by Carl Zimmer This month’s column is a tale of two rats. One rat got lots of attention from its mother when it was young; she licked its fur many times a day. The other rat had a different experience. Its mother hardly licked its fur at all. The two rats grew up and turned out to be very different. The neglected rat was easily startled by noises. It was reluctant to explore new places. When it experienced stress, it churned out lots of hormones. Meanwhile, the rat that had gotten more attention from its mother was not so easily startled, was more curious, and did not suffer surges of stress hormones. The same basic tale has repeated itself hundreds of times in a number of labs. The experiences rats had when they were young altered their behavior as adults. We all intuit that this holds true for people, too, if you replace fur-licking with school, television, family troubles, and all the other experiences that children have. But there’s a major puzzle lurking underneath this seemingly obvious fact of life. Our brains develop according to a recipe encoded in our genes. Each of our brain cells contains the same set of genes we were born with and uses those genes to build proteins and other molecules throughout its life. The sequence of DNA in those genes is pretty much fixed. For experiences to produce long-term changes in how we behave, they must be somehow able to reach into our brains and alter how those genes work. Neuroscientists are now mapping that mechanism. Our experiences don’t actually rewrite the genes in our brains, it seems, but they can do something almost as powerful. Glued to our DNA are thousands of molecules that shut some genes off and allow other genes to be active. Our experiences can physically rearrange the pattern of those switches and, in the process, change the way our brain cells work. This research has a truly exciting implication: It may be possible to rearrange that pattern ourselves and thereby relieve people of psychiatric disorders like severe anxiety and depression. In fact, scientists are already easing those symptoms in mice.

Keyword: Genes & Behavior; Depression
Link ID: 14181 - Posted: 06.24.2010

by Jessica Hamzelou Sea snail venom could become the gold standard for the relief of nerve-related pain following the development of a pill that is 100 times as potent as leading treatments. Current treatments for neuropathic pain include morphine, which is highly addictive, and gabapentin, which both act on nerve receptors. Sea snail venom had been suggested as a good alternative because it consists of a cocktail of peptides, known as conotoxins. These act to immobilise prey by blocking nerve-cell conduction, but in mammals the peptides are an effective analgesic. The only conotoxin-derived drug approved for human use is ziconotide. Unfortunately, the drug is susceptible to breakdown by enzymes in the saliva and gut, so it is administered by a pump surgically inserted into the abdominal wall, making it an invasive and expensive treatment. To solve this problem, David Craik and his team at the University of Queensland in Australia have developed the first "orally active" conotoxin drug. They started with a synthetic version of conotoxin. Since the enzymes that break down the drug usually act at the ends of the conotoxin molecule, the team used a chain of amino acids to join up these ends to form a circular structure. They found this version to be resistant to enzymes in the body. © Copyright Reed Business Information Ltd.

Keyword: Pain & Touch
Link ID: 14180 - Posted: 06.24.2010

Charles Q. Choi Networks of brain cells in a petri dish can be trained to keep time like hourglasses, a new study says. The discovery may help scientists reveal how our brains track time, an ability fundamental to how humans interact with each other and the world. It's also key to how we recognize speech patterns and song rhythms.cn "One issue that's been long debated regarding timing is whether there's a central clock in the brain or whether timing is a general ability in many different circuits of the brain," said study leader Dean Buonomano, a neuroscientist at University of California, Los Angeles. Buonomano and colleagues kept networks of rat brain cells alive in petri dishes and stimulated them with two electrical pulses separated by intervals ranging from a twentieth of a second to a half-second in length. After the cell networks received two hours of "training," a single electrical pulse was given to them to see how the cells would react. In networks trained with short intervals, the communication between cells lasted for only a short while—say, 50 to 100 milliseconds in networks trained on 50-millisecond intervals. However, in networks trained with long intervals, network activity lasted for much longer, according to the study, published June 13 in Nature Neuroscience. When networks trained on half-second intervals were probed, the networks essentially talked to each other for 500 to 600 milliseconds. © 1996-2010 National Geographic Society

Keyword: Biological Rhythms
Link ID: 14179 - Posted: 06.24.2010

Virginia Hughes How long does a fruit fly sleep? That depends on its genetic make-up, according to research presented this weekend at a meeting of the Genetics Society of America in Boston, Massachusetts. Researchers identified nearly 1,000 genes in which certain single-letter changes in DNA, called SNPs (for single nucleotide polymorphisms), are associated with the length of sleep. This preliminary study is the first to come out of the Drosophila Genetic Reference Panel project, a catalogue of variations across the complete genomes of 192 inbred lines of the fruit fly Drosophila melanogaster. So far, the researchers have deposited raw sequence data from 152 lines in a freely available database, spurring roughly 50 other groups to begin genome-wide association (GWA) studies, which compare the SNPs of flies that show various complex behaviours. "Once all of the data are out, there will be an army of people who will immediately go after it," says Charles Langley, a population geneticist at the University of California, Davis, who was not involved in the latest study. Variant flood In the past few years, the field of human genetics has seen a deluge of GWA studies that have identified thousands of genetic variants associated with complex disease. One problem with this approach, however, is that there is no way to know whether the identified SNPs are causal for a disease. © 2010 Nature Publishing Group,

Keyword: Sleep; Genes & Behavior
Link ID: 14178 - Posted: 06.24.2010

By Julie Steenhuysen CHICAGO - A study of brain scans has confirmed the role of several genes linked with Alzheimer's disease, and turned up two others that are worth exploring, U.S. researchers said Monday. A team at Massachusetts General Hospital in Boston used magnetic resonance imaging or MRI scans to study changes in brain structures — such as the size of the hippocampus and amygdala — in 700 healthy volunteers and Alzheimer's patients. They used computer programs to sort through the genetic sequences of the 700 volunteers to see which gene mutations are most linked with these changes. Story continues below ↓advertisement | your ad here The study turned up a known offender — the APOE4 gene — as the most strongly linked with the disease, but it also confirmed three other genes — CLU, CRI, PICALM — that have been more recently linked with Alzheimer's. And they fingered two others — BIN1 and CNTN5 — which have been suspected, but not strongly linked with Alzheimer's. While the findings are preliminary, "they may help prioritize targets for future genetic studies," Drs. Alessandro Biffi and Christopher Anderson of Massachusetts General and the Broad Institute wrote in the Archives of Neurology. Copyright 2010 Reuters.

Keyword: Alzheimers; Brain imaging
Link ID: 14177 - Posted: 06.24.2010

By NATALIE ANGIER Not long ago, Julia Fischer of the German Primate Center in Göttingen was amused to witness two of her distinguished male colleagues preening about a topic very different from the standard academic peacock points — papers published, grants secured, competitors made to look foolish. “One of them said proudly, ‘I have three children,’ ” Dr. Fischer recalled. “The other one replied, ‘Well, I have four children.’ “Some men might talk about their Porsches,” she added. “These men were boasting about their number of children.” And while Dr. Fischer is reluctant to draw facile comparisons between humans and other primates, she couldn’t help thinking of her male Barbary macaques, for whom no display carries higher status, or is more likely to impress the other guys, than to strut around the neighborhood with an infant monkey in tow. Reporting in the current issue of the journal Animal Behaviour, Dr. Fischer and her co-workers describe how male Barbary macaques use infants as “costly social tools” for the express purpose of bonding with other males and strengthening their social clout. Want to befriend the local potentate? Bring a baby. Need to reinforce an existing male-male alliance, or repair a frayed one? Don’t forget the baby. It doesn’t matter if the infant is yours or not. Just so long as it has the downy black fur and wrinkly pinkish face that adult male macaques find impossible to resist. “They will hold up the infant like a holy thing, nuzzling it, chattering their teeth,” Dr. Fischer said. “It can be a bit bewildering to see.” Copyright 2010 The New York Times Company

Keyword: Sexual Behavior
Link ID: 14176 - Posted: 06.24.2010

By Katherine Harmon To function well in the world, people need a good sense of where their body is in space and how it's postured. This "position sense" helps us coordinate high-fives, boot a soccer ball or pick up the remote. But that doesn't seem to mean that our brains have an accurate sense of our body's precise proportions. A new study found that people tend to have rather inaccurate mental models of their own hands. When asked to estimate where the fingertips and knuckles of their hidden hands were, study volunteers were way off. But they were all incorrect in the same directions, guessing that their hands were both shorter and wider than they actually were. The findings come from a study led by Matthew Longo of the Institute of Cognitive Neuroscience at University College London and were published online June 14 in Proceedings of the National Academy of Sciences. "Our results show dramatic distortions of hand shape, which were highly consistent across participants," Longo said in a prepared statement. He and his coauthor, Patrick Haggard, had subjects place their left hand on a platform (using different orientations in different groups), which was then covered with a board to obscure the hand. The subjects were asked to use their free right hand point with a baton to the location of each knuckle and fingertip of their left hand. The process was filmed and compared to before and after pictures of the hand. © 2010 Scientific American,

Keyword: Pain & Touch
Link ID: 14175 - Posted: 06.24.2010

Analysis by Teresa Shipley It sounds like an experiment kids might conduct. Pairs of female jumping spiders were matched off in a mini, gladiator-like arena, while researchers recorded fight tactics in an effort to find a pattern. What did they find? The females fight dirty. While the males "push each other back and forth like sumo wrestlers," lead author Damian Elias of the University of California at Berkeley said in a press release, the females displayed less civil tactics. The research is published online in the journal Behavioral Ecology. "Males have a more gentlemanly form of combat, whereas in females it's an all-out fight," said Elias. "At the drop of a hat they start bashing and biting each other." Another difference was that the female fights were often duels to the death, whereas males tended to resolve things through elaborate dance displays rather than fighting. The researchers were baffled about why this happened. "Nothing we could measure predicted which one would come out on top," Elias said. "That was really unexpected." Finally, they hit upon a hypothesis. What if the females had a reason to fight other than territory? They found that the females who were closer to "molting," a process that happens right before eggs are laid, were more likely to win a fight. The researchers think this may be because molting females are much more vulnerable to predation, and so much more motivated to survive. © 2010 Discovery Communications, LLC.

Keyword: Aggression; Evolution
Link ID: 14174 - Posted: 06.24.2010

By Victoria Gill Have you ever failed to notice a friend's radical new haircut? Or missed a road sign showing a change in the speed limit? This failure to notice what should be very apparent is something we unconsciously experience every day as our brains filter the barrage of visual information which we are flooded with. And apparently it has a name; it is called change blindness. Scientists at Queen Mary, University of London, have invented a unique spot-the-difference-style computer game in order to study it. Milan Verma, a scientist at Queen Mary, explains: "It's the phenomenon where seemingly striking or obvious changes are not noticed." He and his colleagues are asking volunteers to play the game - which involves looking at a screen as it flashes between two images of the same scene. "It flicks between a pre-change version and a post-change version of the scene," Dr Verma explains. "The volunteers simply have to press the button and tell us exactly when they spot the change." Trying out the game at Dr Verma's office, my initial reaction was self-satisfaction; I spotted the difference in the first scene - a picture of a butterfly with orange stripes on its wings - almost immediately. BBC © MMX

Keyword: Vision; Attention
Link ID: 14173 - Posted: 06.24.2010

Janet Fang To follow the scent trail left by their prey across the ocean, sharks swim in the direction of the nostril that sniffed the odour first, scientists have found. Their research challenges the classic notion that sharks orient themselves based on the differences between odour concentration received at each nostril. Shark prey — whether living, injured or dead — leaves behind swirling odour plumes that break apart with distance. The latest work, published today in Current Biology1, suggests that when a shark moves into a patch of odour, the smell hits one nostril before the other — and that tells the shark to turn either left or right. By moving from side to side from one patch to another, the animal maintains contact with the odour plume as it tracks its prey, says Jayne Gardiner at the University of South Florida in Tampa, co-author of the study. Ocean odours mix chaotically, so for sharks to steer using odour concentration, they would need to compare the average concentration at the two nostrils over a period of several minutes to determine the prey's direction. They would then have to reposition themselves and start again — a slow process. But by using timing cues, says Gardiner, sharks receive directionality in under a second. The study centred around lab studies of eight smooth dogfish (Mustelus canis), a small grey-brown shark. To recreate prey odour, Gardiner marinated squid — what she calls "junk food for dogfish" — in 50 litres of seawater. She fitted the sharks with headgear consisting of two tubes delivering this squid marinade to one nostril and then the other. She found that for delays between 0.1 and 0.5 seconds, the sharks turned toward the side receiving the first stimulus. If there was no time lag or if the lag was a second or longer, the sharks were equally likely to turn in either direction. © 2010 Nature Publishing Group,

Keyword: Chemical Senses (Smell & Taste)
Link ID: 14172 - Posted: 06.24.2010

Scientists have discovered that a gene linked to Alzheimer’s disease may play a beneficial role in cell survival by enabling neurons to clear away toxic proteins. A study funded by the National Institute on Aging (NIA), part of the National Institutes of Health, shows the presenilin 1 (PS1) gene is essential to the function of lysosomes, the cell component that digests and recycles unwanted proteins. However, mutations in the PS1 gene — a known risk factor for a rare, early onset form of Alzheimer’s disease — disrupt this crucial process. Ralph Nixon, M.D., Ph.D., of the Nathan Kline Institute, Orangeburg, N.Y., and New York University Langone Medical Center, directed the study involving researchers from the United States, Europe, Japan and Canada. Also supported in part by the Alzheimer’s Association, the study appears in the June 10, 2010, online issue of Cell. Researchers have theorized for more than a decade that PS1 mutations linked to early-onset Alzheimer's, a rare form of the disease that usually affects people between ages 30 and 60, may trigger abnormally high levels of beta-amyloid protein to clump together in the brain. Amyloid deposits and tau protein tangles are hallmarks of both early-onset and the sporadic, more common form of the disease found in people aged 60 and older. These new findings, however, suggest PS1 mutations may play a more general role in the development of early-onset Alzheimer's.

Keyword: Alzheimers; Apoptosis
Link ID: 14171 - Posted: 06.24.2010

by Adam Hadhazy Nerve cells in our sweat glands and blood vessels may constitute an important, previously unrecognized source of sensory info. You are more sensitive than you realize, neuroscientist Frank Rice of Albany Medical College has discovered. His study of patients whose skin lacks normal nerve fibers has revealed a previously unknown source of perception that contributes to the familiar ability to feel texture, temperature, pressure, and pain: the nerve endings surrounding blood vessels and sweat glands in human skin. Rice, neurologist David Bowsher of the University of Liverpool, and their colleagues were studying two patients who were unable to feel pain, yet somehow retained a rudimentary ability to distinguish hot from cold and rough from smooth. On examining skin samples and other biopsies, the researchers found that all of the usual nerve endings associated with skin sensation were missing. The only possible sources of feeling were the nerves of the blood vessels and glands. Scientists knew that such nerves existed but thought they simply regulated blood flow and perspiration. The evidence from the patients examined by Rice and Bowsher suggests that the nerve cells also act as an additional sensory system. “It is very likely that these nerve endings contribute to conscious perception in all of us,” Rice says. If he is correct, problems with this previously unknown system could contribute to poorly understood pain conditions, such as migraines and fibromyalgia. Rice and a group of collaborators are gearing up to investigate this potential link by searching for malformations of the blood-vessel nerves that could affect their function.

Keyword: Pain & Touch
Link ID: 14170 - Posted: 06.24.2010

by John Travis More than 3 years after initially passing peer review and being accepted, a controversial paper addressing how to diagnose psychopathy and whether past criminal behavior is central to the condition has been published in the June issue of Psychological Assessment. The paper has privately circulated among forensic psychologists since 2007, but some of the explanation behind its publishing delay became evident last month when a commentary in International Journal of Forensic Mental Health made it a matter of public knowledge that forensic psychologist Robert Hare of the University of British Columbia,Vancouver, had threatened to file a defamation lawsuit against the authors and the journal's publisher. The Psychological Assessment article, by Jennifer Skeem, a forensic psychologist at the University of California, Irvine, and psychologist David Cooke of Glasgow Caledonian University, is critical of a widely used diagnostic tool developed by Hare called Psychopathy Checklist-Revised (PCL-R) and what the article labels as Hare's construct of psychopathy. Hare, however, saw a copy of the paper prepublication and took exception to Skeem and Cooke's portrayal of PCL-R, his work, and his writings. On 8 November 2007, lawyers representing Hare sent an e-mail to the American Psychological Association (APA), Skeem, and Cooke threatening a defamation lawsuit. "In 40 years, I've engaged in some heated academic debates, but in the journals. This time was different because it had little to do with scientific/academic discourse and everything with taking unwarranted shots at me as a straw man," Hare says. © 2010 American Association for the Advancement of Science.

Keyword: Aggression
Link ID: 14169 - Posted: 06.24.2010

By THE NEW YORK TIMES Dozens of readers had questions about Tourette’s syndrome, the odd and poorly understand disorder that causes uncontrollable tics and vocalizations, after the disorder was profiled in a recent Patient Voices series. Here, Dr. Robert A. King and Dr. James F. Leckman of Yale School of Medicine respond to readers wondering whether Tourette’s is inherited and how common the disorder is. Is Tourette’s Inherited? My daughter is engaged to someone with Tourette’s. I worry about their children inheriting Tourette’s. What is the likelihood of that occurring? Anonymous, San Francisco Dr. King and Dr. Leckman respond: Tourette’s likely has genetic determinants, but they may vary from family to family. When a parent has Tourette’s, sons have a higher risk of inheriting the condition than daughters. On average, about 20 percent of male offspring will have Tourette’s, compared to only about 5 percent of female offspring. The rates for a chronic motor tic disorder are a bit higher: 30 percent of the sons and about 9 percent of the daughters will have such a condition. In contrast, the rates are reversed for obsessive-compulsive disorder, or O.C.D., which sometimes accompanies Tourette’s, with 7 percent of sons and 15 percent of daughters developing symptoms of O.C.D. These are all approximate figures. Copyright 2010 The New York Times Company

Keyword: Tourettes
Link ID: 14168 - Posted: 06.24.2010

By Ferris Jabr NEW YORK—When it comes to brain power, we humans like to think we're the animal kingdom's undisputed champions. But in the past few decades we've had to make a lot of room on our mantle place for shared trophies. Problem-solving? Sorry, but crows and octopuses do that too. Tool use? Primates, birds and even fish have learned that trick. It turns out our human cognitive abilities are just not as unique as we once thought. The collapsing divisions between animal and human minds is exactly what a group of scientists gathered to discuss on Saturday, June 5, at a World Science Festival panel, "All Creatures Great and Smart." WNYC radio host Jad Abumrad mediated the talk. The first topic of conversation was a behavior known as altruism: selflessly helping a stranger. Brian Hare, who studies ape psychology at Duke University, described a recent experiment on this kind of cooperation in bonobos—primates that are in the same genus as chimpanzees. "We wanted to challenge that notion that humans are unique and test whether one of our closest relatives is capable of voluntarily sharing," Hare said. In the study, published earlier this year in Current Biology, researchers showed a bonobo into a room with some food inside. Instead of hogging all the grub, the bonobo consistently chose to unlock the door of an adjacent room and share the food with an unfamiliar bonobo. © 2010 Scientific American,

Keyword: Evolution
Link ID: 14167 - Posted: 06.24.2010

By Katherine Harmon When the body does not properly manage insulin levels, diabetes and other metabolic disorders are familiar outcomes. That hormonal imbalance, however, has also been linked to a higher risk for psychiatric disorders, such as schizophrenia. And a new study has uncovered a potential pathway by which this metabolic hormone can upset the balance of a key neurotransmitter. "We know that people with diabetes have an increased incidence of mood and other psychiatric disorders," Kevin Niswender, an endocrinologist at Vanderbilt University Medical Center and coauthor of the study, said in a prepared statement. Previous researchers, including Aurelio Galli, a neurobiologist at Vanderbilt, had found that insulin was affecting more than blood sugar levels. "Something goes wrong in the brain because insulin isn't signaling the way that it normally does," Galli, a coauthor of the new paper, published online June 8 in the journal PLoS Biology, said in a prepared statement. Although schizophrenia is a complex disease that is thought to have a variety of individual genetic and epigenetic causes, these researchers and others have proposed that a common thread is too little dopamine, a neurotransmitter that is involved in movement, reward and motivation. But just how, molecularly, insulin and dopamine dysfunctions might be linked has yet to be settled. © 2010 Scientific American,

Keyword: Schizophrenia
Link ID: 14166 - Posted: 06.24.2010

By Katherine Harmon Premature infants have a known higher risk for poor neurological development, often leading to developmental and educational issues. However, these babies, born before 37 weeks, make up a small number of any generation, and new research shows that the 40 percent of babies born any more than a week before a full 40-week term are also at higher risk for having special education needs during childhood. By analyzing the 2005 Scottish school census of 407,503 children and national birth records, researchers found that risk for special education needs steadily decreased with gestation duration all the way to 40 and 41 weeks—even though babies born between 37 weeks and 41 weeks are considered "at term." For the survey, special education needs included learning disabilities (such as autism, attention deficit hyperactivity disorder, dyslexia and others) and physical disabilities that can impair learning. The findings were published online June 8 in PLoS Medicine. "The tendency of most previous studies to treat gestation as a binary factor (preterm versus term) has masked a dose-effect across the whole range of gestation," noted the researchers, led by Daniel MacKay, of the University of Glasgow's Section of Public Health. And the sheer number of children who were born before 40 weeks (but after 37 weeks) mean that they constitute a greater percentage of special education children. Whereas preterm births accounted for about 5 percent of deliveries, they made up 3.5 percent of children needing special education. After adjusting for other factors, such as maternal demographics and mode of delivery, early term infants (delivered between 37 weeks and 39 weeks), had a 5.3 percent higher risk (than full term babies) for needing special education later. © 2010 Scientific American,

Keyword: Development of the Brain
Link ID: 14165 - Posted: 06.24.2010

by Ewen Callaway You spend more time window shopping than you may realise. Whether someone intends to buy a product or not can be predicted from their brain activity – even when they are not consciously pondering their choices. The ability to predict from brain scans alone what a person intends to buy, while leaving the potential buyer none the wiser, could bring much-needed rigour to efforts to meld marketing and neuroscience, says Brian Knutson, a neuroscientist at Stanford University in California who was not involved in the research. NeuromarketingMovie Camera, as this field is known, has been employed by drug firms, Hollywood studios and even the Campbell Soup Company to sell their wares, despite little published proof of its effectiveness. Rather than soup, John-Dylan Haynes at the Bernstein Center for Computational Neuroscience in Berlin, Germany, attempted to predict which cars people might unconsciously favour. To do so, he and colleague Anita Tusche used functional MRI to scan the brains of two groups of male volunteers, aged 24 to 32, while they were presented with images of a variety of cars. One group was asked to rate their impressions of the vehicles, while the second performed a distracting visual task while cars were presented in the background. Each volunteer was then shown three cars and asked which they would prefer to buy. © Copyright Reed Business Information Ltd.

Keyword: Emotions; Brain imaging
Link ID: 14164 - Posted: 06.24.2010

by Carlin Flora; Depression is a chemical imbalance, most people think. Researchers, drug manufacturers, and even the Food and Drug Administration assert that antidepressants work by “normalizing” levels of brain neurotransmitters—chemical messengers such as serotonin. And yet hard science supporting this idea is quite poor, says Irving Kirsch, professor of psychology at the University of Hull in the U.K. An expert on the placebo effect, Kirsch has unearthed evidence that antidepressants do not correct brain chemistry gone awry. More important, the drugs are not much more effective against depression than are sugar pills, he says. To support these controversial claims, Kirsch conducted a meta-analysis, digging up data from unpublished clinical trials. When all the evidence is weighed together, Prozac, Paxil, and other such popular pills seem to be at best weakly effective against depression—an argument Kirsch presses in his new book, The Emperor’s New Drugs. Some other research backs up his claims. A study published this winter in the Journal of the American Medical Association found that psychoactive drugs are no better than placebos for people suffering from mild to moderate depression. Where did the idea of depression as a chemical imbalance come from?
 The initial two drugs, imipramine and iproniazid, that were discovered and promoted as effective antidepressants both seemed to increase the amount of serotonin in the brain. It was discovered afterward that one of them seemed to block the reabsorption of serotonin, leaving it to linger longer at cell receptors, and the other blocked the destruction of the serotonin neurotransmitters in the synapses in the brain.

Keyword: Depression
Link ID: 14163 - Posted: 06.24.2010

by Jennifer Couzin-Frankel A new study of nearly 1000 people with autism has confirmed that the genetics of the disease are much more idiosyncratic than some had thought. Rather than a few genes that raise the risk of autism throughout the population, scientists are finding dozens of genes that spur disease, many of them in just one or two people. It appears that these variants do share certain characteristics, however: Many play a role in cell proliferation and cell signaling in the brain. Although scientists are heartened by this new map of autism genetics, they also say that they have a long road ahead in discerning how these genetic changes cause this particular disease. Over the past few years, researchers studying autism and schizophrenia have found that the genomes of patients with one or the other are riddled with so-called copy-number variants: deletions or duplications of stretches of DNA that can encompass many genes. Indeed, the most dramatic of these copy-number variants are even visible with a microscope, as abnormalities in the chromosomes of children afflicted with undiagnosed intellectual disabilities. Some of these disease-causing changes happen spontaneously during embryonic development, whereas others are inherited. The latest study, published online today in Nature, is the second phase of the Autism Genome Project consortium, which comprises more than 120 scientists in 11 countries in North America and Europe. (The first, published in 2007 in Nature Genetics, was a broad analysis of gene changes and copy-number variation, with fewer families and less detailed analysis of rare copy-number variants.) Here the scientists scanned the genomes of 996 children with autism-spectrum disorders, a group of conditions that affect social and communication skills, at high resolution and compared them with the genomes of the children's parents and to 1287 people without the disease. © 2010 American Association for the Advancement of Science.

Keyword: Autism; Genes & Behavior
Link ID: 14162 - Posted: 06.24.2010