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Few genes have made the headlines as much as FOXP2. The first gene associated with language disorders , it was later implicated in the evolution of human speech. Girls make more of the FOXP2 protein, which may help explain their precociousness in learning to talk. Now, neuroscientists have figured out how one of its molecular partners helps Foxp2 exert its effects.
The findings may eventually lead to new therapies for inherited speech disorders, says Richard Huganir, the neurobiologist at Johns Hopkins University School of Medicine in Baltimore, Maryland, who led the work. Foxp2 controls the activity of a gene called Srpx2, he notes, which helps some of the brain's nerve cells beef up their connections to other nerve cells. By establishing what SRPX2 does, researchers can look for defective copies of it in people suffering from problems talking or learning to talk.
Until 2001, scientists were not sure how genes influenced language. Then Simon Fisher, a neurogeneticist now at the Max Planck Institute for Psycholinguistics in Nijmegen, the Netherlands, and his colleagues fingered FOXP2 as the culprit in a family with several members who had trouble with pronunciation, putting words together, and understanding speech. These people cannot move their tongue and lips precisely enough to talk clearly, so even family members often can?t figure out what they are saying. It “opened a molecular window on the neural basis of speech and language,” Fisher says.
Photo credit: Yoichi Araki, Ph.D.
By RON SUSKIND In our first year in Washington, our son disappeared. Just shy of his 3rd birthday, an engaged, chatty child, full of typical speech — “I love you,” “Where are my Ninja Turtles?” “Let’s get ice cream!” — fell silent. He cried, inconsolably. Didn’t sleep. Wouldn’t make eye contact. His only word was “juice.” I had just started a job as The Wall Street Journal’s national affairs reporter. My wife, Cornelia, a former journalist, was home with him — a new story every day, a new horror. He could barely use a sippy cup, though he’d long ago graduated to a big-boy cup. He wove about like someone walking with his eyes shut. “It doesn’t make sense,” I’d say at night. “You don’t grow backward.” Had he been injured somehow when he was out of our sight, banged his head, swallowed something poisonous? It was like searching for clues to a kidnapping. After visits to several doctors, we first heard the word “autism.” Later, it would be fine-tuned to “regressive autism,” now affecting roughly a third of children with the disorder. Unlike the kids born with it, this group seems typical until somewhere between 18 and 36 months — then they vanish. Some never get their speech back. Families stop watching those early videos, their child waving to the camera. Too painful. That child’s gone. In the year since his diagnosis, Owen’s only activity with his brother, Walt, is something they did before the autism struck: watching Disney movies. “The Little Mermaid,” “Beauty and the Beast,” “Aladdin” — it was a boom time for Disney — and also the old classics: “Dumbo,” “Fantasia,” “Pinocchio,” “Bambi.” They watch on a television bracketed to the wall in a high corner of our smallish bedroom in Georgetown. It is hard to know all the things going through the mind of our 6-year-old, Walt, about how his little brother, now nearly 4, is changing. They pile up pillows on our bed and sit close, Walt often with his arm around Owen’s shoulders, trying to hold him — and the shifting world — in place. © 2014 The New York Times Company
Link ID: 19341 - Posted: 03.10.2014
Alison Abbott A simple blood test has the potential to predict whether a healthy person will develop symptoms of dementia within two or three years. If larger studies uphold the results, the test could fill a major gap in strategies to combat brain degeneration, which is thought to show symptoms only at a stage when it too late to treat effectively. The test was identified in a preliminary study involving 525 people aged over 70. The work identified a set of ten lipid metabolites in blood plasma that distinguished with 90% accuracy between people who would remain cognitively healthy from those who would go on to show signs of cognitive impairment. “These findings are potentially very exciting,” says Simon Lovestone, a neuroscientist at the University of Oxford, UK, and a cordinator of a major European public-private partnership seekimg biomarkers for Alzheimer's. But he points out that only 28 participants developed symptoms similar to those of Alzheimer's disease during the latest work. “So the findings need to be confirmed in independent and larger studies.” There is not yet a good treatment for Alzheimer’s disease, which affects 35 million people worldwide. Several promising therapies have been tested in clinical trials over the last few years, but all have failed. However, those trials involved people who had already developed symptoms. Many neuroscientists fear that any benefits of a treatment would be missed in such a study, because it could be impossible to halt the disease once it has manifested. “We desperately need biomarkers which would allow patients to be identified — and recruited into trials — before their symptoms begin,” says Lovestone. © 2014 Nature Publishing Group,
Link ID: 19340 - Posted: 03.10.2014
By INNA GAISLER-SALOMON WE intuitively understand, and scientific studies confirm, that if a woman experiences stress during her pregnancy, it can affect the health of her baby. But what about stress that a woman experiences before getting pregnant — perhaps long before? It may seem unlikely that the effects of such stress could be directly transmitted to the child. After all, stress experienced before pregnancy is not part of a mother’s DNA, nor does it overlap with the nine months of fetal development. Nonetheless, it is undeniable that stress experienced during a person’s lifetime is often correlated with stress-related problems in that person’s offspring — and even in the offspring’s offspring. Perhaps the best-studied example is that of the children and grandchildren of Holocaust survivors. Research shows that survivors’ children have greater-than-average chances of having stress-related psychiatric illnesses like post-traumatic stress disorder, even without being exposed to higher levels of stress in their own lives. Similar correlations are found in other populations. Studies suggest that genocides in Rwanda, Nigeria, Cambodia, Armenia and the former Yugoslavia have brought about distinct psychopathological symptoms in the offspring of survivors. What explains this pattern? Does trauma lead to suboptimal parenting, which leads to abnormal behavior in children, which later affects their own parenting style? Or can you biologically inherit the effects of your parents’ stress, after all? It may be the latter. In a study that I, together with my colleagues Hiba Zaidan and Micah Leshem, recently published in the journal Biological Psychiatry, we found that a relatively mild form of stress in female rats, before pregnancy, affected their offspring in a way that appeared to be unrelated to parental care. © 2014 The New York Times Company
Think you’ll always pick chocolate over a bag of chips? Don’t be so sure. Researchers have found that if they can get people to pay more attention to a particular type of junk food, they will begin to prefer it—even weeks or months after the experiment. The finding suggests a new way to manipulate our decisions and perhaps even encourage us to pick healthy foods. “This paper is provocative and very well done,” says Antonio Rangel, a neuroeconomist at the California Institute of Technology in Pasadena, who was not involved in the new study. “It is exciting because it’s a proof of concept that a relatively simple intervention can have this long-lasting effect.” Economists who study decision-making had previously found that, when deciding between multiple items, people tend to let their gaze linger on the things that they end up choosing. This observation has motivated companies to pursue flashy packaging to attract consumers’ eyes. Tom Schonberg, a neuroscientist at the University of Texas, Austin, wondered whether people’s preferences could be changed before being faced with such a decision by training their brains to pay more attention to certain items. His first task was figuring out what kind of junk food people preferred. He and his colleagues recruited more than 200 university students and set up an auction-style program that asked them how much they were willing to pay for 60 different kinds of snacks, from M&M’s to Fritos. Then, the participants went through a 30- to 50-minute computer training program that showed photos of foods that the participants had already rated. When some treats appeared on the screen, a short tone would play and signal the subject to press a button as fast as possible. When other treats popped up, the computer remained silent and the subject refrained from pressing the button. © 2014 American Association for the Advancement of Science
By BENEDICT CAREY Jack Belliveau, a Harvard scientist whose quest to capture the quicksilver flare of thought inside a living brain led to the first magnetic resonance image of human brain function, died on Feb. 14 in San Mateo, Calif. He was 55. The cause was complications of a gastrointestinal disorder, said his wife, Brigitte Poncelet-Belliveau, a researcher who worked with him at the Athinoula A. Martinos Center for Biomedical Imaging at Massachusetts General Hospital. He lived in Boston. His wife said he died suddenly while visiting an uncle at his childhood home, which he owned. Dr. Belliveau was a 30-year-old graduate student at the Martinos Center when he hatched a scheme to “see” the neural trace of brain activity. Doctors had for decades been taking X-rays and other images of the brain to look for tumors and other lesions and to assess damage from brain injuries. Researchers had also mapped blood flow using positron emission tomography scans, but that required making and handling radioactive trace chemicals, whose signature vanished within minutes. Very few research centers had the technical knowledge or the machinery to pull it off. Dr. Belliveau tried a different approach. He had developed a technique to track blood flow, called dynamic susceptibility contrast, using an M.R.I. scanner that took split-second images, faster than was usual at the time. This would become a standard technique for assessing blood perfusion in stroke patients and others, but Dr. Belliveau thought he would try it to spy on a normal brain in the act of thinking or perceiving. “He went out to RadioShack and bought a strobe light, like you’d see in a disco,” said Dr. Bruce Rosen, director of the Martinos Center and one of Dr. Belliveau’s advisers at the time. “He thought the strobe would help image the visual areas of the brain, where there was a lot of interest.” © 2014 The New York Times Company
Keyword: Brain imaging
Link ID: 19337 - Posted: 03.10.2014
Imagine that, after feeling unwell for a while, you visit your GP. "Ah," says the doctor decisively, "what you need is medication X. It's often pretty effective, though there can be side-effects. You may gain weight. Or feel drowsy. And you may develop tremors reminiscent of Parkinson's disease." Warily, you glance at the prescription on the doctor's desk, but she hasn't finished. "Some patients find that sex becomes a problem. Diabetes and heart problems are a risk. And in the long term the drug may actually shrink your brain … " This scenario may sound far-fetched, but it is precisely what faces people diagnosed with schizophrenia. Since the 1950s, the illness has generally been treated using antipsychotic drugs – which, as with so many medications, were discovered by chance. A French surgeon investigating treatments for surgical shock found that one of the drugs he tried – the antihistamine chlorpromazine – produced powerful psychological effects. This prompted the psychiatrist Pierre Deniker to give the drug to some of his most troubled patients. Their symptoms improved dramatically, and a major breakthrough in the treatment of psychosis seemed to have arrived. Many other antipsychotic drugs have followed in chlorpromazine's wake and today these medications comprise 10% of total NHS psychiatric prescriptions. They are costly items: the NHS spends more on these medications than it does for any other psychiatric drug, including antidepressants. Globally, around $14.5bn is estimated to be spent on antipsychotics each year. Since the 1950s the strategy of all too many NHS mental health teams has been a simple one. Assuming that psychosis is primarily a biological brain problem, clinicians prescribe an antipsychotic medication and everyone does their level best to get the patient to take it, often for long periods. There can be little doubt that these drugs make a positive difference, reducing delusions and hallucinations and making relapse less likely – provided, that is, the patient takes their medication. © 2014 Guardian News and Media Limited
Link ID: 19336 - Posted: 03.08.2014
|By Jason G. Goldman Most people don't spend much time pondering the diameter of their pupils. The fact is that we don't have much control over our pupils, the openings in the center of the irises that allow light into the eyes. Short of chemical interventions—such as the eyedrops ophthalmologists use to widen their patients' pupils for eye exams—the only way to dilate or shrink the pupils is by changing the amount of available light. Switch off the lamp, and your pupils will widen to take in more light. Step out into the sun, and your pupils will narrow. Mechanical though they may be, the workings of pupils are allowing researchers to explore the parallels between imagination and perception. In a recent series of experiments, University of Oslo cognitive neuroscientists Bruno Laeng and Unni Sulutvedt began by displaying triangles of varying brightness on a computer screen while monitoring the pupils of the study volunteers. The subjects' pupils widened for dark shapes and narrowed for bright ones, as expected. Next, participants were instructed to simply imagine the same triangles. Remarkably, their pupils constricted or dilated as if they had been staring at the actual shapes. Laeng and Sulutvedt saw the same pattern when they asked subjects to imagine more complex scenes, such as a sunny sky or a dark room. Imagination is usually thought of as “a private and subjective experience, which is not accompanied by strongly felt or visible physiological changes,” Laeng says. But the new findings, published in Psychological Science, challenge that idea. The study suggests that imagination and perception may rely on a similar set of neural processes: when you picture a dimly lit restaurant, your brain and body respond, at least to some degree, as if you were in that restaurant. © 2014 Scientific American
by Hal Hodson WHETHER striding ahead with pride or slouching sullenly, we all broadcast our emotions through body language. Now a computer has learned to interpret those unspoken cues as well as you or I. Antonio Camurri of the University of Genoa in Italy and colleagues have built a system which uses the depth-sensing, motion-capture camera in Microsoft's Kinect to determine the emotion conveyed by a person's body movements. Using computers to capture emotions has been done before, but typically focuses on facial analysis or voice recording. Reading someone's emotional state from the way they walk across a room or their posture as they sit at a desk means they don't have to speak or look into a camera. "It's a nice achievement," says Frank Pollick, professor of psychology at the University of Glasgow, UK. "Being able to use the Kinect for this is really useful." The system uses the Kinect camera to build a stick figure representation of a person that includes information on how their head, torso, hands and shoulders are moving. Software looks for body positions and movements widely recognised in psychology as indicative of certain emotional states. For example, if a person's head is bowed and their shoulders are drooping, that might indicate sadness or fear. Adding in the speed of movement – slow indicates sadness, while fast indicates fear – allows the software to determine how someone is feeling. In tests, the system correctly identified emotions in the stick figures 61.3 per cent of the time, compared with a 61.9 per cent success rate for 60 human volunteers (arXiv.org/1402.5047). Camurri is using the system to build games that teach children with autism to recognise and express emotions through full-body movements. Understanding how another person feels can be difficult for people with autism, and recognising fear is more difficult than happiness. © Copyright Reed Business Information Ltd.
A man blind since birth is taking up a surprising new hobby: photography. His newfound passion is thanks to a system that turns images into sequences of sound. The technology not only gives “sight” to the blind, but also challenges the way neurologists think the brain is organized. In 1992, Dutch engineer Peter Meijer created vOICe, an algorithm that converts simple grayscale images into musical soundscapes. (The capitalized middle letters sound out “Oh, I see!”). The system scans images from left to right, converting shapes in the image into sound as it sweeps, with higher positions in the image corresponding to higher sound frequencies. For instance, a diagonal line stretching upward from left to right becomes a series of ascending musical notes. While more complicated images, such as a person sitting on a lawn chair, at first seem like garbled noise, with enough training users can learn to “hear” everyday scenes. In 2007, neuroscientist Amir Amedi and his colleagues at the Hebrew University of Jerusalem began training subjects who were born blind to use vOICe. Despite having no visual reference points, after just 70 hours of training, the individuals went from “hearing” simple dots and lines to “seeing” whole images such as faces and street corners composed of 4500 pixels. (For comparison, Nintendo’s Mario was made up of just 192 pixels in his first video game appearance.) By attaching a head-mounted camera to a computer and headphones, the blind users were even able to navigate around a room by the sound cues alone. Every few steps the system snaps a photo and converts it into sound, giving the users their bearings as they traverse tables and trashcans. One patient even took up photography, using the head-mounted system to frame his snapshots. © 2014 American Association for the Advancement of Science.
by Bruce Bower Actor Philip Seymour Hoffman’s February death from a drug overdose triggered media reports blaming the terrible disease of addiction for claiming another life. But calling addiction a “disease” may be misguided, according to an alternative view with some scientific basis. Most people who are addicted to cigarette smoking, alcohol or other drugs manage to quit, usually on their own, after experiencing major attitude adjustments. Although relapses occur, successes ultimately outnumber fatalities. People can permanently walk away from addiction. Evidence that addiction is a solvable coping problem rather than a chronic, recurring disease seems like encouraging news. But it’s highly controversial. Neuroscientists and many clinicians regard drug addictions as brain illnesses best vanquished with the help of medications that fight cravings and withdrawal. From this perspective, drug-induced brain changes increase a person’s thirst for artificial highs and make quitting progressively more difficult. This conflict over addiction’s nature plays out in two lines of research: studies of remission and relapse among treated substance abusers and long-term studies of the general population. Follow-up investigations of people who attend treatment programs report that addicts never completely shake an urge to snort, inject, guzzle or otherwise consume their poisons of choice. Ongoing treatment in psychotherapy, rehab centers or 12-step groups encourages temporary runs of sobriety, but it’s easier to kick the bucket than to kick the habit. Surveys and long-term studies of the general population, however, observe that addicts typically spend their youth in a substance-induced haze but drastically cut back or quit using drugs altogether by early adulthood. Most of those who renounce the “high” life do so without formal treatment. © Society for Science & the Public 2000 - 2013.
Keyword: Drug Abuse
Link ID: 19332 - Posted: 03.08.2014
By SABRINA TAVERNISE Middle and high school students who used electronic cigarettes were more likely to smoke real cigarettes and less likely to quit than students who did not use the devices, a new study has found. They were also more likely to smoke heavily. But experts are divided about what the findings mean. The study’s lead author, Stanton Glantz, a professor of medicine at the University of California, San Francisco, who has been critical of the devices, said the results suggested that the use of e-cigarettes was leading to less quitting, not more. “The use of e-cigarettes does not discourage, and may encourage, conventional cigarette use among U.S. adolescents,” the study concluded. It was published online in the journal JAMA Pediatrics on Thursday. But other experts said the data did not support that interpretation. They said that just because e-cigarettes are being used by youths who smoke more and have a harder time quitting does not mean that the devices themselves are the cause of those problems. It is just as possible, they said, that young people who use the devices were heavier smokers to begin with, or would have become heavy smokers anyway. “The data in this study do not allow many of the broad conclusions that it draws,” said Thomas J. Glynn, a researcher at the American Cancer Society. The study is likely to stir the debate further over what electronic cigarettes mean for the nation’s 45 million smokers, about three million of whom are middle and high school students. Some experts worry that e-cigarettes are a gateway to smoking real cigarettes for young people, though most say the data is too skimpy to settle the issue. Others hope the devices could be a path to quitting. So far, the overwhelming majority of young people who use e-cigarettes also smoke real cigarettes, a large federal survey published last year found. Still, while e-cigarette use among youths doubled from 2011 to 2012, regular cigarette smoking for youths has continued to decline. The rate hit a record low in 2013 of 9.6 percent, down by two-thirds from its peak in 1997. © 2014 The New York Times Company
Keyword: Drug Abuse
Link ID: 19331 - Posted: 03.08.2014
by Graham Lawton In August 2013, professional rugby union player Andy Hazell received a massive blow to the head while playing for his club Gloucester. Six "horrendous" months later he retired from the game, stricken by dizziness, mood swings and a sense of detachment. Hazell isn't the first rugby player to experience concussion during a game, and probably won't be the last to have to retire as a result. According to a campaign launched this week, rugby union players don't know enough about the risks of concussion – and the governing bodies aren't doing enough to prevent it. The problem isn't so much one-off blows like the one that ended Hazell's career, but long-term damage caused by repeated concussions over many years. Studies of boxers and American footballers have shown that these can lead to a degenerative brain disease called Chronic Traumatic Encephalopathy (CTE). CTE leads to memory problems, personality change and slowness of movement. It usually shows up in middle age, long after a sporting career is over. CTE has been an issue in American Football for years. Thousands of ex-professionals sued the National Football League alleging that it knew about the risks but covered them up. Last year the NFL offered a $765 million settlement package. Neurologists have long suspected that other contact sports might also lead to CTE – particularly rugby union because of its emphasis on high-speed "hits". Concussion is the fourth most common injury in the professional game. © Copyright Reed Business Information Ltd.
Keyword: Brain Injury/Concussion
Link ID: 19330 - Posted: 03.08.2014
Londa Schiebinger. In Madrid a couple of years ago, I was interviewed for Spanish newspapers. When I later ran the text through Google Translate, I got a shock: I was referred to repeatedly as “he”. Like much science and technology, Google Translate has a male default. When I drive a car, the seatbelt is not designed to accommodate breast tissue. Any medicines I take are more likely to have been tested on male than on female animals. There are moral issues here: women pay taxes and buy products and should not be short-changed. But scientific objectivity is at stake, too. Because medical research is done mainly in males, there is a male bias in, for example, the choice of drug targets. Science is halving the potential field of innovation. This is not about active discrimination; the bias is largely unconscious. Google Translate defaults to the masculine pronoun because 'he' is more commonly found on the Web than 'she'. Yet that is changing: an analysis of American-English texts in Google Books shows that the ratio of masculine to feminine pronouns has fallen to around 2:1, from a peak of 4:1 in the 1960s. In the summer of 2012, I invited Google and several language-processing experts to a Gendered Innovations workshop at Harvard University in Cambridge, Massachusetts. They listened to the problem for about 20 minutes, then said: “We can fix that!” Although it is complicated, the search for solutions is on. Fixing the problem is great, but constantly retrofitting for women is not the best road forwards. A better way is to include gender at all relevant phases of research — when setting priorities, gathering and analysing data, evaluating results, developing patents and, finally, transferring ideas to markets. Science and technology should take into account the biological and social needs of both women and men. Unconscious sex and gender bias can be socially harmful and expensive. © 2014 Nature Publishing Group
Keyword: Sexual Behavior
Link ID: 19329 - Posted: 03.06.2014
New findings reveal how a mutation, a change in the genetic code that causes neurodegeneration, alters the shape of DNA, making cells more vulnerable to stress and more likely to die. The particular mutation, in the C9orf72 gene, is the most common cause for amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig’s disease), and frontotemporal degeneration (FTD), the second most common type of dementia in people under 65. This research by Jiou Wang, Ph.D., and his colleagues at Johns Hopkins University (JHU) was published in Nature and was partially funded by the National Institutes of Health’s National Institute of Neurological Disorders and Stroke (NINDS). In ALS, the muscle-activating neurons in the spinal cord die, eventually causing paralysis. In FTD neurons in particular brain areas die leading to progressive loss of cognitive abilities. The mutation may also be associated with Alzheimer’s and Huntington’s diseases. DNA contains a person’s genetic code, which is made up of a unique string of bases, chemicals represented by letters. Portions of this code are divided into genes that provide instructions for making molecules (proteins) that control how cells function. The normal C9orf72 gene contains a section of repeating letters; in most people, this sequence is repeated two to 25 times. In contrast, the mutation associated with ALS and FTD can result in up to tens of thousands of repeats of this section.
Clara Moskowitz When mathematicians describe equations as beautiful, they are not lying. Brain scans show that their minds respond to beautiful equations in the same way other people respond to great paintings or masterful music. The finding could bring neuroscientists closer to understanding the neural basis of beauty, a concept that is surprisingly hard to define. In the study, researchers led by Semir Zeki of University College London asked 16 mathematicians to rate 60 equations on a scale ranging from "ugly" to "beautiful." Two weeks later, the mathematicians viewed the same equations and rated them again while lying inside a functional magnetic resonance imaging (fMRI) scanner. The scientists found that the more beautiful an equation was to the mathematician, the more activity his or her brain showed in an area called the A1 field of the medial orbitofrontal cortex. The orbitofrontal cortex is associated with emotion, and this particular region of it has shown in previous tests to be correlated with emotional responses to visual and musical beauty. The researchers wondered whether the trend would extend to mathematical beauty, which "has a much deeper intellectual source than visual or musical beauty, which are more 'sensible' and perceptually based," they wrote in a paper reporting their results published on 13 February in Frontiers of Human Neuroscience. Investigating mathematical beauty allowed the researchers to test the role of culture and learning in aesthetic appreciation. The scientists hypothesized that while people with no musical or artistic training can still appreciate Beethoven’s and Michelangelo's works, only those who understand the meaning behind certain mathematical formulas would find them beautiful. © 2014 Nature Publishing Group,
Link ID: 19327 - Posted: 03.06.2014
By Tara Bahrampour, Alzheimer’s disease likely plays a much larger role in the deaths of older Americans than is reported, according to a new study that says the disease may be the third-leading cause of death in the United States. The Centers for Disease Control and Prevention lists Alzheimer’s as the sixth-leading cause of death, far below heart disease and cancer. But the new report, published Wednesday in the medical journal of the American Academy of Neurology, suggests that the current system of relying on death certificates for causes misses the complexity of dying for many older people and underestimates the impact of Alzheimer’s. While the CDC attributed about 84,000 deaths in 2010 to Alzheimer’s, the report estimated that number to be 503,400 among people 75 and older. That puts it in a close third place, behind heart disease and cancer, and well above chronic lung disease, stroke and accidents, which rank third, fourth and fifth. Alzheimer’s is somewhat of a sleeping giant compared with other leading killers that have received more funding over the years. While deaths from these diseases have been going down thanks to better treatment and prevention, the number of people suffering from Alzheimer’s is quickly rising and the disease is always fatal. More than 5 million people in the United States are estimated to have Alzheimer’s. With the aging of the baby-boom generation, this number is expected to nearly triple by 2050 if there are no significant medical breakthroughs, according to the Alzheimer’s Association. © 1996-2014 The Washington Post
Link ID: 19326 - Posted: 03.06.2014
Virginia Hughes When Brian Dias became a father last October, he was, like any new parent, mindful of the enormous responsibility that lay before him. From that moment on, every choice he made could affect his newborn son's physical and psychological development. But, unlike most new parents, Dias was also aware of the influence of his past experiences — not to mention those of his parents, his grandparents and beyond. Where one's ancestors lived, or how much they valued education, can clearly have effects that pass down through the generations. But what about the legacy of their health: whether they smoked, endured famine or fought in a war? As a postdoc in Kerry Ressler's laboratory at Emory University in Atlanta, Georgia, Dias had spent much of the two years before his son's birth studying these kinds of questions in mice. Specifically, he looked at how fear associated with a particular smell affects the animals and leaves an imprint on the brains of their descendants. Dias had been exposing male mice to acetophenone — a chemical with a sweet, almond-like smell — and then giving them a mild foot shock. After being exposed to this treatment five times a day for three days, the mice became reliably fearful, freezing in the presence of acetophenone even when they received no shock. Ten days later, Dias allowed the mice to mate with unexposed females. When their young grew up, many of the animals were more sensitive to acetophenone than to other odours, and more likely to be startled by an unexpected noise during exposure to the smell. Their offspring — the 'grandchildren' of the mice trained to fear the smell — were also jumpier in the presence of acetophenone. What's more, all three generations had larger-than-normal 'M71 glomeruli', structures where acetophenone-sensitive neurons in the nose connect with neurons in the olfactory bulb. In the January issue of Nature Neuroscience1, Dias and Ressler suggested that this hereditary transmission of environmental information was the result of epigenetics — chemical changes to the genome that affect how DNA is packaged and expressed without altering its sequence. © 2014 Nature Publishing Group,
By Debra Weiner An active lifestyle improves brain health, scientists have long believed. The studies bear this out: physical, intellectual and social activity—or “environmental enrichment,” in the parlance—enhances learning and memory and protects against aging and neurological disease. Recent research suggests one benefit of environmental enrichment at the cellular level: it repairs brain myelin, the protective insulation surrounding axons, or nerve fibers, which can be lost because of aging, injury or diseases such as multiple sclerosis. But how does an enriched environment trigger myelin repair in the first place? The answer appears to involve naturally occurring membrane-wrapped packets called exosomes. A number of different cell types release these little sacs of proteins and genetic material into the body's fluids. Loaded with signaling molecules, exosomes spread through the body “like messages in a bottle,” says R. Douglas Fields, a neurobiologist at the National Institutes of Health. They target particular cells and change their behavior. In animal studies, exosomes secreted by immune cells during environmental enrichment caused cells in the brain to start myelin repair. Researchers think exosomes might find use as biomarkers for diagnosing diseases or as vehicles to deliver cancer drugs or other therapeutic agents. The exosomes produced during environmental enrichment carry microRNAs—small pieces of genetic material—which appear to instruct immature cells in the brain to develop into myelin-making cells called oligodendrocytes. When researchers at the University of Chicago withdrew exosomes from the blood of rats and administered them to aging animals, the older rats' myelin levels rose by 62 percent, the team reported in February in Glia. © 2014 Scientific American
By GRETCHEN REYNOLDS Obesity may have harmful effects on the brain, and exercise may counteract many of those negative effects, according to sophisticated new neurological experiments with mice, even when the animals do not lose much weight. While it’s impossible to know if human brains respond in precisely the same way to fat and physical activity, the findings offer one more reason to get out and exercise. It’s been known for some time that obesity can alter cognition in animals. Past experiments with lab rodents, for instance, have shown that obese animals display poor memory and learning skills compared to their normal-weight peers. They don’t recognize familiar objects or recall the location of the exit in mazes that they’ve negotiated multiple times. But scientists hadn’t understood how excess weight affects the brain. Fat cells, they knew, manufacture and release substances into the bloodstream that flow to other parts of the body, including the heart and muscles. There, these substances jump-start biochemical processes that produce severe inflammation and other conditions that can lead to poor health. Many thought the brain, though, should be insulated from those harmful effects. It contains no fat cells and sits behind the protective blood-brain barrier that usually blocks the entry of undesirable molecules. However, recent disquieting studies in animals indicate that obesity weakens that barrier, leaving it leaky and permeable. In obese animals, substances released by fat cells can ooze past the barrier and into the brain. The consequences of that seepage became the subject of new neurological experiments conducted by researchers at Georgia Regents University in Augusta and published last month in The Journal of Neuroscience. © 2014 The New York Times Company
Link ID: 19323 - Posted: 03.05.2014
By BENEDICT CAREY He heard about the drug trial from a friend in Switzerland and decided it was worth volunteering, even if it meant long, painful train journeys from his native Austria and the real possibility of a mental meltdown. He didn’t have much time, after all, and traditional medicine had done nothing to relieve his degenerative spine condition. “I’d never taken the drug before, so I was feeling — well, I think the proper word for it, in English, is dread,” said Peter, 50, an Austrian social worker, in a telephone interview; he asked that his last name be omitted to protect his identity. “There was this fear that it could all go wrong, that it could turn into a bad trip.” On Tuesday, The Journal of Nervous and Mental Disease is posting online results from the first controlled trial of LSD in more than 40 years. The study, conducted in the office of a Swiss psychiatrist near Bern, tested the effects of the drug as a complement to talk therapy for 12 people nearing the end of life, including Peter. Most of the subjects had terminal cancer, and several died within a year after the trial — but not before having a mental adventure that appeared to have eased the existential gloom of their last days. “Their anxiety went down and stayed down,” said Dr. Peter Gasser, who conducted the therapy and followed up with his patients a year after the trial concluded. The new publication marks the latest in a series of baby steps by a loose coalition of researchers and fund-raisers who are working to bring hallucinogens back into the fold of mainstream psychiatry. Before research was banned in 1966 in the United States, doctors tested LSD’s effect for a variety of conditions, including end-of-life anxiety. But in the past few years, psychiatrists in the United States and abroad — working with state regulators as well as ethics boards — have tested Ecstasy-assisted therapy for post-traumatic stress; and other trials with hallucinogens are in the works. © 2014 The New York Times Company