect. But the older she got, the more distant that dream seemed. By third grade, school had become a struggle. She felt easily distracted and found it impossible to focus in class. Eventually she abandoned her plan to be an architect. Ihme got married, had two kids and began cleaning houses and helping her husband with his business. But even that simpler life felt impossibly difficult. The Michigan mom had trouble keeping track of all the threads of her life. She’d send her kids to school without sneakers on gym day. She’d forget to bring library books back. She felt more overwhelmed than ever before. “I really would try hard to pull it all together,” Ihme told NBC’s Kate Snow in an interview airing on Rock Center Friday. “But when … you’re late for a Christmas concert that your daughter was really looking forward to going to and we get there and her class is walking back to the classroom and the tears in her eyes… you try harder.” Ihme saw history repeating itself in her 10-year-old son, Jacob, who began struggling with school, just as she had. Jacob would spend hours doing his homework, only to forget to bring it to school the next morning. Ihme’s heart ached for her son. © 2013 NBCNews.com

Keyword: ADHD
Link ID: 18001 - Posted: 04.08.2013

Barry Gordon, professor of neurology and cognitive science at the Johns Hopkins University School of Medicine, replies: We are aware of a tiny fraction of the thinking that goes on in our minds, and we can control only a tiny part of our conscious thoughts. The vast majority of our thinking efforts goes on subconsciously. Only one or two of these thoughts are likely to breach into consciousness at a time. Slips of the tongue and accidental actions offer glimpses of our unfiltered subconscious mental life. The intrusive thoughts you may experience throughout the day or before bed illustrate the disconcerting fact that many of the functions of the mind are outside of conscious control. Whether we maintain true control over any mental functions is the central debate about free will. Perhaps this lack of autonomy is to be expected as the foundations for almost all the mind's labors were laid long before our ancestors evolved consciousness. Even deliberate decisions are not completely under our power. Our awareness only sets the start and the end of a goal but leaves the implementation to unconscious mental processes. Thus, a batter can decide to swing at a ball that comes into the strike zone and can delineate the boundaries of that zone. But when the ball comes sailing through, unconscious mental functions take over. The actions required to send him to first base are too complex and unfold too quickly for our comparatively slow conscious control to handle. © 2013 Scientific American

Keyword: Sleep; Consciousness
Link ID: 18000 - Posted: 04.08.2013