By: George Will, Washington Post PRINCETON, N.J. — Fifty years from now, when Malia and Sasha are grandmothers, their father’s presidency might seem most consequential because of a small sum — $100 million —for studying something small. “As humans,” Barack Obama said when announcing the initiative to study the brain, “we can identify galaxies light-years away ... but we still haven’t unlocked the mystery of the three pounds of matter that sits between our ears.” Actually, understanding the brain will be a resounding success without unlocking the essential mystery, which is: How does matter become conscious of itself? Or should we say, how does it become — or acquire — consciousness? Just trying to describe this subject takes scientists onto intellectual terrain long occupied by philosophers. Those whose field is the philosophy of mind will learn from scientists such as Princeton’s David Tank, aleader of the BRAIN Initiative, which aims at understanding how brain regions and cells work together, moment to moment, throughout our lives. If, as is said, a physicist is an atom’s way of knowing about atoms, thena neuroscientist like Tank is a brain cell’s way of knowing about brain cells. Each of us has about 100 billion of those, each of which communicates with an average of 10,000 other nerve cells. The goal of neuroscientists is to discover how these neural conversations give rise to a thought, a memory ora decision. And to understand how the brain functions, from which we may understand disorders such as autism, schizophrenia and epilepsy. © 2013 Forum Communications Co.

Keyword: Brain imaging
Link ID: 18560 - Posted: 08.26.2013

By Brian Mossop A fine line separates creativity and madness. Bipolar disorder teeters along that line, with patients experiencing moments of impulsive thought, which can yield bold insights or quickly descend into confusion or rage. In her new book, Haldol and Hyacinths, Iranian-American author and activist Moezzi presents a captivating autobiographical account of her struggle with bipolar disorder. Using a series of vignettes, she reconstructs her downward spiral into psychosis, which eventually led to a suicide attempt and multiple stays in mental health facilities. From seemingly innocuous bouts of insomnia to full-blown hallucinations, Moezzi describes how she descended into madness. Moezzi's medical issues first emerged in her sophomore year of college, when she began to experience severe abdominal pain, later diagnosed as pancreatitis. Doctors decided to remove her pancreas to save her life and prevent a cyst from festering. Everyone she knew rallied alongside her during this time. Things were much different when Moezzi's bipolar disorder took hold in the years following her physical illness. She soon discovered that mental illness has no heroes, no celebrity spokesperson, no champions. Relying solely on the support of her immediate family and a devoted husband, Moezzi saw that the disorder carries a stigma, exacerbated by inaccurate media portrayals. Even worse is the plight of patients in places such as Moezzi's homeland of Iran, where mental illness is simply ignored. Despite bipolar disorder being the sixth leading cause of disability in the world, there is not even a word for the disease in Farsi. © 2013 Scientific American

Keyword: Schizophrenia
Link ID: 18559 - Posted: 08.26.2013

By Susan Gaidos If you’re someone who enjoys being recognized, Julian Lim is your kind of waiter. Lim, who’s working his way through college waiting tables, remembers the face of everyone that walks through the door of the South Bend, Ind., restaurant where he works. His abilities go beyond making his customers feel special. This spring, when he cut his hand on broken glass, he pegged the emergency room nurse as a fellow student from his grade school days. Though they’d never spoken, and the girl had since undergone changes in appearance, Lim recognized her instantly. Carrie Shanafelt is good with faces, too. A professor of literature at Grinnell College in Iowa, Shanafelt can spot her students outside the classroom, whether it’s the first week of class or years later. And Ajay Jansari, an information technology specialist in London, often has to see a face only once to remember it, even those he meets thousands of miles from home. While some people say they never forget a face, these folks have scientific studies to back their claims. Called “super recognizers,” they’re among a small group of individuals being studied by scientists at Dartmouth College and in England to better understand how some people can recognize almost every face they have ever seen. Scientists are now putting super recognizers’ skills to the test to get a handle on how face-processing areas of the brain work to make a few people so adept at recalling faces. Findings from the studies may advance understanding of how most people categorize faces — a subject that is still poorly understood. © Society for Science & the Public 2000 - 2013

Keyword: Attention
Link ID: 18558 - Posted: 08.24.2013

By GRETCHEN REYNOLDS Our genes may have a more elevated moral sense than our minds do, according to a new study of the genetic effects of happiness. They can, it seems, reward us with healthy gene activity when we’re unselfish — and chastise us, at a microscopic level, when we put our own needs and desires first. To reach that slightly unsettling conclusion, researchers from the University of North Carolina and the University of California, Los Angeles, had 80 healthy volunteers complete an online questionnaire that asked why they felt satisfied with their lives. Then the researchers drew their blood and analyzed their white blood cells. Scientists have long surmised that moods affect health. But the underlying cellular mechanisms were murky until they began looking at gene-expression profiles inside white blood cells. Gene expression is the complex process by which genes direct the production of proteins. These proteins jump-start other processes, which in the case of white blood cells control much of the body’s immune response. It turned out that different forms of happiness were associated with quite different gene-expression profiles. Specifically, those volunteers whose happiness, according to their questionnaires, was primarily hedonic, to use the scientific term, or based on consuming things, had surprisingly unhealthy profiles, with relatively high levels of biological markers known to promote increased inflammation throughout the body. Such inflammation has been linked to the development of cancer, diabetes and cardiovascular disease. They also had relatively low levels of other markers that increase antibody production, to better fight off infections. Copyright 2013 The New York Times Company

Keyword: Emotions; Genes & Behavior
Link ID: 18557 - Posted: 08.24.2013

Virginia Morell A wolf’s howl is one of the most iconic sounds of nature, yet biologists aren’t sure why the animals do it. They’re not even sure if wolves howl voluntarily or if it’s some sort of reflex, perhaps caused by stress. Now, scientists working with captive North American timber wolves in Austria report that they’ve solved part of the mystery. Almost 50 years ago, wildlife biologists suggested that a wolf’s howls were a way of reestablishing contact with other pack members after the animals became separated, which often happens during hunts. Yet, observers of captive wolves have also noted that the pattern of howls differs depending on the size of the pack and whether the dominant, breeding wolf is present, suggesting that the canids’ calls are not necessarily automatic responses. Friederike Range, a cognitive ethologist at the University of Veterinary Medicine in Vienna, was in a unique position to explore the conundrum. Since 2008, she and her colleagues have hand-raised nine wolves at the Wolf Science Center in Ernstbrunn, which she co-directs. “We started taking our wolves for walks when they were 6 weeks old, and as soon as we took one out, the others would start to howl,” she says. “So immediately we became interested in why they howl.” Although the center’s wolves don’t hunt, they do howl differently in different situations, Range says. “So we also wanted to understand these variations in their howling.” © 2012 American Association for the Advancement of Science.

Keyword: Animal Communication; Language
Link ID: 18556 - Posted: 08.24.2013

By CARL ZIMMER Evolutionary biologists have come to recognize humans as a tremendous evolutionary force. In hospitals, we drive the evolution of resistant bacteria by giving patients antibiotics. In the oceans, we drive the evolution of small-bodied fish by catching the big ones. In a new study, a University of Minnesota biologist, Emilie C. Snell-Rood, offers evidence suggesting we may be driving evolution in a more surprising way. As we alter the places where animals live, we may be fueling the evolution of bigger brains. Dr. Snell-Rood bases her conclusion on a collection of mammal skulls kept at the Bell Museum of Natural History at the University of Minnesota. Dr. Snell-Rood picked out 10 species to study, including mice, shrews, bats and gophers. She selected dozens of individual skulls that were collected as far back as a century ago. An undergraduate student named Naomi Wick measured the dimensions of the skulls, making it possible to estimate the size of their brains. Two important results emerged from their research. In two species — the white-footed mouse and the meadow vole — the brains of animals from cities or suburbs were about 6 percent bigger than the brains of animals collected from farms or other rural areas. Dr. Snell-Rood concludes that when these species moved to cities and towns, their brains became significantly bigger. Dr. Snell-Rood and Ms. Wick also found that in rural parts of Minnesota, two species of shrews and two species of bats experienced an increase in brain size as well. Dr. Snell-Rood proposes that the brains of all six species have gotten bigger because humans have radically changed Minnesota. Where there were once pristine forests and prairies, there are now cities and farms. In this disrupted environment, animals that were better at learning new things were more likely to survive and have offspring. © 2013 The New York Times Company

Keyword: Evolution; Brain imaging
Link ID: 18555 - Posted: 08.24.2013

JoNel Aleccia TODAY When doctors told Pete and Michelle Gallagher that they wanted to remove half of their 3-year-old son’s brain, the Attica, Ohio, parents were horrified. But a new study shows the extreme procedure may offer some kids their best shot at a normal life. “We panicked,” said Pete Gallagher, recalling their reaction seven years ago. The couple also knew that the dramatic surgery known as a hemispherectomy might be the only workable option to stop the severe seizures, more than a dozen a day, that were robbing Aiden of his ability to function – and to learn. “He had forgotten his alphabet. He had forgotten how to count. It was all slipping,” the father said. Today, Aiden is a healthy, red-haired fifth-grader who goes to regular school and loves to play baseball and basketball. He hasn’t had a seizure since the rare operation, making the boy a poster child for new research that finds the procedure offers real-world success for children suffering from devastating epilepsy. “The brain has an amazing capacity to work around the function that it has lost,” said Dr. Ajay Gupta, head of pediatric epilepsy at the Cleveland Clinic. In the first large-scale study to look at the everyday capabilities of kids who undergo hemispherectomy, Gupta and his colleagues reviewed 186 operations performed at their center between 1997 and 2009 and took a close look at 115 patients. They confirmed what doctors knew, but had little practical data to support: That removing the diseased hemisphere of a seizure-prone brain allows sufferers to learn and grow and, in some cases, lead normal lives.

Keyword: Epilepsy; Development of the Brain
Link ID: 18554 - Posted: 08.24.2013

By Melinda Wenner Moyer Few phenomena have created as divisive a rift recently among health professionals as the so-called “obesity paradox,” the repeated finding that obese people with certain health conditions live longer than slender people with the same ailments. And when a January meta-analysis involving nearly three million research subjects suggested that overweight people in the general population also live longer than their slimmer counterparts, the head of Harvard University’s nutrition department, Walter Willett, called the work “a pile of rubbish.” A few new studies suggest that these paradoxes may largely be artifacts of flawed research designs, but some experts disagree, accusing the new studies of being inaccurate. Among the biggest questions raised by this new research is the impact of age: whether obesity becomes more or less deadly as people get older and why. The January meta-analysis, led by U.S. Centers for Disease Control and Prevention senior scientist Katherine Flegal, pooled data from 97 studies of the general global population and reported that, in sum, overweight individuals—those with a body mass index of 25 to 29.9—were 6 percent less likely to die over various short time periods than people of normal weight (with a BMI 18.5 to 24.9) were. For people over the age of 65, however, being overweight conferred a 10 percent survival advantage. Flegals' findings also suggest that obesity, which has always been considered a major health risk, is not always dangerous and that it becomes less so with age: Adults with grade 1 obesity (BMIs of 30 to 34.9), she found, were no more likely to die than were normal weight adults; for grade 2 obesity (BMI of 35 to 39.9), the increased death risk for adults of all ages was 29 percent, but restricting the analysis to adults over the age of 65, the increased death risk associated with grade 2 obesity was not statistically significant.. The older a person is, the analysis seemed to say, the safer extra pounds become. © 2013 Scientific American

Keyword: Obesity
Link ID: 18553 - Posted: 08.24.2013

I HAVE been struggling with an addiction to opiates for the past three years. It started with prescription painkillers and progressed to full-blown heroin dependence. In an attempt to kick the habit I signed up for a traditional 30-step inpatient treatment that involved individual and group counselling, and which cost about $30,000. That was a year ago, and it didn't work. I felt unable to stay away from heroin. Now I am at a small clinic in Baja California, Mexico, where I am taking part in the first trial to investigate the effectiveness of treating heroin addiction with a single dose of ibogaine – a psychoactive substance derived from the rainforest shrub Tabernanthe iboga. "Ibogaine can take you many places, causing you to experience a range of emotions, memories and visions. If any of these images become too frightening, just open your eyes." I am reassured by the words of the director of the clinic, Jeff Israel, but the drug's history is not all rosy. Several clinical trials have shown that low doses of ibogaine taken over the course of a few weeks can greatly reduce cravings for heroin and other drugs. There was extensive research on it in the 1990s, with good evidence of safety in animals and a handful of studies in humans. The US National Institute on Drug Abuse invested over $1 million, but then abandoned the project in 1995. A study had shown that at high doses, ibogaine caused some brain cell degeneration in rats. Lower doses similar to those used in human addiction trials showed no such effect, however. © Copyright Reed Business Information Ltd.

Keyword: Drug Abuse
Link ID: 18552 - Posted: 08.24.2013

Posted by Dr. Sushrut Jangi The child's family and physician were making decisions about how to treat this disease. Many readers voted that starting an ADHD medication and behavioral therapy together might be a good way forward. Her doctor agrees with this approach. "A lot of judgement happens the day I talk about starting medicines for young children," Dr. Chan says. Most parents have already tried numerous other routes, such as behavioral therapy which is frequently recommended first. But behavioral therapy alone is hard to implement. "It's hard to access and there's not too many families who can actually carry it out," Chan says. "If you're a single parent working multiple jobs, its really hard to fit the time to take your child regularly. It's a huge time investment." J's parents tried the behavioral therapy route and they worked hard at it. But he wasn't improving. Dr. Chan is more than familiar with the culture of fear that surrounds ADHD medications, but she feels these fears are overinflated. Consequently, children who might benefit from being on medicine get delayed treatments, which can have harmful social effects. "Children in his class already know that he's different, so they react to him differently. Children with ADHD start getting negative feedback from their peers early on." Dr. Chan feels that this is one potential justification for starting medications early. "These medicines can help children get out of cycles of negative-feedback. And we're not condemning children to medicine for the rest of their lives. They can be started as a trial, and then stopped down the line." © 2013 NY Times Co.

Keyword: ADHD; Drug Abuse
Link ID: 18551 - Posted: 08.24.2013

By Jessica Shugart Sometimes it pays to be mediocre. A new study shows that sheep with a 50/50 blend of genes for small and big horns pass along more of their genes over a lifetime than their purely big-horned brethren, who mate more often. The finding offers rare insight into an enduring evolutionary paradox—why some traits persist despite creating a reproductive disadvantage. The results, published online August 21 in Nature, reveal that while big-horned sheep mated most successfully each season, small-horned sheep survived longer. Rams who inherited one of each type of gene from their parents got the best of both worlds: they lived longer than bigger-horned sheep and mated more successfully than those with the smallest horns. As a result, middle-of-the-road sheep passed on more of their genes over time. “They’re the fittest of them all,” says Jon Slate of the University of Sheffield in Scotland, who led the study. “This is a marvelous combination of using the most modern tools available to confirm classic older views of sexual selection,” says evolutionary geneticist Allen Moore of the University of Georgia in Athens, who was not involved in the study. Traits such as bold peacock feathers and giant antlers evolved to garner the attention of prospective females and boost reproductive success. Yet if each generation of females continues to pick the most stellar males, Charles Darwin wondered, how do sub-par versions of a trait continue to persist? “It’s something that has preoccupied evolutionary biologists ever since,” Slate says. © Society for Science & the Public 2000 - 2013

Keyword: Evolution; Sexual Behavior
Link ID: 18550 - Posted: 08.22.2013

By Patrick Cooney The Disney film Finding Nemo lied to your kids! The people at Disney would simply argue that they altered reality to create a more entertaining storyline, but read below for the true story, and you tell me which you think is more entertaining. How Finding Nemo started: Father and mother clownfish are tending to their clutch of eggs at their sea anemone when the mother is eaten by a barracuda. Nemo is the only surviving egg, and he grows up in his father’s anemone before getting lost on a crazy adventure! How Finding Nemo should have started if it were biologically accurate: Father and mother clownfish are tending to their clutch of eggs at their sea anemone when the mother is eaten by a barracuda. Nemo hatches as an undifferentiated hermaphrodite (as all clownfish are born) while his father transforms into a female clownfish now that his female mate is dead. Since Nemo is the only other clownfish around, he becomes male and mates with his father (who is now female). Should his father die, Nemo would change into a female clownfish and mate with another male. Although a much different storyline, it still sounds like a crazy adventure! As you can see, the first minute of Finding Nemo, outside of the talking fish part, is the only biologically accurate part of the movie. Considering that Disney demonstrated reproduction and the killing of the mother in the first minute of the movie, how did it decide that a natural sex change is outside the bubble of viewable material? © 2013 The Slate Group, LLC

Keyword: Sexual Behavior
Link ID: 18549 - Posted: 08.22.2013

By JULIE TURKEWITZ Samantha Dittmeier was the youngest of Karen Allar’s four children. “She was very loving, very compassionate,” said Ms. Allar, 51, an employment counselor who lives on Long Island. “Unfortunately, the addiction got to her.” Ms. Dittmeier, 23, died of a heroin overdose in January, leaving behind her 3-year-old son, Aiden. Ms. Allar is haunted, she said, not just by her daughter’s tumble into addiction, but also by the circumstances of her death. She wonders if her life might have been saved if the emergency workers who treated her had been armed with naloxone, a powerful drug that can reverse the effects of an overdose. “You start to get that sick feeling again,” Ms. Allar said, recounting a frantic race to the hospital just before Ms. Dittmeier’s death. “I’m back at work. I’m trying to think positive about such a horrible situation.” On Long Island and across New York State, drug overdoses are taking an increasing toll. The most common killers are opioids, a class of painkillers that includes prescription drugs like Vicodin, OxyContin and Percocet, as well as illegal narcotics like heroin. In Suffolk and Nassau Counties, the two that make up Long Island, 338 people died of opioid overdoses in 2012, up from 275 in 2008, according to county records. Statewide, opioid overdoses killed 2,051 people in 2011, more than twice the number that they killed in 2004. The spate of deaths is spurred, in part, by the easy access to prescription drugs. As a result, the state has begun several efforts to stem access to prescription drugs. A new law aims to stop addicts from gaining access to multiple rounds of medication by requiring doctors to consult an Internet database that tracks prescriptions. © 2013 The New York Times Company

Keyword: Drug Abuse
Link ID: 18548 - Posted: 08.22.2013

By Cristy Gelling Bacteria can directly trigger the nerves that sense pain, suggesting that the body’s own immune reaction is not always to blame for the extra tenderness of an infected wound. In fact, mice with staph-infected paws showed signs of pain even before immune cells had time to arrive at the site, researchers report online August 21 in Nature. “Most people think that when they get pain during infection it’s due to the immune system,” says coauthor Isaac Chiu of Boston Children’s Hospital and Harvard Medical School. Indeed, immune cells do release pain-causing molecules while fighting off invading microbes. But in recent years scientists have started uncovering evidence that bacteria can also cause pain. Chiu and his colleagues stumbled on this idea when they grew immune cells and pain-sensing cells together in a dish. The researchers were trying to activate the immune cells by adding bacteria to the mix but were surprised to see an immediate response in the nerve cells instead. This made them suspect that nerve cells were sensing the bacteria directly. To take a closer look at a real infection, the team injected the back paws of mice with Staphylococcus aureus, a bacterium that causes painful sores in humans. The researchers measured how tender the infected area was by poking it with flexible filaments of plastic. If the mouse didn’t like being prodded, it would lift its paw, giving a sensitive measure of each infection’s ouch factor. © Society for Science & the Public 2000 - 2013

Keyword: Pain & Touch; Neuroimmunology
Link ID: 18547 - Posted: 08.22.2013

By Caitlin Shure The newest chemical under investigation for managing Alzheimer’s disease (AD) is actually not new at all. Insulin, the therapeutic hormone all-too familiar to individuals with diabetes, has been around for decades. In fact December will mark 90 years since its discoverers earned the Nobel Prize in Physiology or Medicine for the extraction of insulin for clinical use. Yet to say that insulin has been under our noses all these years wouldn’t exactly be correct. Because if it had been under our noses, we might have sensed its neurologic benefits sooner. The latest insulin therapy is not delivered via injection like its diabetes-treating counterparts, nor does it come in the form of a pill or a patch like the cholinesterase inhibitors often prescribed to patients with AD. Instead this novel therapeutic enters the body through the nose—the only entry point that gives insulin a chance of reaching the brain. A large peptide molecule, insulin from the blood cannot float easily into the brain because the blood brain barrier (BBB), a sort of neuroprotective moat, prevents its transport. Fortified by cellular guards called tight junctions, the BBB rejects many pharmacologic hopefuls, allowing entrance only to certain types of substances. Namely small or lipophilic molecules can be administered orally (or via injection, or through the skin) and as long as the relevant chemicals end up in the blood stream, they can casually saunter across the BBB and act on the brain. Large and cumbersome, insulin does not have this luxury and must therefore take a more creative route across the moat. © 2013 Scientific American

Keyword: Alzheimers; Hormones & Behavior
Link ID: 18546 - Posted: 08.22.2013

By Geoffrey Mohan If you can’t quite get that nine-note treble opening to "Fur Elise," just sleep on it. The brain will rehearse, reorganize and nail the sequential motor tasks that help you play piano or type on a keyboard. How that consolidation of memory happens has remained largely a mystery, despite telling evidence that the brain’s motor cortex appears to be quite busy during sleep. Now, a team led by Brown University neuroscientists believes it has found the source of the sleeping piano lesson, and it’s not where many expected it to be. Neuroscience has been fixated since its founding on why the brain “needs” that peculiar mix of dormancy and random activity known as sleep. And it equally wondered why we emerge from it better able to do things. Slowly, evidence accrued that we were “learning” during sleep -- consolidating memory in ways that would make waking tasks more successful. It seemed deepest sleep, not the familiar rapid-eye-movement type, had the most effect on our brain’s abilty to reorganize and prepare to perform better in waking hours. “It has been very difficult to measure brain activation during sleep,” said Brown University neuroscientist Masako Tamaki, lead author of the study published online Tuesday in the Journal of Neuroscience. “So it was unclear what brain region was involved.”

Keyword: Sleep; Learning & Memory
Link ID: 18545 - Posted: 08.22.2013

By Dina Fine Maron Using sensors tucked inside the ears of live gerbils, researchers from Columbia University are providing critical insights into how the ear processes sound. In particular, the researchers have uncovered new evidence on how the cochlea, a coiled portion of the inner ear, processes and amplifies sound. The findings could lay the initial building blocks for better hearing aids and implants. The research could also help settle a long-simmering debate: Do the inner workings of the ear function somewhat passively with sound waves traveling into the cochlea, bouncing along sensory tissue, and slowing as they encounter resistance until they are boosted and processed into sound? Or does the cochlea actively amplify sound waves? The study, published in Biophysical Journal, suggests the latter is the case. The team, led by Elizabeth Olson, a biomedical engineer of Columbia University, used sensors that simultaneously measured small pressure fluctuations and cell-generated voltages within the ear. The sensors allowed the researchers to pick up phase shifts—a change in the alignment of the vibrations of the sound waves within the ear—suggesting that some part of the ear was amplifying sound. What causes that phase shift is still unclear although the researchers think the power behind the phase shift comes from the outer hair cells. Apparently the hair cells’ movement serves to localize and sharpen the frequency region of amplification. The researchers wrote that the mechanism appears to be akin to a child swinging on the playground. If somebody pushes a swing just once, the oscillations will eventually die out. If a child pumps her legs at certain times, however, it will put energy into the oscillations—that is power amplification at work. © 2013 Scientific American

Keyword: Hearing
Link ID: 18544 - Posted: 08.22.2013

By Neuroskeptic An intriguing new paper in the Journal of Neuroscience introduces a new optical illusion – and, potentially, a new way to see ones own brain activity. The article is called The Flickering Wheel Illusion: When α Rhythms Make a Static Wheel Flicker by Sokoliuk and VanRullen. Here’s the illusion: It’s a simple black and white “wheel” with 32 spokes. To see the illusion, get the wheel in your peripheral vision. Look around the edge of your screen and maybe a bit beyond – you should find a ‘sweet spot’ at which the center of the wheel starts to ‘flicker’ on and off like a strobe light. Remarkably, it even works as an afterimage. Find a ‘sweet spot’, stare at that spot for a minute, then look at a blank white wall. You should briefly see a (color-reversed) image of the wheel and it flickers like the real one (I can confirm it works for me). By itself, this is just a cool illusion. There are lots of those around. What makes it neuroscientifically interesting is that – according to Sokoliuk and VanRullen – that flickering reflects brain alpha waves. First some background. Alpha (α) waves are rhythmical electrical fields generated in the brain. They cycle with a frequency of about 10 Hz (ten times per second) and are strongest when you have your eyes closed, but are still present whenever you’re awake. When Hans Berger invented the electroencephalograph (EEG) and hooked it up to the first subjects in 1924, these waves were the first thing he noticed – hence, “alpha”. They’re noticable because they’re both strong and consistent. They’re buzzing through your brain right now. But this raises a mystery – why don’t we see them? Alpha waves are generated by rhythmical changes in neuronal activity, mainly centered on the occipital cortex. Occipital activity is what makes us see things. So why don’t we see something roughly 10 times every second?

Keyword: Vision
Link ID: 18543 - Posted: 08.22.2013

Moheb Costandi Exposure to nicotine in the womb increases the production of brain cells that stimulate appetite, leading to overconsumption of nicotine, alcohol and fatty foods in later life, according to a new study in rats. Smoking during pregnancy is known to alter fetal brain development and increase the risk of premature birth, low birth weight and miscarriage. Prenatal exposure to nicotine also increases the likelihood of tobacco use and nicotine addiction in later life, but exactly how is unclear. To understand the mechanisms behind this effect, Sarah Leibowitz, a behavioural neurobiologist at the Rockefeller University in New York, and her colleagues injected pregnant rats with small doses of nicotine — which the researchers say are comparable to the amount a pregnant woman would get from smoking one cigarette a day — and then examined the brains and behaviour of the offspring. In a paper published today in Journal of Neuroscience1, they found that nicotine increased the production of specific types of neurons in the amygdala and hypothalamus. These cells produce orexin, enkephalin and melanin-concentrating hormone, neuropeptides that stimulate appetite and increase food intake. Rats exposed to nicotine in the womb had more of these cells and produced more of the neuropeptides than those that were not, and this had long-term consequences on their behaviour. As adolescents, they not only self-administered more nicotine, but also ate more fat-rich food and drank more alcohol. © 2013 Nature Publishing Group

Keyword: Drug Abuse; Development of the Brain
Link ID: 18542 - Posted: 08.21.2013

Linda Carroll TODAY contributor Whether it’s “One Flew Over the Cuckoo’s Nest,” “Girl Interrupted,” or “Homeland,” Hollywood’s portrayals of electroconvulsive therapy have never been pretty. And the images from those movies and TV shows have only added to a stigma that keeps many desperate patients from opting for a therapy that might turn their lives around, experts say. “We can’t get past the stigma of all the visuals we’ve seen from movies and the fact that it seems so antiquated when you consider modern medicine,” NBC chief medical editor Dr. Nancy Snyderman told TODAY’s Matt Lauer. “But time and time and time again if you look at patients who have severe depression who don’t respond to medications, they will tell you that ECT works.” That’s certainly true in Denise Stewart’s case. Stewart, a mother of two, suffers from schizoaffective disorder. Her hallucinations were pushing her closer and closer to suicide each day. “There would be voices in my head that would sit there and say, ‘Denise, see the knife in the kitchen? Cut your wrists. Denise, see those pills over there? Take all those pills,’” she told TODAY. After antidepressants made Stewart’s condition worse, her doctors suggested ECT. And the change was dramatic. “If it hadn’t been for the electroconvulsive therapy, I wouldn’t be alive right now,” Stewart said. These days an estimated 100,000 Americans undergo ECT each year – and the process is a lot different from what you see in the media, experts say.

Keyword: Depression; Learning & Memory
Link ID: 18541 - Posted: 08.21.2013