Chapter 7. Life-Span Development of the Brain and Behavior
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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
People with dementia who exercise improve their thinking abilities and everyday life, a body of medical research concludes. The Cochrane Collaboration carried out a systematic review of eight exercise trials involving more than 300 patients living at home or in care. Exercise did little for patients' moods, the research concluded. But it did help them carry out daily activities such as rising from a chair, and boosted their cognitive skills. Whether these benefits improve quality of life is still unclear, but the study authors say the findings are reason for optimism. Dementia affects some 800,000 people in the UK. And the number of people with the condition is steadily increasing because people are living longer. It is estimated that by 2021, the number of people with dementia in the UK will have increased to around one million. With no cure, ways to improve the lives of those living with the condition are vital. Researcher Dorothy Forbes, of the University of Alberta, and colleagues who carried out the Cochrane review, said: "Clearly, further research is needed to be able to develop best practice guidelines to enable healthcare providers to advise people with dementia living at home or in institutions. "We also need to understand what level and intensity of exercise is beneficial for someone with dementia." BBC © 2013
Link ID: 18999 - Posted: 12.05.2013
By James Gallagher Health and science reporter, BBC News The number of people living with dementia worldwide is set to treble by 2050, according to a new analysis. Alzheimer's Disease International says 44 million people live with the disease, but that figure will increase to 135 million by 2050. The figures were released ahead of the G8 dementia summit in London next week. In the UK, dementia research receives one eighth of the amount of funding that is spent on cancer, which charities say is insufficient. Alzheimer's Disease International expects increasing life expectancies to drive a surge in cases in poor and middle-income countries, particularly in South East Asia and Africa. Currently 38% of cases are in rich countries. But that balance is predicted shift significantly by 2050, with 71% of patients being in poor and middle-income countries. The report says most governments are "woefully unprepared for the dementia epidemic". Marc Wortmann, the executive director at Alzheimer Disease International, said: "It's a global epidemic and it is only getting worse - if we look into the future the numbers of elderly people will rise dramatically." Jeremy Hughes, chief executive of the UK's Alzheimer's Society, said: "Dementia is fast becoming the biggest health and social care challenge of this generation. "We must tackle dementia now, for those currently living with the condition across the world and for those millions who will develop dementia in the future. BBC © 2013
Link ID: 18998 - Posted: 12.05.2013
By PAM BELLUCK Scientists have been eager to see if oxytocin, which plays a role in emotional bonding, trust and many biological processes, can improve social behavior in people with autism. Some parents of children with autism have asked doctors to prescribe it, although it is not an approved treatment for autism, or have purchased lower-dose versions of the drug over the counter. Scientifically, the jury is out, and experts say parents should wait until more is known. Some studies suggest that oxytocin, sometimes called the “love hormone,” improves the ability to empathize and connect socially, and may decrease repetitive behaviors. Others find little or no impact, and some research suggests that it can promote clannish and competitive feelings, or exacerbate symptoms in people already oversensitive to social cues. Importantly, nobody knows if oxytocin is safe or desirable to use regularly or long term. Now, the first study of how oxytocin affects the brains of children with autism finds hints of promise — and also suggestions of what its limitations might be. On the promising side, the small study, published Monday in The Proceedings of the National Academy of Sciences, found that the hormone, given as an inhalant, generated increased activity in parts of the brain involved in social connection. This suggests not only that oxytocin can stimulate social brain areas, but also that in children with autism these brain regions are not irrevocably damaged but are plastic enough to be influenced. The limitations could include a finding that oxytocin prompted greater brain activity in children with the least severe autism. Some experts said that this could imply that oxytocin may work primarily in less-impaired people, but others said it might simply suggest that different doses are needed. © 2013 The New York Times Company
by Laura Sanders Last Sunday, the Giants battled the Redskins in our living room, and there was no bigger fan than 9-month-old Baby V. Unlike her father, she was not interested in RG3’s shortcomings. The tiny, colorful guys running around on a bright green field, the psychedelic special effects and the bursts of noise drew her in like a moth to a 42-inch high-definition flame. My friends with kids have noticed the same screen fascination in their little ones. Like adults, kids love colorful, shiny, moving screens. The problem, of course, is that watching TV probably isn’t the best way for little kids to spend their time. Long bouts in front of the tube have been linked to obesity, weaker attention spans and aggression in kids. Now, a new study of Japanese children has linked TV time with changes in the growing brains, effects that have been harder to spot. And the more television a kid watches, the more profound the brain differences, scientists report November 20 in Cerebral Cortex. Researchers studied kids between age 5 and 18 who watched between zero and four hours of television a day. On average, the kids watched TV for about two hours a day. Brain scans revealed that the more television a kid watched, the larger certain parts of the brain were. Gray matter volume was higher in regions toward the front and side of the head in kids who watched a lot of TV. Say that again? Watching television boosts brain volume? Before you rejoice and fire up Season 1 of Breaking Bad, keep in mind: Bigger isn’t always better. In this case, higher brain volume in these kids was associated with a lower verbal IQ. Study coauthor Hikaru Takeuchi Tohoku University in Japan says that these brain areas need to be pruned during childhood to operate efficiently. © Society for Science & the Public 2000 - 2013.
by Bob Holmes Dying cells may play only a small role in the brain decline that accompanies ageing. That is the suggestion from the first computer simulation of brain function that can solve intelligence tests almost as well as university undergraduates. The model promises to reveal how our brains and behaviour are affected by age, and might even offer a way of testing drugs that compensate for cognitive decline. Psychologists have known for many years that our ability to think through novel problems – our "fluid intelligence" – gradually declines with age. However, the reasons for this decline aren't clear, because many features of the brain change as we age: neurons die; connections become sparser between regions of the brain and between individual brain cells; and our mental representation of different concepts becomes less distinct, among other changes. So far, psychologists have been unable to tease apart these possible explanations for cognitive decline. Enter Chris Eliasmith, a theoretical neuroscientist at the University of Waterloo in Ontario, Canada, and his student Daniel Rasmussen. The pair used a computer to simulate the behaviour of about 35,000 individual brain cells wired together in a biologically realistic way. Just like a real brain, their model encoded information as a pattern of electrical activity in particular sets of cells. The researchers set up the system to solve a widely used intelligence test known as Raven's Progressive Matrices, which involves predicting what abstract symbol comes next in a sequence. © Copyright Reed Business Information Ltd.
By KRISTIN WARTMAN THE solution to one of America’s most vexing problems — our soaring rates of obesity and diet-related diseases — may have its roots in early childhood, and even in utero. Researchers at the Monell Chemical Senses Center, a nonprofit research organization in Philadelphia, have found that babies born to mothers who eat a diverse and varied diet while pregnant and breast-feeding are more open to a wide range of flavors. They’ve also found that babies who follow that diet after weaning carry those preferences into childhood and adulthood. Researchers believe that the taste preferences that develop at crucial periods in infancy have lasting effects for life. In fact, changing food preferences beyond toddlerhood appears to be extremely difficult. “What’s really interesting about children is, the preferences they form during the first years of life actually predict what they’ll eat later,” said Julie Mennella, a biopsychologist and researcher at the Monell Center. “Dietary patterns track from early to later childhood but once they are formed, once they get older, it’s really difficult to change — witness how hard it is to change the adult. You can, but it’s just harder. Where you start, is where you end up.” This may have profound implications for the future health of Americans. With some 70 percent of the United States population now overweight or obese and chronic diseases skyrocketing, many parents who are eating a diet high in processed, refined foods are feeding their babies as they feed themselves, and could be setting their children up for a lifetime of preferences for a narrow range of flavors. The Monell researchers have identified several sensitive periods for taste preference development. One is before three and a half months of age, which makes what the mother eats while pregnant and breast-feeding so important. “It’s our fundamental belief that during evolution, we as humans are exposed to flavors both in utero and via mother’s milk that are signals of things that will be in our diets as we grow up and learn about what flavors are acceptable based on those experiences,” said Gary Beauchamp, the director of the Monell Center. © 2013 The New York Times Company
Ewen Callaway Certain fears can be inherited through the generations, a provocative study of mice reports1. The authors suggest that a similar phenomenon could influence anxiety and addiction in humans. But some researchers are sceptical of the findings because a biological mechanism that explains the phenomenon has not been identified. According to convention, the genetic sequences contained in DNA are the only way to transmit biological information across generations. Random DNA mutations, when beneficial, enable organisms to adapt to changing conditions, but this process typically occurs slowly over many generations. Yet some studies have hinted that environmental factors can influence biology more rapidly through 'epigenetic' modifications, which alter the expression of genes, but not their actual nucleotide sequence. For instance, children who were conceived during a harsh wartime famine in the Netherlands in the 1940s are at increased risk of diabetes, heart disease and other conditions — possibly because of epigenetic alterations to genes involved in these diseases2. Yet although epigenetic modifications are known to be important for processes such as development and the inactivation of one copy of the X-chromsome in females, their role in the inheritance of behaviour is still controversial. Kerry Ressler, a neurobiologist and psychiatrist at Emory University in Atlanta, Georgia, and a co-author of the latest study, became interested in epigenetic inheritance after working with poor people living in inner cities, where cycles of drug addiction, neuropsychiatric illness and other problems often seem to recur in parents and their children. “There are a lot of anecdotes to suggest that there’s intergenerational transfer of risk, and that it’s hard to break that cycle,” he says. © 2013 Nature Publishing Group
by Jessica Griggs HAVING type 2 diabetes may mean you are already on the path to Alzheimer's. This startling claim comes from a study linking the two diseases more intimately than ever before. There is some good news: the same research also offers a way to reverse memory problems associated with diabetes – albeit in rats – which may hint at a new treatment for Alzheimer's. "Perhaps you should use Alzheimer's drugs at the diabetes stage to prevent cognitive impairment in the first place," says Ewan McNay from the University at Albany in New York. Alzheimer's cost the US $130 billion in 2011 alone. One of the biggest risk factors is having type 2 diabetes. This kind of diabetes occurs when liver, muscle and fat cells stop responding efficiently to insulin, the hormone that tells them to absorb glucose from the blood. The illness is usually triggered by eating too many sugary and high-fat foods that cause insulin to spike, desensitising cells to its presence. As well as causing obesity, insulin resistance can also lead to cognitive problems such as memory loss and confusion. In 2005, a study by Susanne de la Monte's group at Brown University in Providence, Rhode Island, identified a reason why people with type 2 diabetes had a higher risk of developing Alzheimer's. In this kind of dementia, the hippocampus, a part of the brain involved in learning and memory, seemed to be insensitive to insulin. Not only could your liver, muscle and fat cells be "diabetic" but so it seemed, could your brain. © Copyright Reed Business Information Ltd.
By Tanya Lewis 20 hours ago To understand the human brain, scientists must start small, and what better place than the mind of a worm? The roundworm Caenorhabditis elegans is one of biology's most widely studied organisms, and it's the first to have the complete wiring diagram, or connectome, of its nervous system mapped out. Knowing the structure of the animal's connectome will help explain its behavior, and could lead to insights about the brains of other organisms, scientists say. "You can't understand the brain without understanding the connectome," Scott Emmons, a molecular geneticist at Albert Einstein College of Medicine of Yeshiva University in New York, said in a talk earlier this month at the annual meeting of the Society for Neuroscience in San Diego. In 1963, South African biologist Sydney Brenner of the University of Cambridge decided to use C. elegans as a model organism for developmental biology. He chose the roundworm because it has a simple nervous system, it's easy to grow in a lab and its genetics are relatively straightforward. C. elegans was the first multicellular organism to have its genome sequenced, in 1998. Brenner knew that to understand how genes affect behavior, "you would have to know the structure of the nervous system," Emmons told LiveScience.