Chapter 7. Life-Span Development of the Brain and Behavior
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Stephen S. Hall Hochelaga was the original Iroquoian name for the village that ultimately became Montreal, but it is also the name of a rough-hewn French–Canadian neighbourhood located east of — and a world away from — the cosmopolitan city centre. The district's tidy two- and three-storey brick duplexes, adorned with Montreal's characteristic wrought-iron staircases, predominantly house families that have, because of poverty and lack of education, never quite attained thriving middle-class status. During the 1980s, public-school officials identified Hochelaga and many other impoverished neighbourhoods in the eastern part of Montreal as places where kindergarten children disproportionately displayed severe behavioural problems, such as physical aggression. The school system asked a young University of Montreal psychologist named Richard Tremblay for help. “Their parents didn't have a high-school diploma, and many of the mothers had their first child before the age of 20,” Tremblay says of the families he began to study, as he walks along Rue Ontario in Hochelaga on a sunny afternoon in September. Those were the women, he adds, “most at risk of having children who have problems”. Over the past three decades, Hochelaga and similar neighbourhoods have served as living laboratories in the study of the roots of aggression. Since 1984, Tremblay and his collaborators have followed more than 1,000 children from 53 schools in the city from childhood into adulthood. And in 1985, he initiated a ground-breaking experiment in which some families of at-risk children were given support and counselling to help curb bad behaviour. His research overturned ideas about when aggressive behaviour first emerges, and showed that early intervention can deflect children away from adult criminality. © 2013 Nature Publishing Group
By CARL ZIMMER There are many things that make humans a unique species, but a couple stand out. One is our mind, the other our brain. The human mind can carry out cognitive tasks that other animals cannot, like using language, envisioning the distant future and inferring what other people are thinking. The human brain is exceptional, too. At three pounds, it is gigantic relative to our body size. Our closest living relatives, chimpanzees, have brains that are only a third as big. Scientists have long suspected that our big brain and powerful mind are intimately connected. Starting about three million years ago, fossils of our ancient relatives record a huge increase in brain size. Once that cranial growth was underway, our forerunners started leaving behind signs of increasingly sophisticated minds, like stone tools and cave paintings. But scientists have long struggled to understand how a simple increase in size could lead to the evolution of those faculties. Now, two Harvard neuroscientists, Randy L. Buckner and Fenna M. Krienen, have offered a powerful yet simple explanation. In our smaller-brained ancestors, the researchers argue, neurons were tightly tethered in a relatively simple pattern of connections. When our ancestors’ brains expanded, those tethers ripped apart, enabling our neurons to form new circuits. Dr. Buckner and Dr. Krienen call their idea the tether hypothesis, and present it in a paper in the December issue of the journal Trends in Cognitive Sciences. “I think it presents some pretty exciting ideas,” said Chet C. Sherwood, an expert on human brain evolution at George Washington University who was not involved in the research. Dr. Buckner and Dr. Krienen developed their hypothesis after making detailed maps of the connections in the human brain using f.M.R.I. scanners. When they compared their maps with those of other species’ brains, they saw some striking differences. © 2013 The New York Times Company
By Regina Harrell and Pulse, I am a primary-care doctor who makes house calls in and around Tuscaloosa, Ala. Today my rounds start at a house located down a dirt road a few miles outside town. Gingerly, I cross the front walk; Mrs. Edgars told me that she killed a rattlesnake in her flowerbed last year. She is at the door, expecting my visit. Mr. Edgars sits on the couch, unable to recall that I am his doctor, or even that I am a doctor, but happy to see me nonetheless. We chat about the spring garden and the rain, then we move on to Mr. Edgars’s arthritis. Earlier on in his dementia, he wandered the woods, and his wife was afraid he would get lost and die, although the entire family agreed that this was how he would want it. Now, in a strange twist, his knee arthritis has worsened enough that it has curtailed his wanderings. I suspect that Mrs. Edgars is undertreating the pain to decrease the chance that he’ll wander off again. We talk about how anxious he grows whenever she’s out of his sight and how one of his children comes to sit with him so that she can run errands. She shows me a quilt remnant found in a log cabin on their property; it likely belonged to her husband’s grandfather, making the rough-edged fabric about a century old. I leave carrying a parting gift from her — a jar of homegrown pickled okra. When I get back to the office, I turn on the computer to write a progress note in Mr. Edgars’s electronic health record, or EHR. In addition to recording the details of our visit, I must try to meet the new federal criteria for “meaningful use,” criteria that have been adopted by my office with threats that I won’t get paid for my work if I don’t. © 1996-2013 The Washington Post
Link ID: 19067 - Posted: 12.24.2013
By Alexandra Sifferlin It’s always been conventional wisdom that girls reach maturity more quickly than boys, but now scientists have provided some proof. In new research published in the journal Cerebral Cortex, an international group of researchers led by a team from Newcastle University in England found that girls’ brains march through the reorganization and pruning typical of normal brain development earlier than boys’ brains. In the study, in which 121 people between ages 4 to 40 were scanned using MRIs, the scientists documented the ebb and flow of new neural connections, and found that some brain fibers that bridged far-flung regions of the brain tended to remain stable, while shorter connections, many of which were redundant, were edited away. And the entire reorganization seemed to occur sooner in girls’ brains than in boys’ brains. Females also tended to have more connections across the two hemispheres of the brain. The researchers believe that the earlier reorganization in girls makes the brain work more efficiently, and therefore reach a more mature state for processing the environment. What drives the gender-based difference in timing isn’t clear from the current study, but the results suggest that may be a question worth investigating. © 2013 Time Inc.
Amanda Mascarelli In children with certain gene variants, symptoms similar to common learning disabilities could be omens of serious psychiatric conditions. People who carry high-risk genetic variants for schizophrenia and autism have impairments reminiscent of disorders such as dyslexia, even when they do not yet have a mental illness, a new study has found. The findings offer a window into the brain changes that precede severe mental illness and hold promise for early intervention and even prevention, researchers say. Rare genetic alterations called copy number variants (CNVs), in which certain segments of the genome have an abnormal number of copies, play an important part in psychiatric disorders: Individuals who carry certain CNVs have a several-fold increased risk of developing schizophrenia or autism1. But previous studies were based on individuals who already have a psychiatric disorder, and until now, no one had looked at what effects these CNVs have in the general population. In a study published today in Nature2, researchers report that people with these variants but no diagnosis of autism or a mental illness still show subtle brain changes and impairments in cognitive function. “In psychiatry we always have the problem that disorders are defined by symptoms that patients experience or tell us about, or that we observe,” says study co-author Andreas Meyer-Lindenberg, a psychiatrist and the director the Central Institute of Mental Health in Mannheim, Germany, affiliated with the University of Heidelberg. This work, on the other hand, provides a glimpse into the biological underpinnings of people who are at risk of psychiatric disorders, he says. The team searched a genealogical database of more than 100,000 Icelanders, focusing on 26 genetic variants that have been shown to increase the risk of schizophrenia or autism. They found that 1,178 people in the database, or 1.16% of the sample, carried one or more of these CNVs. © 2013 Nature Publishing Group
By DANNY HAKIM LONDON — European food regulators said on Tuesday that a class of pesticides linked to the deaths of large numbers of honey bees might also harm human health, and they recommended that the European Commission further restrict their use. The commission, which requested the review, has already taken a tougher stance than regulators in other parts of the world against neonicotinoids, a relatively new nicotine-derived class of pesticide. Earlier this year, some were temporarily banned for use on many flowering crops in Europe that attract honey bees, an action that the pesticides’ makers are opposing in court. Now European Union regulators say the same class of pesticides “may affect the developing human nervous system” of children. They focused on two specific versions of the pesticide, acetamiprid and imidacloprid, saying they were safe to use only in smaller amounts than currently allowed. Imidacloprid was one of the pesticides placed under a two-year ban this year. The review was prompted by a Japanese study that raised similar concerns last year. Imidacloprid is one of the most popular insecticides, and is used in agricultural and consumer products. It was developed by Bayer, the German chemicals giant, and is the active ingredient in products like Bayer Advanced Fruit, Citrus & Vegetable Insect Control, which can be purchased at stores internationally, including Home Depot in the United States. Acetamiprid is sold by Nisso Chemical, a German branch of a Japanese company, though it was developed with Bayer’s help. It is used in consumer products like Ortho Flower, Fruit & Vegetable Insect Killer. The action by European regulators could affect the entire category of neonicotinoid pesticides, however. James Ramsay, a spokesman for the European Food Safety Authority, which conducted the review, said the agency was recommending a mandatory submission of studies related to developmental neurotoxicity “as part of the authorization process in the E.U.” © 2013 The New York Times Company
By DONALD G. McNEIL Jr. A long-awaited study has confirmed the fears of Somali residents in Minneapolis that their children suffer from higher rates of a disabling form of autism compared with other children there. The study — by the University of Minnesota, the Centers for Disease Control and Prevention, and the research and advocacy group Autism Speaks — found high rates of autism in two populations: About one Somali child in 32 and one white child in 36 in Minneapolis were on the autism spectrum. The national average is one child in 88, according to Coleen A. Boyle, who directs the C.D.C.’s Center on Birth Defects and Developmental Disabilities. But the Somali children were less likely than the whites to be “high-functioning” and more likely to have I.Q.s below 70. (The average I.Q. score is 100.) The study offered no explanation of the statistics. “We do not know why more Somali and white children were identified,” said Amy S. Hewitt, the project’s primary investigator and director of the University of Minnesota’s Research and Training Center on Community Living. “This project was not designed to answer these questions.” The results echoed those of a Swedish study published last year finding that children from immigrant families in Stockholm — many of them Somali — were more likely to have autism with intellectual disabilities. The Minneapolis study also found that Somali children with autism received their diagnoses late. Age 5 was the average, while autism and learning disabilities can be diagnosed as early as age 2, and children get the most benefit from behavioral treatment when it is started early. Black American-born children and Hispanic children in Minneapolis had much lower autism rates: one in 62 for the former and one in 80 for the latter. © 2013 The New York Times Company
Link ID: 19044 - Posted: 12.17.2013
by Bethany Brookshire “You are what you eat.” We’ve all heard that one. What we eat can affect our growth, life span and whether we develop disease. These days, we know that we also are what our mother eats. Or rather, what our mothers ate while we were in the womb. But are we also what our father eats? A new study shows that in mice, a dietary deficiency in dad can be a big downer for baby. The dietary staple in the study was folic acid, or folate. Folate is one of the B vitamins and is found in dark leafy greens (eat your kale!) and has even been added to some foods like cereals. It is particularly essential to get in the diet because we cannot synthesize it on our own. And it plays roles in DNA repair and DNA synthesis, as well as methylation of DNA. It’s particularly important during development. Without adequate folate, developing fetuses are prone to neural tube disorders, such as spina bifida. Some of the neural tube disorders caused by folate deficiency could result from breaks in the DNA itself. But folic acid is also important in the epigenome. Epigenetics is a mechanism that allows cells to change how genes are used without changing the genes themselves. Instead of altering the DNA itself, epigenetic alterations put chemical “marks” or “notes” —methyl or acetyl groups — on the DNA and the proteins associated with it. The marks can either make a gene more accessible (acetylation) or less accessible (methylation), making it more or less likely to be made into a protein. This means that each cell type can have a different epigenome, allowing a neuron to function differently than a muscle cell, even though they contain the same DNA. Folate affects DNA synthesis, but it can also affect DNA methylation. In fact, DNA methylation requires the presence of folate. So low folate could affect whether genes are turned off or on and by how much. In a developing fetus, that could contribute to developmental problems. © Society for Science & the Public 2000 - 2013.
A study in mice shows how a breakdown of the brain’s blood vessels may amplify or cause problems associated with Alzheimer’s disease. The results published in Nature Communications suggest that blood vessel cells called pericytes may provide novel targets for treatments and diagnoses. “This study helps show how the brain’s vascular system may contribute to the development of Alzheimer’s disease,” said study leader Berislav V. Zlokovic, M.D. Ph.D., director of the Zilkha Neurogenetic Institute at the Keck School of Medicine of the University of Southern California, Los Angeles. The study was co-funded by the National Institute of Neurological Diseases and Stroke (NINDS) and the National Institute on Aging (NIA), parts of the National Institutes of Health. Alzheimer’s disease is the leading cause of dementia. It is an age-related disease that gradually erodes a person’s memory, thinking, and ability to perform everyday tasks. Brains from Alzheimer’s patients typically have abnormally high levels of plaques made up of accumulations of beta-amyloid protein next to brain cells, tau protein that clumps together to form neurofibrillary tangles inside neurons, and extensive neuron loss. Vascular dementias, the second leading cause of dementia, are a diverse group of brain disorders caused by a range of blood vessel problems. Brains from Alzheimer’s patients often show evidence of vascular disease, including ischemic stroke, small hemorrhages, and diffuse white matter disease, plus a buildup of beta-amyloid protein in vessel walls. Furthermore, previous studies suggest that APOE4, a genetic risk factor for Alzheimer’s disease, is linked to brain blood vessel health and integrity.
Link ID: 19033 - Posted: 12.14.2013
Smoking tobacco or marijuana, taking prescription painkillers, or using illegal drugs during pregnancy is associated with double or even triple the risk of stillbirth, according to research funded by the National Institutes of Health. Researchers based their findings on measurements of the chemical byproducts of nicotine in maternal blood samples; and cannabis, prescription painkillers and other drugs in umbilical cords. Taking direct measurements provided more precise information than did previous studies of stillbirth and substance use that relied only on women’s self-reporting. The study findings appear in the journal Obstetrics & Gynecology. “Smoking is a known risk factor for stillbirth, but this analysis gives us a much clearer picture of the risks than before,” said senior author Uma M. Reddy, M.D., MPH, of the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), the NIH institute that supported the study. “Additionally, results from the latest findings also showed that likely exposure to secondhand smoke can elevate the risk of stillbirth.” Dr. Reddy added, “With the legalization of marijuana in some states, it is especially important for pregnant women and health care providers to be aware that cannabis use can increase stillbirth risk.” The study enrolled women between March 2006 and September 2008 in five geographically defined areas delivering at 59 hospitals participating in the Stillbirth Collaborative Research Network External Web Site Policy. Women who experienced a stillbirth and those who gave birth to a live infant participated in the study. The researchers tested blood samples at delivery from the two groups of women and the umbilical cords from their deliveries to measure the exposure to the fetus. They also asked participants to self-report smoking and drug use during pregnancy.
by Rowan Hooper BIOENGINEERS dream of growing spare parts for our worn-out or diseased bodies. They have already succeeded with some tissues, but one has always eluded them: the brain. Now a team in Sweden has taken the first step towards this ultimate goal. Growing artificial body parts in the lab starts with a scaffold. This acts as a template on which to grow cells from the patient's body. This has been successfully used to grow lymph nodes, heart cells and voice boxes from a person's stem cells. Bioengineers have even grown and transplanted an artificial kidney in a rat. Growing nerve tissue in the lab is much more difficult, though. In the brain, new neural cells grow in a complex and specialised matrix of proteins. This matrix is so important that damaged nerve cells don't regenerate without it. But its complexity is difficult to reproduce. To try to get round this problem, Paolo Macchiarini and Silvia Baiguera at the Karolinska Institute in Stockholm, Sweden, and colleagues combined a scaffold made from gelatin with a tiny amount of rat brain tissue that had already had its cells removed. This "decellularised" tissue, they hoped, would provide enough of the crucial biochemical cues to enable seeded cells to develop as they would in the brain. When the team added mesenchymal stem cells – taken from another rat's bone marrow – to the mix, they found evidence that the stem cells had started to develop into neural cells (Biomaterials, doi.org/qfh). The method has the advantage of combining the benefits of natural tissue with the mechanical properties of an artificial matrix, says Alex Seifalian, a regenerative medicine specialist at University College London, who wasn't involved in the study. © Copyright Reed Business Information Ltd.
Keyword: Development of the Brain
Link ID: 19029 - Posted: 12.12.2013
By Janelle Weaver Children with a large vocabulary experience more success at school and in the workplace. How much parents talk to their children plays a major role, but new research shows that it is not just the quantity but also the quality of parental input that matters. Helpful gestures and meaningful glances may allow kids to grasp concepts more easily than they otherwise would. In a study published in June in the Proceedings of the National Academy of Sciences USA, Erica Cartmill of the University of Chicago and her collaborators videotaped parents in their homes as they read books and played games with their 14- or 18-month-old children. The researchers created hundreds of 40-second muted video clips of these interactions. Another set of study participants watched the videos and used clues from the scenes to guess which nouns the parents were saying at various points in the sequences. The researchers used the accuracy of these guesses to rate how well a parent used nonverbal cues, such as gesturing toward and looking at objects, to clarify a word's meaning. Cartmill and her team found that the quality of parents' nonverbal signaling predicted the size of their children's vocabulary three years later. Surprisingly, socioeconomic status did not play a role in the quality of the parents' nonverbal signaling. This result suggests that the well-known differences in children's vocabulary size across income levels are likely the result of how much parents talk to their children, which is known to differ by income, rather than how much nonverbal help they offer during those interactions. © 2013 Scientific American
Ian Sample, science correspondent Differences in children's exam results at secondary school owe more to genetics than teachers, schools or the family environment, according to a study published yesterday. The research drew on the exam scores of more than 11,000 16-year-olds who sat GCSEs at the end of their secondary school education. In the compulsory core subjects of English, maths and science, genetics accounted for on average 58% of the differences in scores that children achieved. Grades in the sciences, such as physics, biology and chemistry, were more heritable than those in humanities subjects, such as art and music, at 58% and 42% respectively. The findings do not mean that children's performance at school is determined by their genes, or that schools and the child's environment have no influence. The overall effect of a child's environment – including their home and school life – accounted for 36% of the variation seen in students' exam scores across all subjects, the study found. "The question we are asking is why do children differ in their GCSE scores? People immediately think it's schools. But if schools accounted for all the variance, then children in one classroom would all be the same," said Robert Plomin, an expert in behavioural genetics who led the study at King's College London. To tease out the genetic contribution to children's school grades, the researchers studied GCSE scores of identical twins (who share 100% of their genes) and non-identical twins (who share on average half of the genes that normally vary between people). Both groups share their environments to a similar extent. © 2013 Guardian News and Media Limited
Taking some heartburn medications for more than two years is linked to a higher risk of vitamin B12 deficiency in adults, a U.S. study suggests. Left untreated, vitamin B12 deficiency can lead to dementia, neurological damage, anemia, and other complications. Knowing that stomach acid aids in vitamin B12 absorption, researchers set out to test whether suppressing the acids can lead to vitamin deficiency. The drugs in question are known as proton pump inhibitors and they include such well known brands as Losec, Nexium, Prabacid and Pariet. Doses of more than 1.5 pills per day were more strongly associated with vitamin D deficiency than doses of less than 0.75 pills per day, Dr. Douglas Corley, a gastroenterologist and research scientist with the Kaiser Permanente Division of Research in Broadway, Calif. and his co-authors said in Wednesday's issue of the Journal of the American Medical Association. "This research raises the question of whether people who are taking acid-depressing medications long term should be screened for vitamin B12 deficiency," Corley said in a release. "It's a relatively simple blood test, and vitamin supplements are an effective way of managing the vitamin deficiency, if it is found." For the study, researchers looked at electronic health records of 25,956 adults diagnosed with vitamin B12 deficiency in Northern California between January 1997 and June 2011, and compared them with 184,199 patients without B12 deficiency during the same time period. Among the 25,956 patients who had vitamin B12 deficiency, 12 per cent used proton pump inhibitors for at least two years, compared with 7.2 per cent of those in the control group. © CBC 2013
By Ingfei Chen The way doctors diagnose Alzheimer's disease may be starting to change. Traditionally clinicians have relied on tests of memory and reasoning skills and reports of social withdrawal to identify patients with Alzheimer's. Such assessments can, in expert hands, be fairly conclusive—but they are not infallible. Around one in five people who are told they have the neurodegenerative disorder actually have other forms of dementia or, sometimes, another problem altogether, such as depression. To know for certain that someone has Alzheimer's, doctors must remove small pieces of the brain, examine the cells under a microscope and count the number of protein clumps called amyloid plaques. An unusually high number of plaques is a key indicator of Alzheimer's. Because such a procedure risks further impairing a patient's mental abilities, it is almost always performed posthumously. In the past 10 years, however, scientists have developed sophisticated brain scans that can estimate the amount of plaque in the brain while people are still alive. In the laboratory, these scans have been very useful in studying the earliest stages of Alzheimer's, before overt symptoms appear. The results are reliable enough that last year the Food and Drug Administration approved one such test called Amyvid to help evaluate patients with memory deficits or other cognitive difficulties. Despite the FDA's approval, lingering doubts about the exact role of amyloid in Alzheimer's and ambivalence about the practical value of information provided by the scan have fueled debate about when to order an Amyvid test. Not everyone who has an excessive amount of amyloid plaque develops Alzheimer's, and at the moment, there is generally no way to predict whom the unlucky ones will be. Recent studies have shown that roughly one third of older citizens in good mental health have moderate to high levels of plaque, with no noticeable ill effects. And raising the specter of the disorder in the absence of symptoms may upset more people than it helps because no effective treatments exist—at least not yet. © 2013 Scientific American
By Dan Hurley Darwin and Freud walk into a bar. Two alcoholic mice — a mother and her son — sit on two bar stools, lapping gin from two thimbles. The mother mouse looks up and says, “Hey, geniuses, tell me how my son got into this sorry state.” “Bad inheritance,” says Darwin. “Bad mothering,” says Freud. For over a hundred years, those two views — nature or nurture, biology or psychology — offered opposing explanations for how behaviors develop and persist, not only within a single individual but across generations. And then, in 1992, two young scientists following in Freud’s and Darwin’s footsteps actually did walk into a bar. And by the time they walked out, a few beers later, they had begun to forge a revolutionary new synthesis of how life experiences could directly affect your genes — and not only your own life experiences, but those of your mother’s, grandmother’s and beyond. The bar was in Madrid, where the Cajal Institute, Spain’s oldest academic center for the study of neurobiology, was holding an international meeting. Moshe Szyf, a molecular biologist and geneticist at McGill University in Montreal, had never studied psychology or neurology, but he had been talked into attending by a colleague who thought his work might have some application. Likewise, Michael Meaney, a McGill neurobiologist, had been talked into attending by the same colleague, who thought Meaney’s research into animal models of maternal neglect might benefit from Szyf’s perspective.
Link ID: 19017 - Posted: 12.11.2013
Researchers striving to understand the origins of dementia are building the case against a possible culprit: lead exposure early in life. A study spanning 23 years has now revealed that monkeys who drank a lead-rich formula as infants later developed tangles of a key brain protein, called tau, linked to Alzheimer's disease. Though neuroscientists say more work is needed to confirm the connection, the research suggests that people exposed to lead as children—as many in America used to be before it was eliminated from paint, car emissions, water, and soil—could have an increased risk of the common, late-onset form of Alzheimer’s disease. Even in small doses, lead can wreak havoc on the heart, intestines, kidneys, and nervous system. Children are especially prone to its pernicious effects, as it curbs brain development. Many studies have linked early lead exposure with lower IQs. Researchers estimate that one in 38 children in the United States still have harmful levels of the metal in their systems, but evidence linking this exposure to dementia later in life has been tenuous. A team led by toxicologist Nasser Zawia, however, has vigorously pursued the lead hypothesis. In one early study, from 2008, the group showed that plaques, insoluble globs of a protein called β-amyloid, marred the brains of five macaques that had consumed a lead-enriched formula as infants. The researchers had compared the preserved brain tissues from those macaques, sacrificed in 2003 at age 23 in a National Institutes of Health lab, with four similarly aged monkeys who had had lead-free formula. The amyloid plaques closely resembled those in the brains of adults with Alzheimer's disease that are thought to contribute to the dementia. © 2013 American Association for the Advancement of Science.
Many physicians and parents report that their autistic children have unusually severe gastrointestinal problems, such as chronic constipation or diarrhea. These observations have led some researchers to speculate that an ailing gut contributes to the disorder in some cases, but scientific data has been lacking. Now, a provocative study claims that a probiotic treatment for gastrointestinal issues can reduce autismlike symptoms in mice and suggests that this treatment could work for humans, too. The reported incidence of gut maladies in people with autism varies wildly between published studies—from zero to more than 80%—making it difficult to establish just how commonly the two conditions go together, says principal investigator Sarkis Mazmanian, a microbiologist at the California Institute of Technology (Caltech) in Pasadena. Overall, however, the evidence seems to point toward a connection. Last year, for example, a Centers for Disease Control and Prevention study of thousands of children with developmental disabilities found that kids with autism were twice as likely as children with other types of disorders to have frequent diarrhea or colitis, an inflammation of the large intestine. For many years, Mazmanian and his and colleagues have been studying the effects of a nontoxic strain of the bacterium Bacteroides fragilis on diseases such as Crohn's disease, which causes intestinal inflammation and allows potentially harmful substances that should pass out of the body to leak through junctions between cells that are normally tight. Although the researchers don’t understand the mechanism, the bacterium appears to restore the damaged gut, possibly by helping close these gaps. © 2013 American Association for the Advancement of Science.
Link ID: 19009 - Posted: 12.06.2013
By Dana Smith Daniel Tammet has memorized Pi to the 22,514th digit. He speaks ten different languages, including one of his own invention, and he can multiply enormous sums in his head within a matter of seconds. However, he is unable to hold down a standard 9-to-5 job, in part due to his obsessive adherence to ritual, down to the precise times he has his tea every day. Daniel is a savant. He is also autistic. And he is a synesthete. Daniel experiences numbers as having color, as well as shape and texture. This helps him perform amazing mathematical feats seemingly without effort, the answer simply materializing to him rather than having to calculate it out. In an interview he gave with The Guardian, Daniel explained, “When I multiply numbers together, I see two shapes. The image starts to change and evolve, and a third shape emerges. That’s the answer. It’s mental imagery. It’s like maths without having to think.” Clearly this man has an extraordinary brain. However, Daniel is perhaps not entirely unique, and it appears that the link between autism and synesthesia is more common than originally thought. This suggests that there is a potential common mechanism between these two conditions, which may even help to explain some of Daniel’s special savant abilities. A new study published in the journal Molecular Autism from a team of researchers at the University of Cambridge now empirically shows that there is an almost three-fold higher occurrence of synesthesia in individuals with autism (18.9%), compared with that of the general population (7.2%). This increased prevalence implies that there is indeed a significant link between autism and synesthesia. © 2013 Scientific American
Link ID: 19008 - Posted: 12.06.2013
By CARL ZIMMER Scientists have found the oldest DNA evidence yet of humans’ biological history. But instead of neatly clarifying human evolution, the finding is adding new mysteries. In a paper in the journal Nature, scientists reported Wednesday that they had retrieved ancient human DNA from a fossil dating back about 400,000 years, shattering the previous record of 100,000 years. The fossil, a thigh bone found in Spain, had previously seemed to many experts to belong to a forerunner of Neanderthals. But its DNA tells a very different story. It most closely resembles DNA from an enigmatic lineage of humans known as Denisovans. Until now, Denisovans were known only from DNA retrieved from 80,000-year-old remains in Siberia, 4,000 miles east of where the new DNA was found. The mismatch between the anatomical and genetic evidence surprised the scientists, who are now rethinking human evolution over the past few hundred thousand years. It is possible, for example, that there are many extinct human populations that scientists have yet to discover. They might have interbred, swapping DNA. Scientists hope that further studies of extremely ancient human DNA will clarify the mystery. “Right now, we’ve basically generated a big question mark,” said Matthias Meyer, a geneticist at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, and a co-author of the new study. Hints at new hidden complexities in the human story came from a 400,000-year-old femur found in a cave in Spain called Sima de los Huesos (“the pit of bones” in Spanish). The scientific team used new methods to extract the ancient DNA from the fossil. “This would not have been possible even a year ago,” said Juan Luis Arsuaga, a paleoanthropologist at Universidad Complutense de Madrid and a co-author of the paper. © 2013 The New York Times Company