by Elizabeth Norton A loving gaze helps firm up the bond between parent and child, building social skills that last a lifetime. But what happens when mom is blind? A new study shows that the children of sightless mothers develop healthy communication skills and can even outstrip the children of parents with normal vision. Eye contact is one of the most important aspects of communication, according to Atsushi Senju, a developmental cognitive neuroscientist at Birkbeck, University of London. Autistic people don't naturally make eye contact, however, and they can become anxious when urged to do so. Children for whom face-to-face contact is drastically reduced—babies severely neglected in orphanages or children who are born blind—are more likely to have traits of autism, such as the inability to form attachments, hyperactivity, and cognitive impairment. To determine whether eye contact is essential for developing normal communication skills, Senju and colleagues chose a less extreme example: babies whose primary caregivers (their mothers) were blind. These children had other forms of loving interaction, such as touching and talking. But the mothers were unable to follow the babies' gaze or teach the babies to follow theirs, which normally helps children learn the importance of the eyes in communication. Apparently, the children don't need the help. Senju and colleagues studied five babies born to blind mothers, checking the children's proficiency at 6 to 10 months, 12 to 15 months, and 24 to 47 months on several measures of age-appropriate communications skills. At the first two visits, babies watched videos in which a woman shifted her gaze or moved different parts of her face while corresponding changes in the baby's face were recorded. Babies also followed the gaze of a woman sitting at a table and looking at various objects. © 2010 American Association for the Advancement of Science

Keyword: Development of the Brain; Aggression
Link ID: 18023 - Posted: 04.11.2013

A rat with some human genes could provide a better way to test Alzheimer's drugs. The genetically modified rat is the first rodent model to exhibit the full range of brain changes found in Alzheimer's, researchers in The Journal of Neuroscience. "It's a big step forward" for drug development, says , a program director at the National Institute of Neurological Disorders and Stroke, or NINDS, which helped fund the work. "The closer the model is to the human condition in representing the disease, the more likely the drug will behave and cure the way it would in humans." In recent years, drug companies have developed several Alzheimer's drugs that seemed to work in animals, but with the disease. A lack of good animal models for Alzheimer's may be one reason for those failures, researchers say. For the past couple of decades, Alzheimer's researchers have relied primarily on mice that carry human gene mutations that cause people to get the disease in their 40s or 50s. Like people, these mice develop so-called amyloid plaques in their brains. But that's where the similarity ends. In people with Alzheimer's, after plaques appear, huge numbers of brain cells die. That's never happened in mice, despite lots of genetic tinkering, Corriveau says. So researchers began to consider a different rodent model: the rat. "Rats are 4 [million] to 5 million years closer evolutionarily to humans," Corriveau says, which means their brains are more like ours. ©2013 NPR

Keyword: Alzheimers; Aggression
Link ID: 18016 - Posted: 04.11.2013

By PAULA SPAN The long list of roles Margaret Thatcher played during her 87 years — potent politician, free-market evangelist, labor antagonist, dominant global leader — includes the one she never publicly discussed: person with dementia. The stroke that killed her on Monday was not her first. Mrs. Thatcher suffered several small strokes more than a decade earlier, canceled all her speaking engagements in 2003 and largely withdrew from public life. Even before the strokes, her daughter, Carol, wrote in a 2008 memoir, she was losing cognitive ground, repeating questions and showing other signs of confusion. Heartbreakingly, she often forgot that her beloved husband, Denis, had died of cancer in 2003. “I had to keep giving her the bad news over and over again,” her daughter wrote. “Every time it finally sank in that she had lost her husband of more than 50 years, she’d look at me sadly and say, ‘Oh’, as I struggled to compose myself. ‘Were we all there?’ she’d ask softly.” At the time, members of her mother’s political circle and other British commentators denounced Carol Thatcher for invading her mother’s privacy and, supposedly, diminishing her dignity. The criticism arose again in some quarters last year, when Meryl Streep won an Oscar for her portrayal of Mrs. Thatcher’s dementia in “The Iron Lady.” © 2013 The New York Times Company

Keyword: Alzheimers
Link ID: 18012 - Posted: 04.10.2013

By Janice Lynch Schuster, My grandmother, who is 92, recently reported that she’d seen three giraffes in her Midwest back yard. She is otherwise sharp (and also kind and funny), but the giraffe episode was further evidence of the mild cognitive impairment that has been slowly creeping into her life. The question for my family has become: How should we respond? One of my sisters tried humor. (“Grandmom, I didn’t know you drank in the middle of the day!”) My father suggested that they were deer (to which she replied, “I’m 92 years old, and I know a giraffe when I see one.”) I tried to learn more about what, exactly, the giraffes were doing out there. (She didn’t seem to know, saying only that “the light shimmered.”) Communicating with a family member who has cognitive impairment can be frustrating and disheartening, even downright depressing for patient and caregiver alike. And it’s a problem faced by a growing number of Americans. According to a report published last week, about 4.1 million Americans have dementia. Alzheimer’s, one of the many forms of dementia, is the most expensive disease in the United States, costing $157 billion to $215 billion a year — more than heart disease and cancer, according to the study, which was sponsored by the National Institute on Aging. As baby boomers reach old age, these numbers are expected to increase dramatically. A number of techniques can not only reduce the frustration but also create new ways of connecting. Among the most effective and popular among experts is the “validation method,” a practice pioneered by geriatric social worker and researcher Naomi Feil in the 1980s. © 1996-2013 The Washington Post

Keyword: Alzheimers; Aggression
Link ID: 18011 - Posted: 04.10.2013

by Dr. Tyeese Gaines African-Americans with a particular gene are twice as likely to develop Alzheimer’s disease in old age as those without it, says a new study published in the Journal of the American Medical Association. This finding is a result of the largest database search for Alzheimer’s genes among African-Americans. “Until now, data on the genetics of Alzheimer’s in this patient population have been extremely limited,” said Dr. Richard Mayeux, chair of neurology at Columbia University Medical Center and senior author of the study. Alzheimer’s disease is the most common cause of dementia — a brain disease that affects memory, personality and the ability to reason. At age 65, only one percent of people have Alzheimer’s, yet over 80 years of age, it increases to 30 percent. A gene called APOE is associated with one in every five cases of Alzheimer’s – known to be a major genetic risk factor for whites and blacks. Yet, in this new research, Mayeux and his team identified an additional gene variant linked to a doubled risk in African-Americans alone, called ABCA7. “ABCA7 is the first major gene implicated in late-onset Alzheimer’s among African-Americans,” said Dr. Christine Reitz, assistant professor of neurology and lead author of the study. To reach this conclusion, researchers examined samples from nearly 6,000 African-American men and women collected between 1989 and 2011 – 2,000 had a diagnosis of probable Alzheimer’s disease and the other 4,000 had no cognitive difficulty. “Although this is a very significant finding, it does not change much for the everyday African-American male or female,” says Rick Kittles, PhD, a human genetics expert who has traced the ancestry of more than 100,000 African-Americans. “There is still much work to do [to] determine how exactly this gene plays a role in Alzheimer’s disease.” ©2013 NBCUniversal

Keyword: Alzheimers; Aggression
Link ID: 18010 - Posted: 04.10.2013

By DENISE GRADY SAN FRANCISCO — Scientists are trained to be skeptics, and Elizabeth H. Blackburn considers herself one of the biggest. Show her the data, and be ready to defend it. But even though she relishes the give and take, Dr. Blackburn admits to impatience at times with the questions some scientists have raised about one of her ventures. “It’s just such a no-brainer, and yet people have such difficulty understanding it,” she said. At issue is a lab test that measures telomeres, stretches of DNA that cap the ends of chromosomes and help keep cells from aging too soon. Unusually short telomeres may be a sign of illness, and Dr. Blackburn, who shared the 2009 Nobel Prize in medicine for her work on telomeres (TEEL-o-meers), thinks measuring them could give doctors and patients a chance to intervene early and maybe even prevent disease. A company she helped found expects to begin offering tests to the public later this year. Other researchers have raised doubts about the usefulness of the measurement, which does not diagnose a specific disease. But Dr. Blackburn, 64, a professor of biology and physiology at the University of California, San Francisco, says she has been convinced by a decade of data from her own team and others, linking short telomeres to heart disease, diabetes, cancer and other diseases, and to chronic stress and post-traumatic stress disorder. With studies that explore the connections among emotional stress, health and telomeres, she has delved into questions that she would have shied away from earlier in her career, as a woman trying to establish herself in science. But now, she has enough confidence and autonomy to follow the leads that intrigue her. The scope of her research has expanded tremendously, from a tight focus on molecular biology to broader questions about the implications of her work for health and public policy. © 2013 The New York Times Company

Keyword: Stress; Aggression
Link ID: 18005 - Posted: 04.09.2013

By DOUGLAS QUENQUA The French geneticist Jérôme Lejeune discovered more than 50 years ago that Down syndrome is caused by the presence of an extra copy of chromosome 21. But to this day it has remained a mystery why that results in impaired physical and cognitive development. Now researchers at the Sanford-Burnham Medical Research Institute think they have found a clue. The scientists, who were investigating Alzheimer’s disease, found that mice that lacked a protein known as SNX27 had many of the same learning and memory defects as mice with Down syndrome. Looking at the brains of people with the syndrome, the researchers discovered that they, too, lacked SNX27. While chromosome 21 is not directly involved in SNX27 production, it does encode a regulator — miR-155 — that inhibits production. According to the study, published in the journal Nature Medicine, levels of miR-155 in the brains of people with Down syndrome correlate almost exactly with the decrease in SNX27. “In the brain, SNX27 keeps certain receptors on the cell surface — receptors that are necessary for neurons to fire properly,” said the study’s senior author, Huaxi Xu, in a statement released by the institute. “So in Down syndrome, we believe lack of SNX27 is at least partly to blame for developmental and cognitive defects.” To test their findings, Dr. Xu’s team introduced more SNX27 to mice with Down syndrome. As they expected, the mice showed immediate improvements in cognitive function and behavior. Now the researchers are investigating molecules that might increase production of SNX27 in the human brain. © 2013 The New York Times Company

Keyword: Development of the Brain; Aggression
Link ID: 18002 - Posted: 04.09.2013

By Neuroskeptic Last year, there was quite a bit of excitement over a “Genetic Test To Predict Risk for Autism”. The test was revealed in a paper in Molecular Psychiatry, by Australian researchers Skafidas and colleagues. The claim was that a statistical classifier could spot patterns of genetic variation that differed between people with autism and healthy controls – with 70% accuracy. For a good discussion of the paper, including comments from the lead author, see here. However, a Letter to Molecular Psychiatry has just cast doubt on the whole thing. The authors write A classifier was recently reported to predict with 70% accuracy if an individual has an autism spectrum disorder using 237 single-nucleotide polymorphisms (SNPs). Biomarkers, genetic or otherwise, that would facilitate earlier autism spectrum disorder diagnosis are crucial; therefore, these results warrant careful scrutiny. So scrutinize it they do, and they find it wanting: In other words, the ‘autism’ genetic variants were indeed more common in the autism cases, compared to controls, but only because the cases and controls were from different places. The classifier worked, but it wasn’t detecting autism, it was detecting ancestry.

Keyword: Autism; Aggression
Link ID: 17996 - Posted: 04.08.2013

By Nathan Seppa Tiny components of amyloid plaques, the notorious protein clumps found littering the brains of people with Alzheimer’s disease, might fight inflammation. Researchers report that several of these sticky protein fragments, or peptides, glom onto inflammatory compounds and reverse paralysis in mice that have a condition similar to multiple sclerosis. A fragment of tau protein, which shows up in other brain deposits in Alzheimer’s patients, has a similar effect. When tested on blood taken from three MS patients, the tau peptide weeded out some inflammatory culprits there, too, researchers report in the April 3 Science Translational Medicine. “This is a seriously good study. It opens up more questions than it answers,” says Jian-Guo Geng, a cell biologist at the University of Michigan in Ann Arbor who wasn’t part of the research team. “But I don’t think we’re anywhere close to using these peptides for treatments.” Amyloid is a broad term for clusters of protein in the brain, including those arising with the aid of misfolded versions of tau or another protein implicated in brain disease called a prion. Viewing amyloid-forming peptides as good guys runs against the scientific thinking, since amyloid plaques are a hallmark of Alzheimer’s disease. But study coauthor Lawrence Steinman, a neurologist at Stanford University, points out that the actual role of amyloid plaques in the disease is unclear. He suggests the tiny peptides holding the plaques together might have an alternative, useful role in the body. © Society for Science & the Public 2000 - 2013

Keyword: Alzheimers
Link ID: 17993 - Posted: 04.05.2013

Genetic markers that could help highlight who is at risk of developing Alzheimer's disease have been identified by US scientists. The research in Neuron identifies mutations that affect the build-up of certain proteins in the brain. High levels of these tau proteins increase the chance of having the disease. UK experts said the study could help understand the changes that occur in the brains of Alzheimer's patients. Tangles of a kind of tau called phosphorylated tau (ptau) are a hallmark of the disease. One of the new gene variants identified by the Washington University School of Medicine team was also shown to be linked to a small increased risk of developing Alzheimer's and a greater risk of cognitive decline. The team used genetic information from more than 1,200 people, significantly larger than previous studies in this area. Dr Alison Goate, who led the study, said: "We anticipate that knowledge about the role of these genes in Alzheimer's disease may lead to the identification of new targets from therapies or new animal or cellular models of the disease. Lifestyle 'plays a role' UK experts said the study adds to the number of genetic markers that have been linked to the development of Alzheimer's disease. BBC © 2013

Keyword: Alzheimers; Aggression
Link ID: 17992 - Posted: 04.05.2013

by Dennis Normile Puberty has always been a time of stress and emotional turmoil for adolescents and for their parents. And scientists have long recognized that kids who start puberty ahead of their peers are particularly likely to have trouble getting along with other children and with adults. New research suggests that those difficulties can be traced back to even earlier ages, indicating that early puberty may not be the root cause. Australian researchers drew on data for 3491 children, roughly half boys and half girls, who were recruited at ages 4 or 5 and then followed until they reached ages 10 or 11. Every 2 years, a researcher visited each subject's home, evaluated the child, and interviewed the primary caregiver, which in most cases was a parent, who later completed and returned a questionnaire about their child's behavior. The primary caregiver was also asked to judge the child's pubertal status, based on indicators for an early phase of puberty such as breast growth in girls, adult-type body odor, and body hair; and growth spurts, deepening voices in boys, and menstruation in girls for a later stage. Girls typically enter puberty at age 10 or 11 and boys at 11 or 12. The researchers found that 16% of the girls and 6% of the boys in the study had entered puberty early, at age 8 or 9. Previously, researchers thought that any negative effects of early puberty showed up only after puberty's onset. But by tracking a cohort of children from age 4 to 5 to age 10 to 11, they found that problems thought restricted to postpuberty children actually appeared well before puberty. Retrospectively, they were able to show that children who later had early onset puberty had difficulty playing with other children and participating in normal school activities, even when they were 4 or 5 years old. Boys, though not girls, in this group had also showed behavior problems, such as being overactive, losing their tempers, and preferring to play alone from a young age. © 2010 American Association for the Advancement of Science.

Keyword: Development of the Brain; Aggression
Link ID: 17987 - Posted: 04.03.2013

By Kathryn Doyle Despite concerns that antidepressant use during pregnancy might affect infants’ growth and development, a small new study finds no size differences in the first year of life between babies exposed and not exposed to the drugs. The medications — known as selective serotonin reuptake inhibitors, or SSRIs, which include fluoxetine (marketed as Prozac) and citalopram (Celexa) — have been tied to premature births and lower birth weight. But their effect on growth during infancy had not been studied. The agency will lift a requirement that the products carry a strict limit on how long they can be used. “It’s a reassuring finding in that when you have an illness during pregnancy, you want to know what is the impact of the illness and what is the impact of the medication,” Katherine Wisner, the study’s lead author, said. Untreated depression also didn’t seem to influence infant growth, according to Wisner, the director of Northwestern University’s Asher Center for the Study and Treatment of Depressive Disorders. That’s important because a baby’s most rapid growth happens in the first year, which sets the stage for growth patterns for the whole life span, she added. Wisner and her colleagues tracked 97 pregnant women without depression, 46 on antidepressants and 31 with depression that was not treated with medication. Their babies were measured and weighed four times over the first year of life. © 1996-2013 The Washington Post

Keyword: Depression; Aggression
Link ID: 17981 - Posted: 04.02.2013

By Bruce Bower Babies take a critical step toward learning to speak before they can say a word or even babble. By 3 months of age, infants flexibly use three types of sounds — squeals, growls and vowel-like utterances — to express a range of emotions, from positive to neutral to negative, researchers say. Attaching sounds freely to different emotions represents a basic building block of spoken language, say psycholinguist D. Kimbrough Oller of the University of Memphis in Tennessee and his colleagues. Any word or phrase can signal any mental state, depending on context and pronunciation. Infants’ flexible manipulation of sounds to signal how they feel lays the groundwork for word learning, the scientists conclude April 1 in the Proceedings of the National Academy of Sciences. Language evolution took off once this ability emerged in human babies, Oller proposes. Ape and monkey researchers have mainly studied vocalizations that have one meaning, such as distress calls. “At this point, the conservative conclusion is that the human infant at 3 months is already vocally freer than has been demonstrated for any other primate at any age,” Oller says. Oller’s group videotaped infants playing and interacting with their parents in a lab room equipped with toys and furniture. Acoustic analyses identified nearly 7,000 utterances made by infants up to 1 year of age that qualified as laughs, cries, squeals, growls or vowel-like sounds. © Society for Science & the Public 2000 - 2013

Keyword: Language; Aggression
Link ID: 17975 - Posted: 04.02.2013

By DAVID W. DUNLAP Words of comfort, encouragement and empathy had been available to Nancy Lanza and her son, Adam, within a pair of books that were found by the police during a search of their home in Newtown, Conn., after Mr. Lanza’s murderous rampage on Dec. 14. “It’s the most widely read book about Asperger’s out there,” said Mr. Robison of his memoir. It is all but impossible to know if mother or son were helped by the books, “Look Me in the Eye: My Life With Asperger’s” and “Born on a Blue Day: Inside the Extraordinary Mind of an Autistic Savant,” or whether either opened, or even had use for, them. While those familiar with Mr. Lanza and his family have said he had an autism variant known as Asperger’s syndrome, investigators have not confirmed the diagnosis. “Look Me in the Eye” (2007), by John Elder Robison, and “Born on a Blue Day” (2006), by Daniel Tammet, are both memoirs that chronicle the painful chasm of misunderstanding that separates people with Asperger’s from the world around them. Both accounts turn hopeful as their writers grow comfortable in their own skins and more successful in communicating with others. That is why Mr. Robison, 55, said it might be expected that his book would have been found among the Lanzas’ belongings. “It’s the most widely read book about Asperger’s out there,” Mr. Robison said by telephone from his home in Amherst, Mass. “Hundreds, if not thousands, of parents have come to me in the years since that book was published to say, ‘Your stories have given me a window into the mind of my son or daughter.’ It’s not a surprise to see that book in the home of any family touched by autism.” The discovery is not entirely welcome, however, if it reinforces an imagined link between autism and violent crime — a link for which experts say there is no evidence. Americans have struggled for three and a half months to understand why Mr. Lanza killed first his mother, then 20 first graders and 6 educators at Sandy Hook Elementary School, before taking his own life. © 2013 The New York Times Company

Keyword: Autism; Aggression
Link ID: 17973 - Posted: 04.01.2013

By JUDITH GRAHAM Three years ago, Kennard Lehmann walked out of a neurologist’s office in Sacramento, Calif., newly diagnosed with early-stage Alzheimer’s disease, a prescription in hand and absolutely no idea where to turn for help. The doctor hadn’t given him a list of resources or discussed how Mr. Lehmann might go about finding them. Knowing nothing about Alzheimer’s, his wife swiped a magazine she had been reading in the doctor’s office to take home and read. Kennard Courtesy of Mary Margaret Lehmann. Kennard “Ken”Lehmann, with his wife, Mary Margaret Lehmann, said monthly get-togethers with other people who also have early-stage Alzheimer’s are “joyful events.” Thus began a journey all too familiar to people with Alzheimer’s — one that Mr. Lehmann, 75, describes as “being put in a box.” “They tell you, you can’t drive, you’re going to get lost,” he told me in a telephone conversation. “Don’t go out at night, you might have sundown syndrome. Don’t try to balance your checkbook, it could be too hard. All these negative things, all these things you’re told you can’t do now that you have Alzheimer’s.” But Mr. Lehmann was lucky. When he and his wife moved to Minneapolis to be near their daughter, they found a group of people like him with early-stage Alzheimer’s who met monthly to socialize and “challenge ourselves so we can continue to grow,” as he put it. The focus was on what people with early-stage dementia can do — dance, write poetry, yoga, visit museums, go to concerts, draw, enjoy one another’s company — not what is no longer within their reach. “These are joyful events,” Mr. Lehmann said, describing how his attitude toward having Alzheimer’s changed after joining the group. “There’s a lot of laughter, a lot of communication. Because we’re all in the same boat, you don’t have that feeling, ‘What is he going to think?’ Everyone there knows you have challenges. There’s no judgment.” © 2013 The New York Times Company

Keyword: Alzheimers
Link ID: 17972 - Posted: 04.01.2013

By Emily Burns Lots of people set themselves goals – like things to do by the time you’re 30. Maybe it’s to find your dream job, meet the love of your life, or travel the world! For sufferers of Cystic Fibrosis, it’s living to see your 30th birthday. Even with all of the advances in medicine and technology, the average life expectancy of someone with Cystic Fibrosis is 33 years. Cystic Fibrosis is an inherited disease that mostly affects the lungs, but also the pancreas, liver and intestines. The body fluids we need – like the mucus in our lungs and intestines – are much thicker than normal, making it extremely difficult to breathe and digest food. Constant physiotherapy, breathing exercises, diet supplements and antibiotics are needed just to get on with daily life. And all of this suffering is caused by one tiny change in our DNA, which then messes up how one single protein folds into the right shape. It’s otherwise known as a protein misfolding disease. There are over 2 million proteins in the human body, carrying out their individual tasks to keep us breathing, thinking – enabling us to live. But their production isn’t easy. It’s an incredibly intricate and specialised process that is constantly going on inside us. If it goes wrong, there are serious consequences to our health, with Cystic Fibrosis being a prime example.... While the primary causes Alzheimer’s and Parkinson’s is still not known, one of the theories suggests that cellular and ER stress results in the cell death that we see. They are known as amyloid diseases, as they’re caused by the accumulation of amyloids in cells. We usually think of amyloids as being associated with Alzheimer’s, so you might think that they were a particular type of protein, but that’s not quite it. Instead, amyloids are protein delinquents: any protein that can form a beta sheet can become an amyloid. When a mutated protein misfolds, the side chains of amino acids (that dictate the specific fold) are no longer so important: the main chain of the polypeptide now causes these amyloid fibres to stick together. These amyloid fibres are formed regardless of the original folded protein structure (meaning that they form the same fibrous shape for every protein) and can penetrate the cells, causing cell stress and death. © 2013 Scientific American

Keyword: Alzheimers; Aggression
Link ID: 17964 - Posted: 03.28.2013

By Melissa Healy, Listening in on the electrical currents of teenagers’ brains during sleep, scientists have begun to hear the sound of growing maturity. It happens most intensively between the ages of 12 and 161 / 2: After years of frenzied fluctuation, the brain’s electrical output during the deepest phase of sleep — the delta, or slow-wave phase, when a child’s brain is undergoing its most restorative rest — becomes practically steady. That reduced fluctuation in electroencephalogram signals appears to coincide with what neuroscientists have described as major architectural changes in the brain that pave the way for cognitive maturity. While babies, toddlers and young children are taking in and making sense of the world, their brain cells are wiring themselves together willy-nilly, creating super-dense networks of interwoven neurons. But as we reach and progress through adolescence, neuroscientists have observed, a period of intensive “synaptic pruning” occurs in which those networks are thinned and the strongest and most evolutionarily useful remain. In a study published last week, scientists from the University of California at Davis say they believe the slowed fluctuations observed during the delta phase of teens’ sleep may be evidence of that pruning process at work. And since major mental illnesses such as schizophrenia appear to take root during adolescence, the authors of the study say the changing architecture of sleep may offer clues as to how and when mental illness sets in. © 1996-2013 The Washington Post

Keyword: Sleep; Aggression
Link ID: 17961 - Posted: 03.28.2013

By Bruce Bower Children with autism may understand more about how other people think than they’re usually given credit for. The trick to exposing this awareness, a new study finds, is to motivate these youngsters to show what they know. In a lab game that requires a child to compete with two adults for a prize, many kids with autism demonstrate insight into how other people’s thoughts shape their behavior, say psychologist Candida Peterson of the University of Queensland in Brisbane, Australia, and her colleagues. The finding suggests that previous research testing this ability, called theory of mind, underestimates how well youngsters with autism can interpret other people’s actions, Peterson’s team reports March 19 in Developmental Science. Studies published since 1985 have found that most high-functioning individuals with autism — those who have serious social and language problems but average or better IQs — fail a standard theory of mind test at least through adolescence. Kids without autism usually pass the test by age 5. In the standard test, called the Sally-Anne test, children watch an experimenter play with a doll named Sally, who has a covered basket, and a doll named Anne, who has a box. Sally puts a marble in her basket and leaves. Anne moves Sally’s marble to the box. Kids with autism usually indicate that, when Sally returns, she will look for her marble in the box, failing to recognize that Sally falsely believes the marble remains in her basket. © Society for Science & the Public 2000 - 2013

Keyword: Autism
Link ID: 17960 - Posted: 03.28.2013

A lack of a protein in Down's syndrome brains could be the cause of learning and memory problems, says a US study. Writing in Nature Medicine, Californian researchers found that the extra copy of chromosome 21 in people with the condition triggered the protein loss. Their study found restoring the protein in Down's syndrome mice improved cognitive function and behaviour. The Down's Syndrome Association said the study was interesting but the causes of Down's were very complex. Prof Huaxi Xu, senior author of the study from the Sanford-Burnham Medical Research Institute, said that in experiments on mice they discovered that the SNX27 protein was important for brain function and memory formation. Mice with less SNX27 had fewer active glutamate receptors and therefore had impaired learning and memory. The SNX27-deficient mice shared some characteristics with Down's syndrome, so the researchers looked at human brains with the condition. This confirmed their findings in the lab - that people with Down's syndrome also have significantly lower levels of SNX27. BBC © 2013

Keyword: Development of the Brain; Aggression
Link ID: 17945 - Posted: 03.25.2013

By Tina Hesman Saey Like many women with parents of the Mad Men generation, Susan Murphy grew up in a household full of cigarette smoke. Both dad and mom smoked heavily, even while Murphy was still in her mother’s womb. “That explains a lot,” Murphy quips, poking fun at herself. But Murphy isn’t worried about her own health. She’s fine. Her children aren’t, though. One boy died of cancer as a toddler. Another has autism. And her daughter has attention deficit disorder. Murphy knows the scientific evidence isn’t in yet, but she still can’t help wondering whether their fates might have been affected by her exposure to tobacco smoke before she was born. Murphy, a researcher at Duke University, studies links between a mother’s diet and chemical exposures during pregnancy with the child’s later health. She and others have established that the womb is the antithesis of Las Vegas; what happens there not only doesn’t stay there, it can influence a child’s health for life. Now, animal studies and a smattering of human data suggest such prenatal effects could reach farther down the family tree: The vices, virtues, inadvertent actions and accidental exposures of a pregnant mother may pose health consequences for her grandchildren and great-grandchildren, and perhaps even their offspring. Scientists have long known that radiation or certain chemicals can cause typos in a developing fetus’s genome — his or her genetic instruction book. Such mutations can get passed along to future generations in the DNA of sperm or egg cells. While exposure to sex hormones or a high-fat diet in the womb doesn’t directly change or damage DNA, those sorts of exposures can induce scribblings in the genome’s margins that can also be passed down. © Society for Science & the Public 2000 - 2013

Keyword: Epigenetics; Aggression
Link ID: 17934 - Posted: 03.23.2013