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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 PAM BELLUCK As a baby’s brain develops, there is an explosion of synapses, the connections that allow neurons to send and receive signals. But during childhood and adolescence, the brain needs to start pruning those synapses, limiting their number so different brain areas can develop specific functions and are not overloaded with stimuli. Now a new study suggests that in children with autism, something in the process goes awry, leaving an oversupply of synapses in at least some parts of the brain. The finding provides clues to how autism develops from childhood on, and may help explain some symptoms like oversensitivity to noise or social experiences, as well as why many people with autism also have epileptic seizures. It could also help scientists in the search for treatments, if they can develop safe therapies to fix the system the brain uses to clear extra synapses. The study, published Thursday in the journal Neuron, involved tissue from the brains of children and adolescents who had died from ages 2 to 20. About half had autism; the others did not. The researchers, from Columbia University Medical Center, looked closely at an area of the brain’s temporal lobe involved in social behavior and communication. Analyzing tissue from 20 of the brains, they counted spines — the tiny neuron protrusions that receive signals via synapses — and found more spines in children with autism. The scientists found that at younger ages, the number of spines did not differ tremendously between the two groups of children, but adolescents with autism had significantly more than those without autism. Typical 19-year-olds had 41 percent fewer synapses than toddlers, but those in their late teenage years with autism had only 16 percent fewer than young children with autism. © 2014 The New York Times Company
By Meeri Kim From ultrasonic bat chirps to eerie whale songs, the animal kingdom is a noisy place. While some sounds might have meaning — typically something like “I'm a male, aren't I great?” — no other creatures have a true language except for us. Or do they? A new study on animal calls has found that the patterns of barks, whistles, and clicks from seven different species appear to be more complex than previously thought. The researchers used mathematical tests to see how well the sequences of sounds fit to models ranging in complexity. In fact, five species including the killer whale and free-tailed bat had communication behaviors that were definitively more language-like than random. The study was published online Wednesday in the Proceedings of the Royal Society B. “We're still a very, very long way from understanding this transition from animal communication to human language, and it's a huge mystery at the moment,” said study author and zoologist Arik Kershenbaum, who did the work at the National Institute for Mathematical and Biological Synthesis. “These types of mathematical analyses can give us some clues.” While the most complicated mathematical models come closer to our own speech patterns, the simple models — called Markov processes — are more random and have been historically thought to fit animal calls. “A Markov process is where you have a sequence of numbers or letters or notes, and the probability of any particular note depends only on the few notes that have come before,” said Kershenbaum. So the next note could depend on the last two or 10 notes before it, but there is a defined window of history that can be used to predict what happens next. “What makes human language special is that there's no finite limit as to what comes next,” he said.
By Jane C. Hu Last week, people around the world mourned the death of beloved actor and comedian Robin Williams. According to the Gorilla Foundation in Woodside, California, we were not the only primates mourning. A press release from the foundation announced that Koko the gorilla—the main subject of its research on ape language ability, capable in sign language and a celebrity in her own right—“was quiet and looked very thoughtful” when she heard about Williams’ death, and later became “somber” as the news sank in. Williams, described in the press release as one of Koko’s “closest friends,” spent an afternoon with the gorilla in 2001. The foundation released a video showing the two laughing and tickling one another. At one point, Koko lifts up Williams’ shirt to touch his bare chest. In another scene, Koko steals Williams’ glasses and wears them around her trailer. These clips resonated with people. In the days after Williams’ death, the video amassed more than 3 million views. Many viewers were charmed and touched to learn that a gorilla forged a bond with a celebrity in just an afternoon and, 13 years later, not only remembered him and understood the finality of his death, but grieved. The foundation hailed the relationship as a triumph over “interspecies boundaries,” and the story was covered in outlets from BuzzFeed to the New York Post to Slate. The story is a prime example of selective interpretation, a critique that has plagued ape language research since its first experiments. Was Koko really mourning Robin Williams? How much are we projecting ourselves onto her and what are we reading into her behaviors? Animals perceive the emotions of the humans around them, and the anecdotes in the release could easily be evidence that Koko was responding to the sadness she sensed in her human caregivers. © 2014 The Slate Group LLC.
|By Jason G. Goldman When you do not know the answer to a question, say, a crossword puzzle hint, you realize your shortcomings and devise a strategy for finding the missing information. The ability to identify the state of your knowledge—thinking about thinking—is known as metacognition. It is hard to tell whether other animals are also capable of metacognition because we cannot ask them; studies of primates and birds have not yet been able to rule out simpler explanations for this complex process. Scientists know, however, that some animals, such as western scrub jays, can plan for the future. Western scrub jays, corvids native to western North America, are a favorite of cognitive scientists because they are not “stuck in time”—that is, they are able to remember past events and are known to cache their food in anticipation of hunger, according to psychologist Arii Watanabe of the University of Cambridge. But the question remained: Are they aware that they are planning? Watanabe devised a way to test them. He let five birds watch two researchers hide food, in this case a wax worm. The first researcher could hide the food in any of four cups lined up in front of him. The second had three covered cups, so he could place the food only in the open one. The trick was that the researchers hid their food at the same time, forcing the birds to choose which one to watch. If the jays were capable of metacognition, Watanabe surmised, the birds should realize that they could easily find the second researcher's food. The wax worm had to be in the singular open cup. They should instead prefer keeping their eyes on the setup with four open cups because witnessing where that food went would prove more useful in the future. And that is exactly what happened: the jays spent more time watching the first researcher. The results appeared in the July issue of the journal © 2014 Scientific American,
by Sarah Zielinski PRINCETON, N.J. — Learning can be a quick shortcut for figuring out how to do something on your own. The ability to learn from watching another individual — called social learning — is something that hasn’t been documented in many species outside of primates and birds. But now a lizard can be added to the list of critters that can learn from one another. Young eastern water skinks were able to learn by watching older lizards, Martin Whiting of Macquarie University in Sydney reported August 10 at the Animal Behavior Society meeting at Princeton University. The eastern water skink, which reaches a length of about 30 centimeters, can be found near streams and waterways in eastern Australia. The lizards live up to eight years, and while they don’t live in groups, they often see each other in the wild. That could provide an opportunity for learning from each other. Whiting and his colleagues worked with 18 mature (older than 5 years) and 18 young (1.5 to 2 years) male skinks in the lab. The lizards were placed in bins with a barrier in the middle that was either opaque or transparent. In the first of two experiments, the skinks were given a yellow-lidded container with a mealworm inside. They had to learn to open the lid to get the food. In that task, skinks that could see a demonstrator through a transparent barrier were no better at opening the lid than those who had to figure it out on their own. After watching a demonstrator lizard (top row), the skink in the other half of the tub was supposed to have learned that a mealworm was beneath the blue lid. The skink in the middle arena, however, failed the task when he opened the white lid first.D.W.A. Noble et al/Biology Letters 2014 © Society for Science & the Public 2000 - 2013.
by Philippa Skett It's the strangest sweet tooth in the world. Birds lost the ability to taste sugars, but nectar-feeding hummingbirds re-evolved the capacity by repurposing receptors used to taste savoury food. To differentiate between tastes, receptors on the surface of taste buds on the tongue, known as T1Rs, bind to molecules in certain foods, triggering a neurological response. In vertebrates such as humans, a pair of these receptors – T1R2 and T1R3 – work together to deliver the sweet kick we experience from sugar. But Maude Baldwin at Harvard University and her colleagues found that birds don't have the genes that code for T1R2. They are found in lizards, though, suggesting that they were lost at some point during the evolution of birds or the dinosaurs they evolved from. But hummingbirds clearly can detect sugar: not only do they regularly sup on nectar, taste tests show they prefer sweet tasting foods over blander options. Now Baldwin and her team have worked out why: another pair of receptors – T1R1 and T1R3 – work together to detect sugar. Other vertebrates use T1R1 to taste savoury foods. It seems that in hummingbirds the proteins on the surface of the two receptors have been modified so that they respond to sugars instead. © Copyright Reed Business Information Ltd.
By ELEANOR LEW I was watching Diane Sawyer on the evening news, wondering how she manages year after year to look so young, when suddenly her face disappeared. Now you see. Now you don’t. One second. That’s all it took. A dense black inkblot shaped like a map of England and southern Norway suddenly blocked my view of Diane so that all I could see was her blond hair and shoulders. At first, I thought it was the television set. Changing channels didn’t bring her face back, nor did rubbing my eyes. “It’s permanent vision loss,” my ophthalmologist said. “Your optic nerve and retina buckled.” He drew a picture of the inside of my right eye, the affected one, and explained that my degenerative myopia, an inherited condition that is far less common than ordinary nearsightedness but still a leading cause of blindness worldwide, had caused my eyeball to elongate excessively. It looked like a house whose walls had been stretched so thin that the roof caved. The doctor didn’t say much else, didn’t make any recommendations for physical or occupational therapy, didn’t tell me to call him if I noticed any changes. I left his office shaken. “What if it happens in my other eye? What if…?” In the weeks that followed, I began to notice bizarre changes in my right eye. Frequent flashing lights, like a dying neon tube, sometimes flickering color or bright white light, so intense I swore I could hear them buzz. I observed my peripheral vision diminishing. England and Norway morphed into a large, bushy oak tree with a short and wide trunk. At a park, I came upon children playing. When I covered my good eye with my hand, I could see only a sliver of sky, and legs and shoes of children running in and out of the tree. I wrote off the psychedelic changes to the “buckling” and didn’t bother to call my ophthalmologist. But I was scared and needed help. © 2014 The New York Times Company
Link ID: 19982 - Posted: 08.22.2014
By CARL ZIMMER Your body is home to about 100 trillion bacteria and other microbes, collectively known as your microbiome. Naturalists first became aware of our invisible lodgers in the 1600s, but it wasn’t until the past few years that we’ve become really familiar with them. This recent research has given the microbiome a cuddly kind of fame. We’ve come to appreciate how beneficial our microbes are — breaking down our food, fighting off infections and nurturing our immune system. It’s a lovely, invisible garden we should be tending for our own well-being. But in the journal Bioessays, a team of scientists has raised a creepier possibility. Perhaps our menagerie of germs is also influencing our behavior in order to advance its own evolutionary success — giving us cravings for certain foods, for example. “One of the ways we started thinking about this was in a crime-novel perspective,” said Carlo C. Maley, an evolutionary biologist at the University of California, San Francisco, and a co-author of the new paper. “What are the means, motives and opportunity for the microbes to manipulate us? They have all three.” The idea that a simple organism could control a complex animal may sound like science fiction. In fact, there are many well-documented examples of parasites controlling their hosts. Some species of fungi, for example, infiltrate the brains of ants and coax them to climb plants and clamp onto the underside of leaves. The fungi then sprout out of the ants and send spores showering onto uninfected ants below. How parasites control their hosts remains mysterious. But it looks as if they release molecules that directly or indirectly can influence their brains. © 2014 The New York Times Company
by Bethany Brookshire When a laboratory mouse and a house mouse come nose to nose for the first time, each one is encountering something it has never seen before. They are both Mus musculus. But the wild mouse is facing a larger, fatter, calmer and less aggressive version of itself that’s the result of brother-to-sister inbreeding for generations, resulting in mice that are almost completely genetically identical. Laboratory mice are incredibly valuable tools for research into diseases from Alzheimer’s to Zellweger syndrome. Scientists have a deep understanding of lab mouse DNA, and can use that knowledge to study how specific genes may control certain behaviors and underlie disease. But with all the inbreeding comes some traits that, while desirable in a lab mouse, may not reflect the behavior of an animal in the wild. So for some questions, and some behaviors, scientists might need something a bit wilder. A new study takes lab mice back to their roots and along the way uncovers a new gene function. Lea Chalfin and colleagues at the Weizmann Institute of Science in Rohovot, Israel, bred laboratory mice with wild mice for 10 generations. The result was a mouse with wild mouse genes and wild mouse behavior — with a few important lab mouse genes mixed in. The technique allows scientists to place specific mutations in a wild mouse. The results have interesting implications for studying the mouse species, and might provide some new ways to study human disease as well. Chalfin and her colleagues were especially interested in behaviors linked to female aggression. © Society for Science & the Public 2000 - 2013
By James Gallagher Health editor, BBC News website Stimulating the part of the brain which controls movement may improve recovery after a stroke, research suggests. Studies showed firing beams of light into the brains of mice led to the animals moving further and faster than those without the therapy. The research, published in Proceedings of the National Academy of Science, could help explain how the brain recovers and lead to new treatments. The Stroke Association said the findings were interesting. Strokes can affect memory, movement and the ability to communicate. Brain cells die when their supply of oxygen and sugars is cut off by a blood clot. Stroke care is focused on rapid treatment to minimise the damage, but some recovery is possible in the following months as the brain rewires itself. The team at Stanford University School of Medicine investigated whether brain stimulation aided recovery in animal experiments. They used a technique called optogenetics to stimulate just the neurons in the motor cortex - the part of the brain responsible for voluntary movements - following a stroke. After seven days of stimulation, mice were able to walk further down a rotating rod than mice which had not had brain stimulation. After 10 days they were also moving faster. The researchers believe the stimulation is affecting how the wiring of the brain changes after a stroke. They detected higher levels of chemicals linked to the formation of new connections between brain cells. Lead researcher Prof Gary Steinberg said it was a struggle to give people drugs to protect brain cells in time as the "time window is very short". BBC © 2014
Link ID: 19979 - Posted: 08.20.2014
|By Matthew H. Schneps “There are three types of mathematicians, those who can count and those who can’t.” Bad joke? You bet. But what makes this amusing is that the joke is triggered by our perception of a paradox, a breakdown in mathematical logic that activates regions of the brain located in the right prefrontal cortex. These regions are sensitive to the perception of causality and alert us to situations that are suspect or fishy — possible sources of danger where a situation just doesn’t seem to add up. Many of the famous etchings by the artist M.C. Escher activate a similar response because they depict scenes that violate causality. His famous “Waterfall” shows a water wheel powered by water pouring down from a wooden flume. The water turns the wheel, and is redirected uphill back to the mouth of the flume, where it can once again pour over the wheel, in an endless cycle. The drawing shows us a situation that violates pretty much every law of physics on the books, and our brain perceives this logical oddity as amusing — a visual joke. The trick that makes Escher’s drawings intriguing is a geometric construction psychologists refer to as an “impossible figure,” a line-form suggesting a three-dimensional object that could never exist in our experience. Psychologists, including a team led by Catya von Károlyi of the University of Wisconsin-Eau Claire, have used such figures to study human cognition. When the team asked people to pick out impossible figures from similarly drawn illustrations that did not violate causality, they were surprised to discover that some people were faster at this than others. And most surprising of all, among those who were the fastest were those with dyslexia. © 2014 Scientific American
By James Gallagher Health editor, BBC News website Breastfeeding can halve the risk of post-natal depression, according to a large study of 14,000 new mothers. However, there is a large increase in the risk of depression in women planning to breastfeed who are then unable to do so. The study, published in the journal Maternal and Child Health, called for more support for women unable to breastfeed. A parenting charity said mental health was a "huge issue" for many mothers. The health benefits of breastfeeding to the baby are clear-cut and the World Health Organization recommends feeding a child nothing but breast milk for the first six months. However, researchers at the University of Cambridge said the impact on the mother was not as clearly understood. 'Highest risk' One in 10 women will develop depression after the birth of their child. The researchers analysed data from 13,998 births in the south-west of England. It showed that, out of women who were planning to breastfeed, there was a 50% reduction in the risk of post-natal depression if they started breastfeeding. But the risk of depression more than doubled among women who wanted to, but were not able to, breastfeed. Dr Maria Iacovou, one of the researchers, told the BBC: "Breastfeeding does appear to have a protective effect, but there's the other side of the coin as well. "Those who wanted to and didn't end up breastfeeding had the highest risk of all the groups." BBC © 2014
By TARA PARKER-POPE When the antidrug educator Tim Ryan talks to students, he often asks them what they know about marijuana. “It’s a plant,” is a common response. But more recently, the answer has changed. Now they reply, “It’s legal in Colorado.” These are confusing times for middle and high school students, who for most of their young lives have been lectured about the perils of substance abuse, particularly marijuana. Now it seems that the adults in their lives have done an about-face. Recreational marijuana is legal in Colorado and in Washington, and many other states have approved it for medical use. Lawmakers, the news media and even parents are debating the merits of full-scale legalization. “They are growing up in a generation where marijuana used to be bad, and maybe now it’s not bad,” said Mr. Ryan, a senior prevention specialist with FCD Educational Services, an antidrug group that works with students in the classroom. “Their parents are telling them not to do it, but they may be supporting legalization of it at the same time.” Antidrug advocates say efforts to legalize marijuana have created new challenges as they work to educate teenagers and their parents about the unique risks that alcohol, marijuana and other drugs pose to the developing teenage brain. These educators say their goal is not to vilify marijuana or take a stand on legalization; instead, they say their role is to convince young people and their parents that the use of drugs is not just a moral or legal issue, but a significant health issue. “The health risks are real,” said Steve Pasierb, the chief executive of the Partnership for Drug-Free Kids. “Every passing year, science unearths more health risks about why any form of substance use is unhealthy for young people.” © 2014 The New York Times Company
Claudia M. Gold When I hear debate over the association between SSRI’s (selective serotonin re-uptake inhibitors, a class of antidepressant medication) and suicidal behavior in children and adolescents, I am immediately brought back to a night in the early 2000's. As the covering pediatrician I was called to the emergency room to see a young man, a patient of a pediatrician in a neighboring town, who had attempted suicide by taking a nearly lethal overdose. That night, as I watched over him in the intensive care unit, I learned that he was a high achieving student and athlete who, struggling under the pressures of the college application process, had been prescribed an SSRI by his pediatrician. His parents described a transformation in his personality over the months preceding the suicide attempt that was so dramatic that I ordered a CT scan to see if he had a brain tumor. It was normal. When, in the coming years the data emerged about increasing suicidal behavior following use of SSRI's, I recognized in retrospect that his change in behavior was a result of the medication. But at the time I knew nothing of these serious side effects. At that time, coinciding with pharmaceutical industry's aggressive marketing campaign directed at the public as well as a professional audience, these drugs were becoming increasingly popular with pediatricians. As the possible serious side effects of these medications came increasingly in to awareness, the FDA issued the controversial "black box warning" that the drugs carried an increased risk of suicidal behavior. Following the black box warning, pediatricians, myself included, became reluctant to prescribe these medications. We did not have the time or experience to provide the recommended increased monitoring and close follow-up.
by Clare Wilson Figuring out how the brain works is enough to make your head spin. But now we seem to have a handle on how it gets its folded shape. The surface layer of the brain, or cortex, is also referred to as our grey matter. Mammals with larger brains have a more folded cortex, and the human brain is the most wrinkled of all, cramming as much grey matter into our skulls as possible. L. Mahadevan at Harvard University and his colleagues physically modelled how the brain develops in the embryo, using a layer of gel to stand in for the grey matter. This gel adhered to the top of a solid hemisphere of gel representing the white matter beneath. In the embryo, grey matter grows as neurons are created or others migrate to the cortex from the brain's centre. By adding a solvent to make the grey matter gel expand, the team mimicked how the cortex might grow in the developing brain. They didn't model what effect, if any, the skull would have had. Hills and valleys The team varied factors such as the stiffness of the gels and the depth of the upper layer to find a combination that led to similarly shaped wrinkles as those of the human brain, with smooth "hills" and sharply cusped "valleys". There are several theories about how the brain's folds form. These include the possibility that more neurons migrate to the hills, making them rise above the valleys, or that the valleys are pulled down by the axons – fibres that connect neurons to each other – linking highly interconnected parts of the brain together. © Copyright Reed Business Information Ltd.
Keyword: Development of the Brain
Link ID: 19974 - Posted: 08.19.2014
Sara Reardon The National Science Foundation (NSF)’s role in the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative is starting to take shape. On 18 August, the NSF awarded 36 small grants totalling US$10.8 million to projects studying everything from electrodes that measure chemical and electronic signals to artificial intelligence programs to identify brain structures. The three agencies participating in the BRAIN Initiative have taken markedly different approaches. The Defense Advanced Research Projects Agency, which received $50 million this year for the neuroscience programme, is concentrating on prosthetics and treatments for brain disorders that affect veterans, such as post-traumatic stress disorder. It has already awarded multi-million dollar grants to several teams. The National Institutes of Health, which received $40 million this year, has put together a 146-page plan to map and observe the brain over the next decade, and will announce its first round of grant recipients next month. The NSF, by contrast, has cast a wider net. The agency sent an request in March for informal, two-page project ideas. The only criterion was that the projects somehow address the properties of neural circuits. The response was overwhelming, says James Deshler, deputy director of the NSF’s Division of Biological Infrastructure. The agency had expected to fund about 12 grants, but decided to triple that number after receiving nearly 600 applications. “People started finding money in different pockets,” Deshler says. The wide-ranging list of winning projects includes mathematical models that help computers recognize different parts and patterns in the brain, physical tools such as new types of electrodes, and other tools that integrate and link neural activity to behaviour. © 2014 Nature Publishing Group
|By Karen Hopkin They say that the nose knows. But it still gets its marching orders from the brain—at least when it comes to the lungs. Got that? Nose to brain to lungs. Because a new study shows that when people with asthma think they’re smelling something noxious, their airways become inflamed—even when the odor is harmless. The finding is in the Journal of Psychosomatic Research. [Cristina Jaén and Pamela Dalton, Asthma and odors: The role of risk perception in asthma exacerbation] Asthma attacks can be triggered by pollen, dust, harsh chemicals or scents. These environmental annoyances constrict the airways in the lung, making breathing difficult. In this study, researchers wanted to see whether an individual’s assumptions have any influence over this breathtaking series of events. So they exposed 17 asthma sufferers to a benign chemical that smells like roses for 15 minutes. Nine subjects were told the fragrance was a potential irritant, the other eight that it would be therapeutic. The results were as plain as the nose on your face: subjects who expected an irritant experienced inflammation. And those who were primed to be soothed had no adverse reactions—even if they were normally bothered by perfumes. The results suggest that a rose by any other name would smell as sweet. Or be as irritating as you expect it will. © 2014 Scientific American
Keyword: Chemical Senses (Smell & Taste)
Link ID: 19972 - Posted: 08.19.2014
Helen Shen For most adults, adding small numbers requires little effort, but for some children, it can take all ten fingers and a lot of time. Research published online on 17 August in Nature Neuroscience1 suggests that changes in the hippocampus — a brain area associated with memory formation — could help to explain how children eventually pick up efficient strategies for mathematics, and why some children learn more quickly than others. Vinod Menon, a developmental cognitive neuroscientist at Stanford University in California, and his colleagues presented single-digit addition problems to 28 children aged 7–9, as well as to 20 adolescents aged 14–17 and 20 young adults. Consistent with previous psychology studies2, the children relied heavily on counting out the sums, whereas adolescents and adults tended to draw on memorized information to calculate the answers. The researchers saw this developmental change begin to unfold when they tested the same children at two time points, about one year apart. As the children aged, they began to move away from counting on fingers towards memory-based strategies, as measured by their own accounts and by decreased lip and finger movements during the task. Using functional magnetic resonance imaging (fMRI) to scan the children's brains, the team observed increased activation of the hippocampus between the first and second time point. Neural activation decreased in parts of the prefrontal and parietal cortices known to be involved in counting, suggesting that the same calculations had begun to engage different neural circuits. © 2014 Nature Publishing Group
Vaughan Bell For thousands of years, direct studies of the human brain required the dead. The main method of study was dissection, which needed, rather inconveniently for the owner, physical access to their brain. Despite occasional unfortunate cases where the living brain was exposed on the battlefield or the surgeon's table, corpses and preserved brains were the source of most of our knowledge. When brain scanning technologies were invented in the 20th century they allowed the structure and function of the brain to be shown in living humans for the first time. This was as important for neuroscientists as the invention of the telescope and the cadaver slowly faded into the background of brain research. But recently, scrutiny of the post-mortem brain has seen something of a revival, a resurrection you might say, as modern researchers have become increasingly interested in applying their new scanning technologies to the brains of the deceased. Forensic pathologists have the job of working out the cause and manner of death to present as legal evidence and have been partly responsible for this curious full circle. One of their main jobs is the autopsy, where the pathologist examines the body, inside and out, to assess its condition at the point of death. Although the traditional autopsy has many advantages, not least the microscopic examination of body tissue, there are drawbacks. One is that within some religions cutting up the dead body is seen as an infringement of human dignity and may delay burial beyond the customary period. The other is that an autopsy is a one-shot deal. If someone disagrees with the way it has been carried out or its interpretation, it is usually too late to do anything except re-examine photos or, on the rare occasions when they may have been kept, tissue samples. © 2014 Guardian News and Media Limited
Keyword: Brain imaging
Link ID: 19970 - Posted: 08.18.2014
by Andy Coghlan Pioneering studies of post-mortem brain tissues have yielded the first evidence of a potential association between Alzheimer's disease and the epigenetic alteration of gene function. The researchers stress, however, that more research is needed to find out if the changes play a causal role in the disease or occur as a result of it. We already have some evidence that the risk of developing Alzheimer's might be elevated by poor diet, lack of exercise, and inflammatory conditions such as diabetes, obesity and clogging of blood vessels with fatty deposits. The new research hints that the lifestyle changes that raise Alzheimer's risk may be taking effect through epigenetic changes. The idea is strengthened by the fact that the brain tissue samples studied in the new work came from hundreds of people, many of whom had Alzheimer's when they died, and that a number of genes identified were found by two teams working independently, one in the UK and one in the US. "The results are compelling and consistent across four cohorts of patients taken across the two studies," says Jonathan Mill at the University of Exeter, who led the UK-based team. "It's illuminated new genetic pathways affecting the disease and, given the lack of success tackling Alzheimer's so far, new leads are going to be vital." "We can now focus our efforts on understanding how these genes are associated with the disease," says Philip De Jager of the Brigham and Women's Hospital in Boston, who headed the US team. © Copyright Reed Business Information Ltd.