by Claudia M Gold I recently had the privilege of being appointed to the Massachusetts Commission on Postpartum Depression (PPD). Lately I have been writing a lot about love, and this new role brings me again to this subject. When we support caregivers (I use this word rather than mother, as while the primary caregiver is usually the mother, it may be the father or another relative) who are struggling with postpartum depression, we are dealing with disruptions in passionate love relationships. Depression is, in fact, only one potential cause of such disruption. Perhaps our conversation should focus on relationships from the beginning. Education material about PPD does address the impact of PPD on child development, but the language is often focused on the caregiver, rather than the caregiver-child relationship. Across the ocean in Scotland my friend and colleague Suzanne Zeedyk has had a good deal of success in calling attention to the need to support early parent-child relationships. The departments of education, health care, finance and even law enforcement are on board in recognizing this need. On her website under "what I do" she writes: Science is helping us to better understand how relationships shape the development of human brains and human communities. I make this knowledge understandable for parents, professionals and policymakers Suzanne has created a beautiful DVD, The Connected Baby. There is a live streaming of the film today March 1st on the blog Mothering.com. One segment entitled "The Dance of the Nappy" films a mother changing her baby's diaper, interspersing commentary. In this simple and elegant way she shows the exquisite attunement between mother and baby that goes on in countless minute to minute interactions throughout the day. It is in this relationship that a baby's brain grows and develops. It is how he develops a sense of himself. © 2012 NY Times Co.

Keyword: Depression
Link ID: 16471 - Posted: 03.05.2012

By PATRICIA PEARSON A friend recently told me about a new app for the treatment of phobias. You stare at pictures of dental drills, snakes or airplane interiors, depending on your affliction, and these totems of menace — interspersed with reassuring images of teddy bears — gradually cease to provoke you. Does it work? We can’t know. My friend has a phobia of stuffed animals. It’s something, he says, about the soulless glass eyes. We were talking on the phone, but I could picture him shuddering. I, meanwhile, feel fine about snakes, jets and needles, but am haunted by heights and clusters. I haven’t seen apps for those, at least not yet. Of all the manifestations of anxiety, specific phobias are by far the most idiosyncratic. About 6 percent of Americans have an acute fear of animals like rats and birds. But after that, the sources of terror are myriad. Why objects bunched tightly together should send me into states of high alarm, I cannot say. My daughter once festooned a sock puppet with googly eyes from the craft store, and when I encountered it in the house, I reared like a spooked horse. Being a conscientious mother, I managed to conceal my sense of horror, but she has since witnessed my reaction to stands of mushrooms in the woods, and to dandelion buds in the grass. There is something — some hint of unchecked growth, of aggressive profusion — that I spy in certain geometric arrangements. Could it pertain to disgust, a burgeoning field of research? Might the underlying fear be one of chaos, or of the rapidly multiplying cells in cancer? © 2012 The New York Times Company

Keyword: Emotions; Learning & Memory
Link ID: 16470 - Posted: 03.05.2012

David T. Blake After training, animals and humans can make their thoughts interact directly with computers. A study provides evidence that the corticostriatal system of the brain is essential for this learning process. Brain–machine interfaces have a rich history in the sci-fi genre: in The Matrix films, human brains are plugged into a computer-based simulation that then becomes their 'reality'. But using our thoughts to directly control computers or other devices is not just in the realm of fantasy. Monkeys can learn to use visual cues to instruct a brain–machine interface to move a robotic arm or a computer cursor1, 2. And electrode arrays were implanted into the brain of a paralysed man in 2006, enabling him to control an artificial arm, to move a cursor on a computer screen and even to open e-mail3. Over time, an individual learns to improve their control over the brain–machine interface by modifying the activity of their brain, but how this happens is not well understood. In an article published on Nature's website today, Koralek et al.4 report that the corticostriatal system of the brain is involved in learning mental actions and skills that do not involve physical movement, such as those required for control of brain–machine interfaces. The corticostriatal system has a unique pattern of connectivity that enables sensory inputs to be associated with appropriate motor or cognitive responses5. It consists of a cortical component, the primary motor cortex, that exerts control over muscles, and a striatal component, the basal ganglia, that receives direct inputs from the motor cortex. The basal ganglia are involved in a wide range of learning conditions and are crucial to the motor deficits observed in Parkinson's and Huntington's diseases. Both corticostriatal components have a role in the learning and execution of physical skills requiring movement. © 2012 Nature Publishing Group

Keyword: Robotics
Link ID: 16469 - Posted: 03.05.2012

A cheap antibiotic normally prescribed to teenagers for acne is to be tested as a treatment to alleviate the symptoms of psychosis in patients with schizophrenia, in a trial that could advance scientific understanding of the causes of mental illness. The National Institute for Health Research is funding a £1.9m trial of minocycline, which will begin recruiting patients in the UK next month. The research follows case reports from Japan in which the drug was prescribed to patients with schizophrenia who had infections and led to dramatic improvements in their psychotic symptoms. The chance observation caused researchers to test the drug in patients with schizophrenia around the world. Trials in Israel, Pakistan and Brazil have shown significant improvement in patients treated with the drug. Scientists believe that schizophrenia and other mental illnesses including depression and Alzheimer's disease may result from inflammatory processes in the brain. Minocycline has anti-inflammatory and neuroprotective effects which they believe could account for the positive findings. Details of the trial were presented to the independent Schizophrenia Commission by Bill Deakin, professor of psychiatry at the University of Manchester, who is the lead investigator. The 12-member commission, set up by the mental health charity Rethink, is looking into the treatment and care of people with schizophrenia, and is due to report in the summer. The first account of minocycline's effects appeared in 2007 when a 23-year-old Japanese man was admitted to hospital suffering from persecutory delusions and paranoid ideas. He had no previous psychiatric history but became agitated and suffered auditory hallucinations, anxiety and insomnia. © independent.co.uk

Keyword: Schizophrenia
Link ID: 16468 - Posted: 03.03.2012

By Ferris Jabr In a 2006, season 2 episode of The Office entitled "Drug Testing," Dwight Schrute interrogates his fellow employees about the partially smoked joint he found in the parking lot. Dwight is determined to identify the culprit, but Jim Halpert turns the tables: Jim: I'm just saying that you can't be sure that it wasn't you. Dwight: That's ridiculous. Of course it wasn't me. Jim: Marijuana is a memory-loss drug, so maybe you just don't remember. Half a joint is unlikely to obliterate entire memories, but studies have shown that regularly smoking marijuana for many years does impair working memorythe ability to temporarily hold information in your head, such as a telephone number or the name of someone you just met. Exactly what marijuana does to the brain to muddle up memory formation has remained unclear. Now, a team of researchers has proposed that marijuana hinders the process not by acting on neurons, but rather by acting on non-neuronal brain cells called astrocytes. The finding adds to a growing heap of evidence that such non-electrical structural cells, collectively known as glia, play a far more active role in neural activity than researchers once realized. Memory depends on a balance of two opposing cellular processes: long-term potentiation, in which connected neurons learn to fire in sync, and long-term depression, the weakening of unnecessary connections among neurons. Xia Zhang of the University of Ottawa Institute of Mental Health Research and his colleagues think that marijuana impairs working memory by throwing off this balance, bolstering long-term depression (LTD) at the expense of long-term potentiation (LTP). Their new study suggests that marijuana increases LTD by triggering a chemical cascade that starts in astrocytes. © 2012 Scientific American,

Keyword: Glia; Learning & Memory
Link ID: 16467 - Posted: 03.03.2012

By Rachael Rettner Caffeine will get you going during the day but could leave you tossing and turning at night unless you're a "night owl" to begin with, a new study suggests. In the study, "morning people" who consumed caffeine during the day appeared more likely than late risers to awaken in the middle of their nighttime sleep. The researchers said this is the first study to link caffeine intake with "chronotype," the categorizing of people by the time of day they are most alert and active. The findings are preliminary and more research is needed to confirm them, the researchers added. Fifty college students were asked to record their caffeine consumption and their sleeping and waking times for a week. The students wore wrist devices that monitored their movements, to assess whether they had periods of wakefulness after they had fallen asleep. The researchers also measured caffeine levels in the students' saliva over the week. As college students, they tended to be so sleep-deprived that, for most, "it didn't matter how much caffeine they had"  they slept well whenever they finally hit the sack, said study researcher Jamie Zeitzer, an assistant professor of psychiatry and behavioral sciences at Stanford University. However, for the early risers, the more caffeine in their bodies, the more time they spent awake during the night after initially falling asleep. This was not seen in the night owls. © 2012 Scientific American,

Keyword: Sleep; Drug Abuse
Link ID: 16466 - Posted: 03.03.2012

Anne Trafton, MIT News Office MIT neuroscientists have shown that an enzyme overproduced in the brains of Alzheimer’s patients creates a blockade that shuts off genes necessary to form new memories. Furthermore, by inhibiting that enzyme in mice, the researchers were able to reverse Alzheimer’s symptoms. The finding suggests that drugs targeting the enzyme, known as HDAC2, could be a promising new approach to treating the disease, which affects 5.4 million Americans. The number of Alzheimer’s victims worldwide is expected to double every 20 years, and President Barack Obama recently set a target date of 2025 to find an effective treatment. Li-Huei Tsai, leader of the research team, says that HDAC2 inhibitors could help achieve that goal, though it would likely take at least 10 years to develop and test such drugs. “I would really strongly advocate for an active program to develop agents that can contain HDAC2 activity,” says Tsai, director of the Picower Institute for Learning and Memory at MIT. “The disease is so devastating and affects so many people, so I would encourage more people to think about this.” Tsai and her colleagues report the findings in the Feb. 29 online edition of Nature. Lead author of the paper is Johannes Gräff, a postdoc at the Picower Institute.

Keyword: Alzheimers
Link ID: 16465 - Posted: 03.03.2012

A repression of gene activity in the brain appears to be an early event affecting people with Alzheimer's disease, researchers funded by the National Institutes of Health have found. In mouse models of Alzheimer's disease, this epigenetic blockade and its effects on memory were treatable. "These findings provide a glimpse of the brain shutting down the ability to form new memories gene by gene in Alzheimer's disease, and offer hope that we may be able to counteract this process," said Roderick Corriveau, Ph.D., a program director at NIH's National Institute of Neurological Disorders and Stroke (NINDS), which helped fund the research. The study was led by Li-Huei Tsai, Ph.D., who is director of The Picower Institute for Learning and Memory at the Massachusetts Institute of Technology and an investigator at the Howard Hughes Medical Institute. It was published online February 29 in Nature. Dr. Tsai and her team found that a protein called histone deacetylase 2 (HDAC2) accumulates in the brain early in the course of Alzheimer's disease in mouse models and in people with the disease. HDAC2 is known to tighten up spools of DNA, effectively locking down the genes within and reducing their activity, or expression. In the mice, the increase in HDAC2 appears to produce a blockade of genes involved in learning and memory. Preventing the build-up of HDAC2 protected the mice from memory loss.

Keyword: Learning & Memory; Genes & Behavior
Link ID: 16464 - Posted: 03.01.2012

Erika Check Hayden The intersection of Mission and Sixth streets in San Francisco's South of Market neighbourhood is considered one of the most crime-riddled in the city. Liquor shops, adult bookshops and single-resident-occupancy hotels inhabit most of the buildings. Homeless people sit on the pavements or shuffle by, many of them showing symptoms of mental illness or drug abuse. Yet behind the walls of an unassuming outpatient psychiatric clinic, researchers are conducting experiments that they believe could fundamentally change the landscape of psychiatric care. Inside the San Francisco Citywide and Community Focus Center, in a room about the size of a large walk-in wardrobe, two people wearing headphones sit staring at computer screens. Despite the hubbub — the din of a nearby group session, clients milling in the hallway and the internal turmoil caused by their mental disorders — they are mesmerized by the games on the screens. Both have schizophrenia, and they are taking part in a study that aims to determine whether a controversial method of treatment can succeed where modern medicine has largely failed. The man behind the games is Michael Merzenich, an emeritus professor at the University of California, San Francisco, and a pioneering advocate for neuroplasticity — the notion that the brain can reshape and remodel its neural pathways even into adulthood. He has gained notoriety for his unabashed promotion of video games designed to tap into that plasticity. These have been marketed to treat everything from reading difficulties in children to driving impairment in elderly people. His zeal has, at times, attracted criticism. There is little solid evidence, say critics, that brain training makes a long-lasting difference in the lives of either ill or healthy people. © 2012 Nature Publishing Group

Keyword: Schizophrenia; Learning & Memory
Link ID: 16463 - Posted: 03.01.2012

A DRUG which minimises brain damage when given three hours after stroke has proved successful in monkeys and humans. A lack of oxygen in the brain during a stroke can cause fatal brain damage. There is only one approved treatment - tissue plasminogen activator - but it is most effective when administered within 90 minutes after the onset of stroke. Immediate treatment isn't always available, however, so drugs that can be given at a later time have been sought. In a series of experiments, Michael Tymianski and colleagues at Toronto Western Hospital in Ontario, Canada, replicated the effects of stroke in macaques before intravenously administering a PSD-95 inhibitor, or a placebo. PSD-95 inhibitors interfere with the process that triggers cell death when the brain is deprived of oxygen. To test its effectiveness the team used MRI to measure the volume of damaged brain for 30 days following the treatment, and conducted behavioural tests at various intervals within this time. Monkeys treated with the PSD-95 inhibitor one hour after stroke had 55 per cent less damaged tissue in the brain after 24 hours and 70 per cent less after 30 days, compared with those that took a placebo. These animals also did better in behavioural tests. Importantly, the drug was also effective three hours after stroke (Nature, DOI: 10.1038/nature10841). © Copyright Reed Business Information Ltd

Keyword: Stroke
Link ID: 16462 - Posted: 03.01.2012

By BENEDICT CAREY Daily doses of a drug used to treat Parkinson’s disease significantly improved function in severely brain-injured people thought to be beyond the reach of treatment, scientists reported on Wednesday, providing the first rigorous evidence to date that any therapy reliably helps such patients. The improvements were modest, experts said, and hardly amounted to a cure, or a quick means of “waking up” someone who has long been unresponsive. But the progress was meaningful, experts said, and, if replicated, would give rehabilitation doctors something they have never had: a standard treatment for injuries that are not at all standard or predictable in the ways they affect the brain. Some 50,000 to 100,000 Americans live in states of partial consciousness, and perhaps 15,000 in an unresponsive “vegetative” condition. According to the Department of Defense, more than 6,000 veterans have had severe brain injuries since 2000 and would potentially benefit from this therapy. The new report, appearing in The New England Journal of Medicine, gives doctors a solid basis to address such injuries, if not yet a predictable outcome. “This study puts the traumatic brain injury field on the first step of the ladder to developing scientific treatments. We’ve been trying to get there for a long time,” said Dr. Ramon Diaz-Arrastia, director of clinical research at the Center for Neuroscience and Regenerative Medicine at the Uniformed Services University of the Health Sciences in Rockville, Md., who was not involved in the research. “And there’s no reason to doubt that this therapy would also be effective in people with less severe brain injuries” than in the study. © 2012 The New York Times Company

Keyword: Brain Injury/Concussion; Parkinsons
Link ID: 16461 - Posted: 03.01.2012

By Sheila Eldred In the weeks and months following a tragedy like this week's school shooting in Ohio, experts and lawyers and school psychologists and classmates will try to make sense of the actions of the 17-year-old suspect. In all likelihood, though, no one will ever be able to pinpoint a single reason, said pyschologist David Walsh, author of "Why Do They Act That Way? A Survival Guide to the Adolescent Brain for You and Your Teen." "There are usually multiple factors that take a long time to sort out," Walsh said. "It's irrational, so looking for a reason can be somewhat frustrating. There are many kids who probably share that profile who don't do anything remotely like what he did. Science, however, can shed some light on how he and other teenagers think. "Adolescents can make good decisions," insists B. J. Casey, a neuroscientist at Weill Cornell Medical College. "They can make better decisions than you or I. But it is in the heat of the moment that they get into trouble." That's because the reward-sensitive areas of the brain are maturing with the onset of puberty. There's been a long-held view that teens make poor decisions because they don't think through consequences. Since the 1990s, we've known that brains go through extensive development in adolescence. © 2012 Discovery Communications, LLC

Keyword: Development of the Brain; Emotions
Link ID: 16460 - Posted: 03.01.2012

By Janet Raloff Exposure to certain pollutants early in a rat’s pregnancy can foster disease in her offspring during their adulthood as well as in subsequent generations, a new study shows. A wide range of pollutants elicited such lasting effects, despite future generations never encountering the triggering pollutant. Some chemicals tested led to premature puberty among great-granddaughters, with an increased risk of disease in reproductive tissues. In some tests, the chemicals disrupted ovarian function, something that in humans could lead to infertility or premature menopause. And another chemical exposure caused premature death of sperm-forming cells in the great-grandsons, researchers report online February 28 in PLoS ONE. Rather than altering genes, the tested pollutants altered chemical switches that regulate genes, reports Michael Skinner and his colleagues at Washington State University in Pullman. These epigenetic switches can lock a gene on or off. These master switches for DNA are fairly easy to modify throughout life. Early in development, a fetus erases any epigenetic changes acquired during its parents’ lifetimes, resetting those switches back to healthy, default programming. Because the fetus has a mechanism to erase such changes, a pollutant’s epigenetic effects shouldn’t occur in subsequent generations, says epigeneticist John McCarrey of the University of Texas at San Antonio, who was not involved in the study. That they did emerge in the new study “is pretty heavy in terms of their potential significance,” he says. © Society for Science & the Public 2000 - 2012

Keyword: Development of the Brain; Epigenetics
Link ID: 16459 - Posted: 03.01.2012

by Elizabeth Norton Bottlenose dolphins have a knack for language. They can understand both the meaning and the order of words conveyed through human hand gestures—correctly putting an item on the right side of their tank into a basket on the left, for example. Now humans, too, are beginning to understand dolphin language as more than just a cacophony of clicks, pulses, and whistles. A new study shows that dolphins use their own unique calls, known as signature whistles, to introduce themselves to others when meeting at sea. Until recently, researchers could study signature whistles only in captive animals—raising the question of whether the whistle developed in response to capture, isolation, or stress. A 2004 study showed that a group of free-swimming bottlenose dolphins in Florida did indeed use signature whistles. But information about how they used these sounds was scant. Marine biologists Vincent Janik and Nicola Quick of the Sea Mammal Research Unit at the University of St. Andrews in the United Kingdom were focusing on signature whistles as a way of understanding how dolphins communicate in the natural world. "Dolphins are comparable to great apes in their cognitive skills, but all we know is what they do in a lab," Janik explains. "We wanted to understand how dolphins use their intelligence outside of the tasks that humans set for them." © 2010 American Association for the Advancement of Science.

Keyword: Animal Communication; Language
Link ID: 16458 - Posted: 03.01.2012

By Jason G. Goldman When you dive into the frigid waters of the Pacific Ocean off the coast of southern California, the first thing you notice is the silence. Other than the bitter cold. Your body begins to adapt to the chilly water as blades of slimy kelp brush across your ankles. You spit out the bit of brackish saltwater that inevitably seeps into your mouth. Then you quickly dunk your head into the sea so that you might wet your hair and wipe it away from your eyes. It’s in that moment – when you’re entirely submerged under the rolling waves – that you notice the silence. You can almost hear the oscillating thuds of the waves breaking against the sand. As your heart beats faster to push warm blood into your arms and legs, perhaps you might even be able to hear your own heartbeat. Even against the auditory backdrop of the pounding of the waves and your heart, you can’t help but perceive the quiet. If only it were so for the blue whales that call this corner of the ocean home, at least for part of the year. Each summer, groups of endangered blue whales (Balaenoptera musculus) pass along the coast of Southern California between San Diego and Los Angeles. It isn’t a secret that the ocean is a noisy place if you’re a whale. In addition to the natural soundscape of the ocean, whales can hear sounds that have human origins, like sonar, passing ships, or underwater explosions. Considerable scientific attention has been paid to the effects of high-intensity anthropogenic noise on the communication abilities of whales and other marine mammals. After all, these animals communicate over vast distances by producing clicks, whistles, and songs. Previous findings have confirmed that the presence of ships interrupts blue whale songs. And some whales have been observed increasing the amplitude of their foraging calls in noisy environments, in an effort to aid others in distinguishing their communication from the undersea cacophony. Imagine having to pick out the sounds of only the cellos from amid an entire orchestra. © 2012 Scientific American

Keyword: Animal Communication; Hearing
Link ID: 16457 - Posted: 03.01.2012

The belief that older people tend to suffer worse sleep may be false - in fact the reverse may be true, according to US researchers. A telephone survey of more than 150,000 adults suggested that, apart from a blip in your 40s, sleep quality gets better with age. Those in their 80s reported the best sleep, says the study in Sleep journal. A UK sleep researcher said while poor health could affect sleep, it was a "myth" that age alone was a factor. While universities have equipment which can measure sleep duration and disturbance in study volunteers, this does not always match the volunteer's own opinion on their night's rest. The research, conducted by the Center for Sleep and Circadian Neurobiology at the University of Pennsylvania, instead focused on asking large numbers of randomly selected people about their sleep. They were also asked about their race, income, education, mood and general health. While being depressed or having health problems was linked to poor sleep quality, once the researchers had adjusted the results to compensate for this, a distinct pattern emerged. BBC © 2012

Keyword: Sleep; Development of the Brain
Link ID: 16456 - Posted: 03.01.2012

By Stephen Dougherty Today anesthetics are considered as routine as a trip to the dentist. They have been around at least since the 18th century when a talented chemist named Humphry Davy discovered the mysterious effect of nitrous oxide (laughing gas). Davy, young and ambitious, set out to rigorously test the gas’s effect, inhaling nitrous oxide daily for several months. Under slightly less rigorous conditions, Davy shared the gas with a distinguished group of friends including Samuel Taylor Coleridge, James Watt, and Robert Southey—who wrote in a letter that “the atmosphere of the highest of all possible heavens must be composed of this gas.” These early trials laid the foundation for anesthesia’s emergence in medicine today. Yet in the modern era, despite tremendous advances in the quality and selectivity of anesthetics, we still have a poor understanding of how anesthetics work in the brain. Highlighting these fundamental gaps in knowledge, a group of researchers recently made a surprising discovery about how we transition out of consciousness and back. The common view holds that going under (induction) and coming back up (emergence) are the same process, albeit in different directions. However, a recent study published in the journal PLoS ONE suggests that going under is not the same as coming back up. The researchers, led by Dr. Max Kelz at the University of Pennsylvania School of Medicine, observed that less anesthetic is required to keep the brain anesthetized than to induce unconsciousness. To explain these observations, the researchers have introduced a concept they call “neural inertia,” referring to the brain’s resistance to transitions between consciousness and unconsciousness. © 2012 Scientific American

Keyword: Sleep
Link ID: 16455 - Posted: 03.01.2012

By Lena Groeger Our five senses–sight, hearing, touch, taste and smell–seem to operate independently, as five distinct modes of perceiving the world. In reality, however, they collaborate closely to enable the mind to better understand its surroundings. We can become aware of this collaboration under special circumstances. In some cases, a sense may covertly influence the one we think is dominant. When visual information clashes with that from sound, sensory crosstalk can cause what we see to alter what we hear. When one sense drops out, another can pick up the slack. For instance, people who are blind can train their hearing to play double duty. Those who are both blind and deaf can make touch step in—to say, help them interpret speech. For a few individuals with a condition called synesthesia, the senses collide dramatically to form a kaleidoscope world in which chicken tastes like triangles, a symphony smells of baked bread or words bask in a halo of red, green or purple. (For more on how the senses can cross each other and into unusual territory, see “Edges of Perception,” by Ariel Bleicher, Scientific American Mind, March/April 2012.) Our senses must also regularly meet and greet in the brain to provide accurate impressions of the world. Our ability to perceive the emotions of others relies on combinations of cues from sounds, sights and even smells (see “I Know How You Feel,” by Janina Seubert and Christina Regenbogen, Scientific American Mind, March/April 2012). Perceptual systems, particularly smell, connect with memory and emotion centers to enable sensory cues to trigger feelings and recollections, and to be incorporated within them. © 2012 Scientific American

Keyword: Vision; Hearing
Link ID: 16454 - Posted: 03.01.2012

By Stephani Sutherland The lifelong mental benefits of exercising have long been known, from improving learning in kids to staving off dementia in seniors. Yet how working up a sweat leads to better cognition is much less clear. A study in the Journal of Applied Physiology reveals that the key may lie in the body’s power supply. Just as a booming metropolis might build new power plants to meet a rising need for electricity, our muscles respond to the demands of exercise by producing new mitochondria, the tiny structures inside cells that supply the body with energy. J. Mark Davis, a physiologist at the University of South Carolina, and his colleagues wondered if brain cells might do the same thing. While studying mice, they found that quantities of a signaling molecule, dubbed by researchers “a master regulator” of mitochondria production, increased in the brain after half an hour a day of treadmill running. The mice’s brain cells also had more mitochondrial DNA—distinct from the regular cellular DNA found in the nucleus—providing “gold standard” evidence of more mitochondria. It appears that the brain “adapts and changes by bringing more of these power­houses” online, Davis says. The increased energy supply allows the brain to work faster and more efficiently. The finding could help scientists understand how exercise staves off age- and disease-related declines in brain function, because neurons naturally lose mito­chondria as we age, Davis explains. Although past research has shown that exercise encourages the growth of new neurons in certain regions, the widespread expansion of the energy supply could underlie the benefits of exercise to more general brain functions such as mood regulation and dementia pre­vention. “The evidence is accumulating rapidly that exercise keeps the brain younger,” Davis says. © 2012 Scientific American

Keyword: Alzheimers
Link ID: 16453 - Posted: 03.01.2012

By Maia Szalavitz Sticks and stones may break your bones, but names can hurt just as much. Indeed, according to converging evidence reported in a new review in Current Directions in Psychological Science, physical and social pain are processed in some of the same regions of the brain. Naomi Eisenberger, co-director of the Social Cognitive Neuroscience Lab at UCLA, published the first brain-imaging paper revealing the overlap in 2003. She had been studying participants’ reactions to being rejected by other players (actually just a computer opponent) in a video game. “The first time we noticed the similarity, I was analyzing data next to a colleague of mine who was analyzing data on physical pain in irritable bowel syndrome,” she says. “We noticed similarities in the way that the neural data looked.” Physical pain has two components, Eisenberger explains: sensory and emotional. The sensory part of physical pain is mapped in the brain depending on which part of the body is hurt, but the emotional component — how distressing your brain determines the pain to be — is registered in the dorsal anterior cingulate cortex (dACC). That’s also where the sting of social pain is processed. “The affective component, which tells you more how much the pain is bothering [you], how much suffering it is causing — that experience seems to be more localized to the dACC and the anterior insula,” Eisenberger says. © 2012 Time Inc.

Keyword: Emotions; Pain & Touch
Link ID: 16452 - Posted: 03.01.2012